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Vitamin D

Master Evidence Library

Explore human trials, animal models, reviews and one human-cell study. Read the findings beside their limitations, then follow the original publication.

Browse 48 records →
Conceptual research notebook and magnifying glass; decorative charts are not study data
48 publications · 24 fields · one transparent collection

What This Collection Contains

22Human studies
14Animal studies
11Reviews & meta-analyses
1Human cell experiments

The supplied workbook contains 44 records. Four targeted additions cover the direct senescence-marker trial, two contrasting telomere analyses and primary human-macrophage evidence. Publication counts are not independent-trial or participant counts.

Read each evidence type differently. Reviews share underlying trials; animal and cell experiments support mechanisms, not human clinical benefit. “Positive” describes a reported outcome, not study quality or a recommendation.

Master Evidence

Start with the human studies

Trials test outcomes in people. Look at who participated and what was actually measured.

Understand the mechanism

Cell and animal experiments explain pathways; they do not establish a benefit in people.

Keep aging claims in perspective

A changed biomarker is a finding to investigate, not proof of immune rejuvenation.

48 records

Human studiesH01 · 2009

Li-Ng et al., 2009

Epidemiology and infection

What the study found

No reduction in URI incidence, duration, or severity despite increased 25(OH)D.

Limits: Winter trial; baseline vitamin D status generally not severely deficient.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H01
IDH01
CitationLi-Ng et al., 2009
Year2009
JournalEpidemiology and infection
Evidence ClassHuman RCT
Study DesignRandomized, placebo-controlled
Research AreaRespiratory infection
Population / ModelAdults
N162
Baseline 25(OH)D~63–64 nmol/L
Vitamin D FormVitamin D3
Dose / Regimen2,000 IU/day
Duration12 weeks
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)Symptomatic URI incidence, duration, severity
Main FindingNo reduction in URI incidence, duration, or severity despite increased 25(OH)D.
Key Statistical ResultURI 48 vs 50; P=0.57; duration P=0.86
Evidence DirectionNeutral / Negative
Key Limitations / NotesWinter trial; baseline vitamin D status generally not severely deficient.
PMID19296870
DOI10.1017/S0950268809002404
PubMed / Source URLPubMed ↗
ImmuneForward UseQualifies claims that supplementation prevents respiratory infections.
Human studiesH02 · 2010

Urashima et al., 2010

The American journal of clinical nutrition

What the study found

Lower incidence of influenza A in vitamin D group.

Limits: Specific pediatric population and influenza season; outcome-specific.

PubMed ↗DOI ↗Positive outcomes
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H02
IDH02
CitationUrashima et al., 2010
Year2010
JournalThe American journal of clinical nutrition
Evidence ClassHuman RCT
Study DesignRandomized, double-blind, placebo-controlled
Research AreaInfluenza
Population / ModelSchoolchildren
N334
Baseline 25(OH)DNot extracted
Vitamin D FormVitamin D3
Dose / Regimen1,200 IU/day
DurationDec 2008–Mar 2009
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)Laboratory/physician-diagnosed influenza A
Main FindingLower incidence of influenza A in vitamin D group.
Key Statistical Result10.8% vs 18.6%; RR 0.58 (95% CI 0.34–0.99); P=0.04
Evidence DirectionPositive
Key Limitations / NotesSpecific pediatric population and influenza season; outcome-specific.
PMID20219962
DOI10.3945/ajcn.2009.29094
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports possible infection-specific benefit in children.
Human studiesH03 · 2010

Laaksi et al., 2010

The Journal of infectious diseases

What the study found

Trial tested vitamin D for prevention of ARTI in young men; include in respiratory RCT evidence base.

Limits: PubMed metadata verified; no abstract available in the retrieved record. Full numerical extraction requires primary-article review before claim-level use.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H03
IDH03
CitationLaaksi et al., 2010
Year2010
JournalThe Journal of infectious diseases
Evidence ClassHuman RCT
Study DesignRandomized, double-blind
Research AreaRespiratory infection
Population / ModelYoung Finnish men
NNot extracted
Baseline 25(OH)DNot extracted
Vitamin D FormVitamin D3
Dose / RegimenDaily supplementation
DurationWinter study
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)Acute respiratory tract infection
Main FindingTrial tested vitamin D for prevention of ARTI in young men; include in respiratory RCT evidence base.
Key Statistical ResultSee primary publication
Evidence DirectionMixed / requires full extraction
Key Limitations / NotesPubMed metadata verified; no abstract available in the retrieved record. Full numerical extraction requires primary-article review before claim-level use.
PMID20632889
DOI10.1086/654881
PubMed / Source URLPubMed ↗
ImmuneForward UseRespiratory-infection RCT evidence.
Human studiesH04 · 2012

Camargo et al., 2012

Pediatrics

What the study found

Vitamin D-fortified milk reduced reported ARIs.

Limits: Subset of larger cluster trial; very low baseline 25(OH)D; parent-reported outcome.

PubMed ↗DOI ↗Positive outcomes
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H04
IDH04
CitationCamargo et al., 2012
Year2012
JournalPediatrics
Evidence ClassHuman RCT
Study DesignCluster randomized, double-blind comparison
Research AreaRespiratory infection
Population / ModelMongolian schoolchildren with marked vitamin D deficiency
N247
Baseline 25(OH)DMedian 7 ng/mL
Vitamin D FormVitamin D3
Dose / Regimen300 IU/day in fortified milk
Duration~3 months winter
ComparatorUnfortified milk
Immune Endpoint(s)—
Clinical Endpoint(s)Parent-reported ARI
Main FindingVitamin D-fortified milk reduced reported ARIs.
Key Statistical ResultRate ratio 0.52 (95% CI 0.31–0.89); adjusted RR 0.50 (0.28–0.88)
Evidence DirectionPositive
Key Limitations / NotesSubset of larger cluster trial; very low baseline 25(OH)D; parent-reported outcome.
PMID22908115
DOI10.1542/peds.2011-3029
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports benefit in severely deficient children.
Human studiesH05 · 2012

Murdoch et al., 2012 (VIDARIS)

JAMA

What the study found

High-dose monthly vitamin D did not reduce incidence or severity of URTIs.

Limits: Bolus regimen; participants not markedly deficient at baseline.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H05
IDH05
CitationMurdoch et al., 2012 (VIDARIS)
Year2012
JournalJAMA
Evidence ClassHuman RCT
Study DesignRandomized, double-blind, placebo-controlled
Research AreaRespiratory infection
Population / ModelHealthy adults
N322
Baseline 25(OH)DMean 29 ng/mL
Vitamin D FormVitamin D3
Dose / Regimen200,000 IU initial + 200,000 IU at 1 month, then 100,000 IU monthly
Duration18 months
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)URTI incidence, duration, severity, missed work
Main FindingHigh-dose monthly vitamin D did not reduce incidence or severity of URTIs.
Key Statistical ResultRR 0.97 (95% CI 0.85–1.11) for URTIs/person
Evidence DirectionNeutral / Negative
Key Limitations / NotesBolus regimen; participants not markedly deficient at baseline.
PMID23032549
DOI10.1001/jama.2012.12505
PubMed / Source URLPubMed ↗
ImmuneForward UseStrong negative evidence for intermittent high-dose supplementation.
Human studiesH06 · 2012

Bergman et al., 2012

BMJ open

What the study found

Daily vitamin D produced favorable infection-related outcomes in a selected high-risk population.

Limits: Selected clinical population; not generalizable to healthy adults.

PubMed ↗DOI ↗Positive outcomes
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H06
IDH06
CitationBergman et al., 2012
Year2012
JournalBMJ open
Evidence ClassHuman RCT
Study DesignRandomized, double-blind, placebo-controlled
Research AreaRespiratory infection
Population / ModelAdults with frequent RTIs and/or antibody deficiency
N140
Baseline 25(OH)DNot extracted
Vitamin D FormVitamin D3
Dose / Regimen4,000 IU/day
Duration1 year
ComparatorPlacebo
Immune Endpoint(s)Antimicrobial/immune context
Clinical Endpoint(s)Infectious symptoms, antibiotic use
Main FindingDaily vitamin D produced favorable infection-related outcomes in a selected high-risk population.
Key Statistical ResultSee primary publication
Evidence DirectionPositive
Key Limitations / NotesSelected clinical population; not generalizable to healthy adults.
PMID23242238
DOI10.1136/bmjopen-2012-001663
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports possible benefit in selected high-risk patients.
Human studiesH07 · 2013

Rees et al., 2013

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America

What the study found

No significant reduction in winter URTI, colds, or influenza-like illness.

Limits: Respiratory outcomes were secondary; diary subset n=759.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H07
IDH07
CitationRees et al., 2013
Year2013
JournalClinical infectious diseases : an official publication of the Infectious Diseases Society of America
Evidence ClassHuman RCT
Study DesignRandomized controlled trial / secondary infection analysis
Research AreaRespiratory infection
Population / ModelAdults aged 45–75 with prior colorectal adenoma
N2259
Baseline 25(OH)D≥12 ng/mL
Vitamin D FormVitamin D3
Dose / Regimen1,000 IU/day
DurationMulti-year parent trial
ComparatorPlacebo / calcium factorial
Immune Endpoint(s)—
Clinical Endpoint(s)Winter URTI, colds, influenza-like illness
Main FindingNo significant reduction in winter URTI, colds, or influenza-like illness.
Key Statistical ResultURTI RR 0.93 (95% CI 0.79–1.09)
Evidence DirectionNeutral / Negative
Key Limitations / NotesRespiratory outcomes were secondary; diary subset n=759.
PMID24014734
DOI10.1093/cid/cit549
PubMed / Source URLPubMed ↗
ImmuneForward UseNegative evidence in generally healthy midlife/older adults.
Human studiesH08 · 2014

Goodall et al., 2014

BMC infectious diseases

What the study found

Clinical URTI reduction was not statistically significant, but laboratory-confirmed URTI was lower with vitamin D.

Limits: Factorial trial also tested gargling; completion varied.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H08
IDH08
CitationGoodall et al., 2014
Year2014
JournalBMC infectious diseases
Evidence ClassHuman RCT
Study DesignRandomized controlled trial
Research AreaRespiratory infection
Population / ModelUniversity students
N600
Baseline 25(OH)DNot extracted
Vitamin D FormVitamin D3
Dose / RegimenNot extracted
DurationNot extracted
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)Clinical and laboratory-confirmed URTI
Main FindingClinical URTI reduction was not statistically significant, but laboratory-confirmed URTI was lower with vitamin D.
Key Statistical ResultClinical RR 0.79 (95% CI 0.61–1.03); lab-confirmed RR 0.54 (0.34–0.84)
Evidence DirectionMixed / Positive for lab-confirmed endpoint
Key Limitations / NotesFactorial trial also tested gargling; completion varied.
PMID24885201
DOI10.1186/1471-2334-14-273
PubMed / Source URLPubMed ↗
ImmuneForward UseShows endpoint-dependent respiratory findings.
Human studiesH09 · 2014

Urashima et al., 2014

Food & function

What the study found

No reduction in influenza A incidence.

Limits: Specific pandemic season; contrasts with earlier pediatric influenza trial.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H09
IDH09
CitationUrashima et al., 2014
Year2014
JournalFood & function
Evidence ClassHuman RCT
Study DesignRandomized, double-blind, placebo-controlled
Research AreaInfluenza
Population / ModelJapanese high-school students
N247
Baseline 25(OH)DNot extracted
Vitamin D FormVitamin D3
Dose / Regimen2,000 IU/day
Duration2 months
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)Influenza A during 2009 H1N1 pandemic
Main FindingNo reduction in influenza A incidence.
Key Statistical Result13.5% vs 12.1%
Evidence DirectionNeutral / Negative
Key Limitations / NotesSpecific pandemic season; contrasts with earlier pediatric influenza trial.
PMID25088394
DOI10.1039/c4fo00371c
PubMed / Source URLPubMed ↗
ImmuneForward UseBalances positive influenza findings.
Human studiesH10 · 2015

Grant et al., 2015

Acta paediatrica (Oslo, Norway : 1992)

What the study found

Vitamin D supplementation was associated with reduced primary-care respiratory infection visits in the trial follow-up.

Limits: Maternal/infant intervention; population and dosing differ from adult supplementation.

PubMed ↗DOI ↗Positive outcomes
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H10
IDH10
CitationGrant et al., 2015
Year2015
JournalActa paediatrica (Oslo, Norway : 1992)
Evidence ClassHuman RCT
Study DesignRandomized, double-blind, placebo-controlled
Research AreaRespiratory infection
Population / ModelPregnancy/infancy supplementation cohort
NNot extracted
Baseline 25(OH)DNot extracted
Vitamin D FormVitamin D3
Dose / RegimenPregnancy and infancy dosing arms
DurationInfancy follow-up
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)Primary-care ARI visits
Main FindingVitamin D supplementation was associated with reduced primary-care respiratory infection visits in the trial follow-up.
Key Statistical ResultSee primary publication
Evidence DirectionPositive
Key Limitations / NotesMaternal/infant intervention; population and dosing differ from adult supplementation.
PMID25283480
DOI10.1111/apa.12819
PubMed / Source URLPubMed ↗
ImmuneForward UsePediatric/perinatal respiratory evidence.
Human studiesH11 · 2016

Konijeti et al., 2016

The Journal of clinical endocrinology and metabolism

What the study found

Higher-dose vitamin D reduced stimulated CD4+ T-cell ATP release versus the lower dose; this is immune modulation, not enhanced protection.

Limits: Small ancillary study; low-dose active comparator rather than placebo.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H11
IDH11
CitationKonijeti et al., 2016
Year2016
JournalThe Journal of clinical endocrinology and metabolism
Evidence ClassHuman RCT / ancillary
Study DesignDouble-blind randomized dose comparison
Research AreaT-cell function
Population / ModelVitamin-D-deficient adults with untreated pre/early hypertension
N38
Baseline 25(OH)DVitamin D deficient
Vitamin D FormVitamin D3
Dose / Regimen400 vs 4,000 IU/day
Duration6 months; immune endpoint at 2 months
ComparatorLow-dose vitamin D
Immune Endpoint(s)CD4+ T-cell activation / intracellular ATP after stimulation
Clinical Endpoint(s)Not measured as a clinical outcome
Main FindingHigher-dose vitamin D reduced stimulated CD4+ T-cell ATP release versus the lower dose; this is immune modulation, not enhanced protection.
Key Statistical Result38 participants; immune testing at 2 months; OR 3.43 for lower ATP release. The abstract confidence interval appears typographically inconsistent and is not reproduced.
Evidence DirectionMechanistically Positive
Key Limitations / NotesSmall ancillary study; low-dose active comparator rather than placebo.
PMID26653112
DOI10.1210/jc.2015-3599
PubMed / Source URLPubMed ↗
ImmuneForward UseDirect human evidence that supplementation can modulate T-cell function.
Human studiesH12 · 2016

Sharifi et al., 2016

Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association

What the study found

Vitamin D increased cathelicidin gene expression and reduced hs-CRP and ESR versus placebo.

Limits: Disease-specific population; very large bolus; not evidence of general immune benefit.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H12
IDH12
CitationSharifi et al., 2016
Year2016
JournalSaudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association
Evidence ClassHuman RCT
Study DesignRandomized placebo-controlled
Research AreaCathelicidin / inflammation
Population / ModelUlcerative colitis patients in remission
N90
Baseline 25(OH)DNot extracted
Vitamin D FormVitamin D
Dose / Regimen300,000 IU intramuscular once
Duration90 days
ComparatorSaline placebo
Immune Endpoint(s)Cathelicidin hCAP18 expression, hs-CRP, ESR
Clinical Endpoint(s)Inflammatory biomarkers
Main FindingVitamin D increased cathelicidin gene expression and reduced hs-CRP and ESR versus placebo.
Key Statistical Resulths-CRP P=0.023; ESR P<0.001; hCAP18 increased
Evidence DirectionPositive mechanistic
Key Limitations / NotesDisease-specific population; very large bolus; not evidence of general immune benefit.
PMID27488327
DOI10.4103/1319-3767.187606
PubMed / Source URLPubMed ↗
ImmuneForward UseMechanistic human evidence for antimicrobial peptide/inflammation pathways.
Human studiesH13 · 2019

Loeb et al. / Vietnam trial, 2019

Influenza and other respiratory viruses

What the study found

No reduction in influenza; moderate reduction in non-influenza respiratory viral infection and all respiratory viruses combined.

Limits: Benefit depended on virologic endpoint; baseline vitamin D not severely low.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H13
IDH13
CitationLoeb et al. / Vietnam trial, 2019
Year2019
JournalInfluenza and other respiratory viruses
Evidence ClassHuman RCT
Study DesignRandomized, placebo-controlled
Research AreaRespiratory viral infection
Population / ModelChildren and adolescents in Vietnam
N1300
Baseline 25(OH)D~65 nmol/L
Vitamin D FormVitamin D
Dose / RegimenTrial supplementation
DurationNot extracted
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)RT-PCR influenza and non-influenza respiratory viruses
Main FindingNo reduction in influenza; moderate reduction in non-influenza respiratory viral infection and all respiratory viruses combined.
Key Statistical ResultInfluenza HR 1.18 (0.79–1.78); non-influenza HR 0.76 (0.61–0.94); all viruses HR 0.81 (0.66–0.99)
Evidence DirectionMixed
Key Limitations / NotesBenefit depended on virologic endpoint; baseline vitamin D not severely low.
PMID30328294
DOI10.1111/irv.12615
PubMed / Source URLPubMed ↗
ImmuneForward UseDemonstrates pathogen-specific heterogeneity.
Human studiesH14 · 2020

Ganmaa et al., 2020

The New England journal of medicine

What the study found

Vitamin D substantially raised 25(OH)D but did not reduce tuberculosis infection, TB disease, or ARI hospitalization.

Limits: Large, long-duration trial; highly relevant negative evidence despite correction of deficiency.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H14
IDH14
CitationGanmaa et al., 2020
Year2020
JournalThe New England journal of medicine
Evidence ClassHuman RCT
Study DesignRandomized, double-blind, placebo-controlled
Research AreaTuberculosis / respiratory infection
Population / ModelVitamin-D-deficient Mongolian schoolchildren
N~8,800
Baseline 25(OH)DDeficient
Vitamin D FormVitamin D3
Dose / RegimenWeekly supplementation
Duration3 years
ComparatorPlacebo
Immune Endpoint(s)TB infection (QFT)
Clinical Endpoint(s)TB infection/disease; ARI hospitalization
Main FindingVitamin D substantially raised 25(OH)D but did not reduce tuberculosis infection, TB disease, or ARI hospitalization.
Key Statistical ResultQFT adjusted RR 1.10 (0.87–1.38); TB disease RR 0.87 (0.49–1.55)
Evidence DirectionNeutral / Negative
Key Limitations / NotesLarge, long-duration trial; highly relevant negative evidence despite correction of deficiency.
PMID32706534
DOI10.1056/NEJMoa1915176
PubMed / Source URLPubMed ↗
ImmuneForward UseStrong negative evidence for TB prevention.
Human studiesH15 · 2022

Jolliffe et al., 2022 (CORONAVIT)

BMJ (Clinical research ed.)

What the study found

Test-and-treat vitamin D strategy did not establish prevention of all-cause ARI or COVID-19.

Limits: Open-label; intervention was an offer/test-and-treat strategy rather than simple blinded supplementation.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H15
IDH15
CitationJolliffe et al., 2022 (CORONAVIT)
Year2022
JournalBMJ (Clinical research ed.)
Evidence ClassHuman RCT
Study DesignPhase 3 open-label randomized controlled trial
Research AreaRespiratory infection / COVID-19
Population / ModelUK adults ≥16 years
N6200
Baseline 25(OH)DTest-and-treat threshold <75 nmol/L
Vitamin D FormVitamin D3
Dose / Regimen800 or 3,200 IU/day when <75 nmol/L
Duration6 months
ComparatorNo offer of testing/supplementation
Immune Endpoint(s)—
Clinical Endpoint(s)All-cause ARI and COVID-19
Main FindingTest-and-treat vitamin D strategy did not establish prevention of all-cause ARI or COVID-19.
Key Statistical ResultSee primary publication
Evidence DirectionNeutral / Negative
Key Limitations / NotesOpen-label; intervention was an offer/test-and-treat strategy rather than simple blinded supplementation.
PMID36215226
DOI10.1136/bmj-2022-071230
PubMed / Source URLPubMed ↗
ImmuneForward UseLarge modern trial relevant to ARI/COVID prevention.
Human studiesH16 · 2022

Jolliffe et al., 2022 (CORONAVIT vaccine substudy)

Nutrients

What the study found

Supplementation raised 25(OH)D but did not improve vaccine immunogenicity or efficacy.

Limits: Nested substudies; SARS-CoV-2 vaccines specifically.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H16
IDH16
CitationJolliffe et al., 2022 (CORONAVIT vaccine substudy)
Year2022
JournalNutrients
Evidence ClassHuman RCT substudy
Study DesignNested randomized trial substudies
Research AreaVaccination
Population / ModelUK adults with suboptimal vitamin D status
N2808 / 1853 / 100 across substudies
Baseline 25(OH)D<75 nmol/L entry criterion
Vitamin D FormVitamin D3
Dose / Regimen800 or 3,200 IU/day
DurationDuring vaccination follow-up
ComparatorNo offer
Immune Endpoint(s)Anti-Spike IgGAM, neutralizing antibodies, IFN-γ cellular response
Clinical Endpoint(s)Breakthrough SARS-CoV-2 infection
Main FindingSupplementation raised 25(OH)D but did not improve vaccine immunogenicity or efficacy.
Key Statistical ResultBreakthrough aHR 1.28 and 1.17 vs no offer; no antibody/IFN-γ benefit
Evidence DirectionNeutral / Negative
Key Limitations / NotesNested substudies; SARS-CoV-2 vaccines specifically.
PMID36145196
DOI10.3390/nu14183821
PubMed / Source URLPubMed ↗
ImmuneForward UseStrong negative evidence against routine vitamin D to boost SARS-CoV-2 vaccine response.
Human studiesH17 · 2024

Camargo et al., 2024 (VITAL URI analysis)

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America

What the study found

Daily vitamin D3 did not significantly lower self-reported recent upper respiratory infection risk in older adults.

Limits: Predominantly vitamin-D-sufficient population; URI self-report.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H17
IDH17
CitationCamargo et al., 2024 (VITAL URI analysis)
Year2024
JournalClinical infectious diseases : an official publication of the Infectious Diseases Society of America
Evidence ClassHuman RCT
Study DesignPrespecified analysis of randomized placebo-controlled trial
Research AreaRespiratory infection
Population / ModelGenerally healthy older adults
N15,804
Baseline 25(OH)DMean 31 ng/mL; 2.4% <12 ng/mL
Vitamin D FormVitamin D3
Dose / Regimen2,000 IU/day
Duration1 year primary URI analysis
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)Self-reported recent URI
Main FindingDaily vitamin D3 did not significantly lower self-reported recent upper respiratory infection risk in older adults.
Key Statistical ResultOR 0.96 (95% CI 0.86–1.06); primary endpoint at 1 year.
Evidence DirectionNeutral / Negative
Key Limitations / NotesPredominantly vitamin-D-sufficient population; URI self-report.
PMID38113446
DOI10.1093/cid/ciad770
PubMed / Source URLPubMed ↗
ImmuneForward UseLarge daily-dose trial in older adults.
Human studiesH18 · 2024

A. Laaksi et al., 2024

Open forum infectious diseases

What the study found

Supplementation had no effect on ARI or days off; baseline insufficiency was associated with more ARI and lower cathelicidin.

Limits: Important distinction between association and supplementation effect.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H18
IDH18
CitationA. Laaksi et al., 2024
Year2024
JournalOpen forum infectious diseases
Evidence ClassHuman RCT + observational follow-up
Study DesignRandomized placebo-controlled
Research AreaRespiratory infection / cathelicidin
Population / ModelYoung men; follow-up cohort 412
NRCT N not extracted; cohort 412
Baseline 25(OH)DInsufficiency defined <50 nmol/L
Vitamin D FormVitamin D3
Dose / Regimen20 µg/day (800 IU/day)
Duration14 weeks
ComparatorPlacebo
Immune Endpoint(s)Cathelicidin
Clinical Endpoint(s)ARI and days off
Main FindingSupplementation had no effect on ARI or days off; baseline insufficiency was associated with more ARI and lower cathelicidin.
Key Statistical ResultBaseline insufficiency ARI OR 2.1 (1.2–3.7); supplementation null
Evidence DirectionMixed: RCT neutral, observational association
Key Limitations / NotesImportant distinction between association and supplementation effect.
PMID39301110
DOI10.1093/ofid/ofae482
PubMed / Source URLPubMed ↗
ImmuneForward UseExcellent example of observational association not translating into RCT benefit.
Human studiesH19 · 2025

Clerico et al., 2025

European journal of nutrition

What the study found

Fewer days with acute respiratory infection and with febrile respiratory infection; no difference in other measured outcomes.

Limits: Secondary analysis of a factorial Danish trial; generally vitamin-D-replete, white children aged 6–8; illness reported by parents. This measures sick days, not universal infection prevention.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · H19
IDH19
CitationClerico et al., 2025
Year2025
JournalEuropean journal of nutrition
Evidence ClassHuman RCT
Study DesignRandomized clinical trial
Research AreaRespiratory infection
Population / ModelChildren aged 6–8 years
N200 randomized; 189 with complete infection questionnaires
Baseline 25(OH)D79.8 ± 17.2 nmol/L
Vitamin D FormVitamin D
Dose / Regimen20 µg/day (800 IU/day) vitamin D3
Duration24 weeks
ComparatorControl
Immune Endpoint(s)—
Clinical Endpoint(s)Acute respiratory tract infections
Main FindingFewer days with acute respiratory infection and with febrile respiratory infection; no difference in other measured outcomes.
Key Statistical ResultSick days RR 0.83 (95% CI 0.76–0.90); febrile sick days RR 0.57 (0.48–0.67); both P<0.001.
Evidence DirectionMixed / Positive
Key Limitations / NotesSecondary analysis of a factorial Danish trial; generally vitamin-D-replete, white children aged 6–8; illness reported by parents. This measures sick days, not universal infection prevention.
PMID40310565
DOI10.1007/s00394-025-03674-1
PubMed / Source URLPubMed ↗
ImmuneForward UseRecent pediatric RCT.
Human studiesH20 · 2025 · Added source

Rastgoo et al., 2025

Frontiers in Immunology

What the study found

5,000 IU/day reduced selected PBMC senescence-associated markers versus 1,000 IU/day; some NAC combinations also changed markers. Serum IL-6, CRP and NLR did not differ significantly between groups.

Limits: Short biomarker trial with active comparators; does not establish whole-system immune rejuvenation. 5,000 IU/day exceeds the usual adult upper intake level. Corrigendum PMID 40510343 corrects a 50,000/5,000 IU table-label typo.

PubMed ↗DOI ↗Mechanism / biomarker
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Complete study record · H20
IDH20
CitationRastgoo et al., 2025
Year2025
JournalFrontiers in Immunology
Evidence ClassHuman RCT
Study DesignRandomized, double-blind, four active-treatment groups
Research AreaImmune aging / cellular senescence
Population / ModelVitamin-D-deficient older adults in Iran
N88; 22 per group
Baseline 25(OH)DVitamin D deficient
Vitamin D FormVitamin D
Dose / Regimen1,000 or 5,000 IU/day, with or without NAC 600 mg/day
Duration8 weeks
Comparator1,000 IU/day vitamin D; no untreated placebo
Immune Endpoint(s)PBMC p16, p21, IL6, TNF; SA-β-gal activity; serum IL-6, CRP, NLR
Clinical Endpoint(s)No clinical infection or vaccine outcome
Main Finding5,000 IU/day reduced selected PBMC senescence-associated markers versus 1,000 IU/day; some NAC combinations also changed markers. Serum IL-6, CRP and NLR did not differ significantly between groups.
Key Statistical Result88 completed; p21 changes were not significant. See corrected full text for endpoint-specific tests.
Evidence DirectionPositive mechanistic
Key Limitations / NotesShort biomarker trial with active comparators; does not establish whole-system immune rejuvenation. 5,000 IU/day exceeds the usual adult upper intake level. Corrigendum PMID 40510343 corrects a 50,000/5,000 IU table-label typo.
PMID40421021
DOI10.3389/fimmu.2025.1570441
PubMed / Source URLPubMed ↗
ImmuneForward UseDirect but preliminary human immune-aging-marker evidence from the supplied ImmAge document.
Human studiesH21 · 2025 · Added source

Zhu et al., 2025 (VITAL telomere substudy)

American Journal of Clinical Nutrition

What the study found

Vitamin D reduced leukocyte telomere attrition compared with placebo. This biomarker result does not establish immune rejuvenation.

Limits: Ancillary analysis; telomere measurement is not a clinical immunity outcome; differs from the negative monthly-dose D-Health study.

PubMed ↗DOI ↗Mechanism / biomarker
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Complete study record · H21
IDH21
CitationZhu et al., 2025 (VITAL telomere substudy)
Year2025
JournalAmerican Journal of Clinical Nutrition
Evidence ClassHuman RCT substudy
Study DesignAncillary study of a randomized double-blind factorial trial
Research AreaAging biomarkers / telomeres
Population / ModelUS men ≥50 and women ≥55 years
N1,031 participants with telomere measurements
Baseline 25(OH)DNot selected for deficiency
Vitamin D FormVitamin D3
Dose / Regimen2,000 IU/day
Duration4 years
ComparatorPlacebo
Immune Endpoint(s)Leukocyte telomere length
Clinical Endpoint(s)No direct immune-function or infection endpoint in this analysis
Main FindingVitamin D reduced leukocyte telomere attrition compared with placebo. This biomarker result does not establish immune rejuvenation.
Key Statistical ResultBetween-group difference in attrition 0.14 kb (95% CI 0.007–0.27), P=0.039.
Evidence DirectionPositive biomarker
Key Limitations / NotesAncillary analysis; telomere measurement is not a clinical immunity outcome; differs from the negative monthly-dose D-Health study.
PMID40409468
DOI10.1016/j.ajcnut.2025.05.003
PubMed / Source URLPubMed ↗
ImmuneForward UseAdds aging-biomarker context without claiming a younger immune system.
Human studiesH22 · 2023 · Added source

Rahman et al., 2023 (D-Health telomere substudy)

The Journal of Nutrition, Health & Aging

What the study found

Monthly supplementation did not change relative telomere length.

Limits: No baseline telomere change measurement in this comparison; monthly regimen and population differ from VITAL.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

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Complete study record · H22
IDH22
CitationRahman et al., 2023 (D-Health telomere substudy)
Year2023
JournalThe Journal of Nutrition, Health & Aging
Evidence ClassHuman RCT substudy
Study DesignAncillary analysis of randomized double-blind trial
Research AreaAging biomarkers / telomeres
Population / ModelAustralian adults aged 60–84 years, largely vitamin D replete
N1,519
Baseline 25(OH)DLargely vitamin D replete
Vitamin D FormVitamin D3
Dose / Regimen60,000 IU monthly
DurationTelomeres measured 4 or 5 years after randomization
ComparatorPlacebo
Immune Endpoint(s)Relative leukocyte telomere length
Clinical Endpoint(s)No immune-function endpoint in this analysis
Main FindingMonthly supplementation did not change relative telomere length.
Key Statistical ResultAdjusted T/S-ratio difference −0.001 (95% CI −0.02 to 0.02).
Evidence DirectionNeutral / Negative
Key Limitations / NotesNo baseline telomere change measurement in this comparison; monthly regimen and population differ from VITAL.
PMID37702332
DOI10.1007/s12603-023-1948-3
PubMed / Source URLPubMed ↗
ImmuneForward UseBalances positive VITAL biomarker evidence.
Animal studiesA01 · 2009

Bruce et al., 2009

International immunology

What the study found

VDR-KO mice cleared primary and secondary Listeria infections, with somewhat delayed kinetics; old VDR-KO mice had fewer memory T cells but elevated nonspecific cytokine/antibody responses.

Limits: Important aging model: amplified immune responses did not translate into better pathogen clearance.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

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Complete study record · A01
IDA01
CitationBruce et al., 2009
Year2009
JournalInternational immunology
Evidence ClassAnimal Study
Study DesignVDR knockout infection model; young and old mice
Research AreaImmune aging / Listeria infection
Population / ModelYoung and old VDR-KO and WT mice
NNot extracted
Baseline 25(OH)DN/A
Vitamin D FormVDR genetic deletion
Dose / RegimenVDR knockout
DurationPrimary and secondary infection
ComparatorWild-type controls
Immune Endpoint(s)Memory T cells, cytokines, antibodies
Clinical Endpoint(s)Listeria monocytogenes clearance
Main FindingVDR-KO mice cleared primary and secondary Listeria infections, with somewhat delayed kinetics; old VDR-KO mice had fewer memory T cells but elevated nonspecific cytokine/antibody responses.
Key Statistical ResultComplete clearance despite altered immune phenotype
Evidence DirectionMixed / Mechanistic
Key Limitations / NotesImportant aging model: amplified immune responses did not translate into better pathogen clearance.
PMID19088060
DOI10.1093/intimm/dxn129
PubMed / Source URLPubMed ↗
ImmuneForward UseShows VDR effects on immune aging and regulation without simple loss of antimicrobial competence.
Animal studiesA02 · 2001

Mathieu et al., 2001

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

What the study found

VDR-KO mice showed lower anti-CD3 proliferation and impaired macrophage chemotaxis, but several abnormalities normalized when calcium homeostasis was corrected.

Limits: Highlights major calcium-homeostasis confounding in VDR-KO models.

PubMed ↗DOI ↗Mechanism / biomarker
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Complete study record · A02
IDA02
CitationMathieu et al., 2001
Year2001
JournalJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
Evidence ClassAnimal Study
Study DesignVDR knockout immune phenotyping
Research AreaInnate & adaptive immunity
Population / ModelVDR-KO and wild-type mice
NNot extracted
Baseline 25(OH)DN/A
Vitamin D FormVDR genetic deletion
Dose / RegimenVDR knockout
DurationIn vivo/in vitro
ComparatorWild-type
Immune Endpoint(s)Anti-CD3 proliferation, macrophage chemotaxis, phagocytosis/killing
Clinical Endpoint(s)Graft rejection; streptozotocin diabetes
Main FindingVDR-KO mice showed lower anti-CD3 proliferation and impaired macrophage chemotaxis, but several abnormalities normalized when calcium homeostasis was corrected.
Key Statistical ResultAnti-CD3 SI 13±4 vs 24±9; macrophage chemotaxis 41±19% vs 60±18%
Evidence DirectionMixed / Mechanistic
Key Limitations / NotesHighlights major calcium-homeostasis confounding in VDR-KO models.
PMID11697802
DOI10.1359/jbmr.2001.16.11.2057
PubMed / Source URLPubMed ↗
ImmuneForward UseCautions against attributing every VDR-KO immune phenotype directly to vitamin D signaling.
Animal studiesA03 · 2010

Wu et al., 2010

The American journal of pathology

What the study found

VDR deletion produced a pro-inflammatory intestinal phenotype and increased Salmonella burden and mortality.

Limits: Genetic receptor model; demonstrates VDR-dependent host regulation, not supplementation efficacy.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

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Complete study record · A03
IDA03
CitationWu et al., 2010
Year2010
JournalThe American journal of pathology
Evidence ClassAnimal Study
Study DesignVDR knockout + Salmonella infection
Research AreaBacterial infection / NF-κB
Population / ModelVDR-/- and VDR+/+ mice
NNot extracted
Baseline 25(OH)DN/A
Vitamin D FormVDR genetic deletion
Dose / RegimenVDR knockout
DurationAcute infection
ComparatorWild-type
Immune Endpoint(s)Intestinal NF-κB, IL-6, epithelial responses
Clinical Endpoint(s)Salmonella burden and mortality
Main FindingVDR deletion produced a pro-inflammatory intestinal phenotype and increased Salmonella burden and mortality.
Key Statistical ResultSee primary publication
Evidence DirectionNegative effect of VDR loss
Key Limitations / NotesGenetic receptor model; demonstrates VDR-dependent host regulation, not supplementation efficacy.
PMID20566739
DOI10.2353/ajpath.2010.090998
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports VDR/NF-κB and mucosal host-defense mechanisms.
Animal studiesA04 · 2012

Ryz et al., 2012

American journal of physiology. Gastrointestinal and liver physiology

What the study found

Active vitamin D suppressed mucosal Th17 responses and REG3γ and increased pathogen burden and pathology.

Limits: Important negative animal result: immune suppression can impair host defense.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

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Complete study record · A04
IDA04
CitationRyz et al., 2012
Year2012
JournalAmerican journal of physiology. Gastrointestinal and liver physiology
Evidence ClassAnimal Study
Study DesignCalcitriol treatment during enteric infection
Research AreaCitrobacter / Th17
Population / ModelC. rodentium-infected mice
NNot extracted
Baseline 25(OH)DN/A
Vitamin D Form1,25(OH)2D3
Dose / RegimenActive vitamin D treatment
DurationDuring infection
ComparatorVehicle/control
Immune Endpoint(s)Th17, Th1, Treg, REG3γ
Clinical Endpoint(s)Pathogen burden, tissue pathology
Main FindingActive vitamin D suppressed mucosal Th17 responses and REG3γ and increased pathogen burden and pathology.
Key Statistical ResultSee primary publication
Evidence DirectionAdverse / Mechanistically informative
Key Limitations / NotesImportant negative animal result: immune suppression can impair host defense.
PMID23019194
DOI10.1152/ajpgi.00320.2012
PubMed / Source URLPubMed ↗
ImmuneForward UseBalances claims that vitamin D immune modulation is universally beneficial.
Animal studiesA05 · 2013

Ooi et al., 2013

The Journal of nutrition

What the study found

Vitamin D/VDR deficiency caused dysbiosis and greater colitis susceptibility; 1,25(OH)2D3 treatment reduced colitis severity in Cyp-KO mice.

Limits: Complex microbiome-mediated model; not direct human evidence.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

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Complete study record · A05
IDA05
CitationOoi et al., 2013
Year2013
JournalThe Journal of nutrition
Evidence ClassAnimal Study
Study DesignVitamin D/VDR/CYP27B1 deficiency and DSS colitis
Research AreaMicrobiome / colitis
Population / ModelWT, VDR-KO and Cyp27b1-KO mice
NNot extracted
Baseline 25(OH)DN/A
Vitamin D Form1,25(OH)2D3 / VDR
Dose / RegimenDietary treatment in Cyp KO
DurationExperimental colitis
ComparatorWT / untreated
Immune Endpoint(s)Tolerogenic dendritic cells, E-cadherin, microbiota
Clinical Endpoint(s)DSS colitis severity
Main FindingVitamin D/VDR deficiency caused dysbiosis and greater colitis susceptibility; 1,25(OH)2D3 treatment reduced colitis severity in Cyp-KO mice.
Key Statistical ResultSee primary publication
Evidence DirectionPositive mechanistic
Key Limitations / NotesComplex microbiome-mediated model; not direct human evidence.
PMID23966330
DOI10.3945/jn.113.180794
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports vitamin D–microbiome–mucosal immunity interactions.
Animal studiesA06 · 2013

Liu et al., 2013

The Journal of clinical investigation

What the study found

Intestinal epithelial VDR expression protected against several experimental colitis models and rescued severe disease in VDR-null mice.

Limits: Tissue-specific genetic model; not supplementation evidence.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

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Complete study record · A06
IDA06
CitationLiu et al., 2013
Year2013
JournalThe Journal of clinical investigation
Evidence ClassAnimal Study
Study DesignEpithelial VDR transgenic/rescue colitis models
Research AreaMucosal immunity / colitis
Population / ModelMultiple mouse colitis models
NNot extracted
Baseline 25(OH)DN/A
Vitamin D FormVDR signaling
Dose / RegimenEpithelial VDR expression/rescue
DurationExperimental colitis
ComparatorWT / VDR-deficient
Immune Endpoint(s)Epithelial barrier and inflammatory responses
Clinical Endpoint(s)Colitis severity and survival
Main FindingIntestinal epithelial VDR expression protected against several experimental colitis models and rescued severe disease in VDR-null mice.
Key Statistical ResultSee primary publication
Evidence DirectionPositive mechanistic
Key Limitations / NotesTissue-specific genetic model; not supplementation evidence.
PMID23945234
DOI10.1172/JCI65842
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports epithelial VDR as a regulator of mucosal inflammation.
Animal studiesA07 · 2016

Reeme & Robinson, 2016

Journal of immunology (Baltimore, Md. : 1950)

What the study found

Vitamin-D-replete diet reduced late pulmonary inflammation and immunopathology but did not significantly reduce bacterial burden.

Limits: Strong example that immune modulation and pathogen killing are distinct outcomes.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

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Complete study record · A07
IDA07
CitationReeme & Robinson, 2016
Year2016
JournalJournal of immunology (Baltimore, Md. : 1950)
Evidence ClassAnimal Study
Study DesignDietary vitamin D3 in experimental tuberculosis
Research AreaTuberculosis / immunopathology
Population / ModelC3HeB/FeJ mice infected with M. tuberculosis
N3–4/group/timepoint
Baseline 25(OH)DN/A
Vitamin D FormVitamin D3
Dose / RegimenVitamin-D-high vs deficient diet
DurationUp to 92 days post-infection
ComparatorVitamin-D-low diet
Immune Endpoint(s)IL-12/23p40, IFN-γ, T-cell accumulation, myeloid cells
Clinical Endpoint(s)M. tuberculosis burden; pulmonary pathology
Main FindingVitamin-D-replete diet reduced late pulmonary inflammation and immunopathology but did not significantly reduce bacterial burden.
Key Statistical ResultLung burden P=0.1444; spleen P=0.6109
Evidence DirectionMixed / Positive immunopathology
Key Limitations / NotesStrong example that immune modulation and pathogen killing are distinct outcomes.
PMID26729807
DOI10.4049/jimmunol.1500931
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports anti-inflammatory effects without claiming antimycobacterial efficacy.
Animal studiesA08 · 2016

Penkert et al., 2016

Clinical and vaccine immunology : CVI

What the study found

Vitamin D deficiency alone had limited effects, while combined A+D deficiency further reduced respiratory antibody responses; supplementation restored responses dose-dependently.

Limits: Combined nutrient model prevents attribution of rescue solely to vitamin D.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

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Complete study record · A08
IDA08
CitationPenkert et al., 2016
Year2016
JournalClinical and vaccine immunology : CVI
Evidence ClassAnimal Study
Study DesignVitamin A/D deficiency and live attenuated influenza vaccination
Research AreaVaccination / mucosal antibody
Population / ModelVitamin-deficient mice
NNot extracted
Baseline 25(OH)DN/A
Vitamin D FormVitamins A and D
Dose / RegimenSupplementation at immunization
DurationVaccination study
ComparatorDeficient controls
Immune Endpoint(s)Mucosal antibody responses
Clinical Endpoint(s)Influenza vaccine immunogenicity
Main FindingVitamin D deficiency alone had limited effects, while combined A+D deficiency further reduced respiratory antibody responses; supplementation restored responses dose-dependently.
Key Statistical ResultSee primary publication
Evidence DirectionMixed / Combination evidence
Key Limitations / NotesCombined nutrient model prevents attribution of rescue solely to vitamin D.
PMID26740391
DOI10.1128/CVI.00739-15
PubMed / Source URLPubMed ↗
ImmuneForward UseAnimal vaccine evidence; clearly label combined vitamin A/D intervention.
Animal studiesA09 · 2016

Zhang et al., 2016

Scientific reports

What the study found

Vitamin D attenuated TNBS-induced colitis and suppressed Th1/Th17-related cytokines, but did not improve oxazolone colitis.

Limits: Effect differed by immune/pathologic model.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

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Complete study record · A09
IDA09
CitationZhang et al., 2016
Year2016
JournalScientific reports
Evidence ClassAnimal Study
Study DesignVitamin D treatment in TNBS and oxazolone colitis
Research AreaTh1/Th17 / colitis
Population / ModelC57BL/6 mice
NNot extracted
Baseline 25(OH)DN/A
Vitamin D FormVitamin D
Dose / RegimenPretreatment
DurationExperimental colitis
ComparatorVehicle
Immune Endpoint(s)Th1, Th17, Th2, Treg cytokines
Clinical Endpoint(s)Colitis pathology
Main FindingVitamin D attenuated TNBS-induced colitis and suppressed Th1/Th17-related cytokines, but did not improve oxazolone colitis.
Key Statistical ResultSee primary publication
Evidence DirectionMixed / Model-dependent
Key Limitations / NotesEffect differed by immune/pathologic model.
PMID27620138
DOI10.1038/srep32889
PubMed / Source URLPubMed ↗
ImmuneForward UseShows immune effects depend on inflammatory context.
Animal studiesA10 · 2019

Cantorna et al., 2019

Frontiers in immunology

What the study found

Vitamin-D-sufficient mice had more colonic regulatory T cells and were less susceptible to colitis; microbiota transfer reproduced aspects of the phenotype.

Limits: Microbiota-dependent; developmental timing mattered.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

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Complete study record · A10
IDA10
CitationCantorna et al., 2019
Year2019
JournalFrontiers in immunology
Evidence ClassAnimal Study
Study DesignVitamin D regulation of colonic Tregs and microbiota
Research AreaTreg / microbiome / colitis
Population / ModelVitamin-D-sufficient and deficient mice; germ-free recipients
NNot extracted
Baseline 25(OH)DN/A
Vitamin D FormVitamin D / 1,25(OH)2D
Dose / RegimenDietary status and treatment
DurationDevelopment + colitis
ComparatorVitamin-D-deficient
Immune Endpoint(s)FoxP3+ and RORγt/FoxP3+ Tregs
Clinical Endpoint(s)Colitis susceptibility
Main FindingVitamin-D-sufficient mice had more colonic regulatory T cells and were less susceptible to colitis; microbiota transfer reproduced aspects of the phenotype.
Key Statistical ResultSee primary publication
Evidence DirectionPositive mechanistic
Key Limitations / NotesMicrobiota-dependent; developmental timing mattered.
PMID31417552
DOI10.3389/fimmu.2019.01772
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports vitamin D–microbiome–Treg axis.
Animal studiesA11 · 2020

Yamamoto et al., 2020

Nutrients

What the study found

25(OH)D3-fed mice had significantly lower lung viral titers than standard-fed controls.

Limits: High-dose metabolite in mice; cannot be generalized to standard human D3 supplementation.

PubMed ↗DOI ↗Positive outcomes
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Complete study record · A11
IDA11
CitationYamamoto et al., 2020
Year2020
JournalNutrients
Evidence ClassAnimal Study
Study DesignOral 25(OH)D3 supplementation before influenza challenge
Research AreaInfluenza infection
Population / ModelInfluenza A-infected mice
NNot extracted
Baseline 25(OH)DN/A
Vitamin D Form25-hydroxyvitamin D3
Dose / RegimenHigh-dose dietary 25(OH)D3
DurationProphylactic feeding
ComparatorStandard diet
Immune Endpoint(s)Inflammatory/antiviral lung responses
Clinical Endpoint(s)Pulmonary viral titers
Main Finding25(OH)D3-fed mice had significantly lower lung viral titers than standard-fed controls.
Key Statistical ResultSee primary publication
Evidence DirectionPositive preclinical
Key Limitations / NotesHigh-dose metabolite in mice; cannot be generalized to standard human D3 supplementation.
PMID32635656
DOI10.3390/nu12072000
PubMed / Source URLPubMed ↗
ImmuneForward UsePreclinical antiviral evidence.
Animal studiesA12 · 2022

Cantorna group, 2022

Nutrients

What the study found

Deficiency or inability to generate 1,25(OH)2D worsened H1N1 outcomes; supplementation reduced inflammation in mice, but viral replication was not consistently reduced and hamster results differed.

Limits: Species- and endpoint-dependent; distinguishes inflammation/survival from viral replication.

PubMed ↗DOI ↗Mixed findings
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Complete study record · A12
IDA12
CitationCantorna group, 2022
Year2022
JournalNutrients
Evidence ClassAnimal Study
Study DesignVitamin D deficiency, CYP27B1 KO, H1N1 and SARS-CoV-2 models
Research AreaRespiratory viral infection
Population / ModelMice and hamsters
NNot extracted
Baseline 25(OH)DN/A
Vitamin D FormVitamin D / 1,25(OH)2D
Dose / RegimenDeficiency/sufficiency; supplementation
DurationInfection studies
ComparatorSufficient WT controls
Immune Endpoint(s)Lung inflammation, vitamin D activation
Clinical Endpoint(s)Survival, viral gene expression, weight recovery
Main FindingDeficiency or inability to generate 1,25(OH)2D worsened H1N1 outcomes; supplementation reduced inflammation in mice, but viral replication was not consistently reduced and hamster results differed.
Key Statistical ResultSee primary publication
Evidence DirectionMixed / Positive host tolerance
Key Limitations / NotesSpecies- and endpoint-dependent; distinguishes inflammation/survival from viral replication.
PMID35893921
DOI10.3390/nu14153061
PubMed / Source URLPubMed ↗
ImmuneForward UseModern respiratory-virus animal evidence with important limitations.
Animal studiesA13 · 2002

Meehan & DeLuca, 2002

Archives of biochemistry and biophysics

What the study found

Calcitriol suppressed EAE through the canonical vitamin D receptor; VDR was required for the effect.

Limits: Pharmacologic active hormone in autoimmune model, not nutritional supplementation.

PubMed ↗DOI ↗Mechanism / biomarker
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Complete study record · A13
IDA13
CitationMeehan & DeLuca, 2002
Year2002
JournalArchives of biochemistry and biophysics
Evidence ClassAnimal Study
Study DesignVDR requirement for calcitriol suppression of EAE
Research AreaAutoimmunity / EAE
Population / ModelEAE mice with/without functional VDR
NNot extracted
Baseline 25(OH)DN/A
Vitamin D Form1,25(OH)2D3
Dose / RegimenCalcitriol
DurationEAE course
ComparatorVehicle / genotype controls
Immune Endpoint(s)Autoimmune T-cell responses
Clinical Endpoint(s)EAE severity
Main FindingCalcitriol suppressed EAE through the canonical vitamin D receptor; VDR was required for the effect.
Key Statistical ResultSee primary publication
Evidence DirectionPositive mechanistic
Key Limitations / NotesPharmacologic active hormone in autoimmune model, not nutritional supplementation.
PMID12464272
DOI10.1016/s0003-9861(02)00580-5
PubMed / Source URLPubMed ↗
ImmuneForward UseEstablishes VDR dependence of calcitriol's autoimmune effects.
Animal studiesA14 · 2011

Mayne et al., 2011

European journal of immunology

What the study found

Calcitriol acted directly through T-cell VDR to inhibit EAE; Foxp3+ proportions were not the key mechanism in this model.

Limits: Disease model and pharmacologic calcitriol; not general immune-health evidence.

PubMed ↗DOI ↗Mechanism / biomarker
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Complete study record · A14
IDA14
CitationMayne et al., 2011
Year2011
JournalEuropean journal of immunology
Evidence ClassAnimal Study
Study DesignT-cell-specific VDR targeting in EAE
Research AreaAutoimmunity / T cells
Population / ModelEAE mice with conditional VDR targeting
NNot extracted
Baseline 25(OH)DN/A
Vitamin D Form1,25(OH)2D3 / VDR
Dose / RegimenCalcitriol / genetic targeting
DurationEAE course
ComparatorControls
Immune Endpoint(s)Pathogenic CD4+ T cells, Foxp3+ Tregs
Clinical Endpoint(s)EAE severity
Main FindingCalcitriol acted directly through T-cell VDR to inhibit EAE; Foxp3+ proportions were not the key mechanism in this model.
Key Statistical ResultSee primary publication
Evidence DirectionPositive mechanistic
Key Limitations / NotesDisease model and pharmacologic calcitriol; not general immune-health evidence.
PMID21287548
DOI10.1002/eji.201040632
PubMed / Source URLPubMed ↗
ImmuneForward UseDirect evidence for T-cell VDR-mediated immunoregulation.
Reviews & meta-analysesR01 · 2019

Martineau/Jolliffe et al., 2019 IPD meta-analysis

Health technology assessment (Winchester, England)

What the study found

Overall protection was reported; stronger effects were observed with daily/weekly dosing without bolus and among very deficient participants in those regimens.

Limits: Based on older trial set; later larger meta-analyses changed the overall inference.

PubMed ↗DOI ↗Positive outcomes
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Complete study record · R01
IDR01
CitationMartineau/Jolliffe et al., 2019 IPD meta-analysis
Year2019
JournalHealth technology assessment (Winchester, England)
Evidence ClassSystematic Review / Meta-analysis
Study DesignIndividual participant data meta-analysis of 25 RCTs
Research AreaRespiratory infection
Population / ModelParticipants aged 0–95 years
N11321
Baseline 25(OH)DStratified including <25 nmol/L
Vitamin D FormD2/D3
Dose / RegimenMultiple regimens
DurationMultiple
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)ARI
Main FindingOverall protection was reported; stronger effects were observed with daily/weekly dosing without bolus and among very deficient participants in those regimens.
Key Statistical ResultaOR 0.88 (0.81–0.96); daily/weekly aOR 0.81; <25 nmol/L subgroup aOR 0.30
Evidence DirectionPositive meta-analytic evidence
Key Limitations / NotesBased on older trial set; later larger meta-analyses changed the overall inference.
PMID30675873
DOI10.3310/hta23020
PubMed / Source URLPubMed ↗
ImmuneForward UseHistorical synthesis explaining earlier positive interpretation.
Reviews & meta-analysesR02 · 2021

Jolliffe et al., 2021

The lancet. Diabetes & endocrinology

What the study found

Small overall reduction in ARI was reported, with heterogeneity; no significant interaction by prespecified modifiers.

Limits: Superseded by newer 2025 update with additional large trials.

PubMed ↗DOI ↗Positive outcomes
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Complete study record · R02
IDR02
CitationJolliffe et al., 2021
Year2021
JournalThe lancet. Diabetes & endocrinology
Evidence ClassSystematic Review / Meta-analysis
Study DesignAggregate-data meta-analysis
Research AreaRespiratory infection
Population / Model43 trials; ages 0–95
N48488
Baseline 25(OH)DStratified
Vitamin D FormD2/D3/25(OH)D
Dose / RegimenMultiple
DurationVarious
ComparatorPlacebo/low-dose
Immune Endpoint(s)—
Clinical Endpoint(s)ARI
Main FindingSmall overall reduction in ARI was reported, with heterogeneity; no significant interaction by prespecified modifiers.
Key Statistical ResultOR 0.92 (0.86–0.99)
Evidence DirectionSmall Positive / heterogeneous
Key Limitations / NotesSuperseded by newer 2025 update with additional large trials.
PMID33798465
DOI10.1016/S2213-8587(21)00051-6
PubMed / Source URLPubMed ↗
ImmuneForward UseShows evolution of evidence over time.
Reviews & meta-analysesR03 · 2022

Cho et al., 2022

Nutrients

What the study found

No significant overall prevention; apparent daily/short-term subgroup effects disappeared in high-quality-study subgroup analyses.

Limits: Subgroup heterogeneity; quality-sensitive results.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R03
IDR03
CitationCho et al., 2022
Year2022
JournalNutrients
Evidence ClassSystematic Review / Meta-analysis
Study DesignMeta-analysis of RCTs
Research AreaARI prevention
Population / Model30 RCTs
N30263
Baseline 25(OH)DVarious
Vitamin D FormVitamin D
Dose / RegimenVarious
DurationVarious
ComparatorControl
Immune Endpoint(s)—
Clinical Endpoint(s)ARI prevention
Main FindingNo significant overall prevention; apparent daily/short-term subgroup effects disappeared in high-quality-study subgroup analyses.
Key Statistical ResultRR 0.96 (0.91–1.01)
Evidence DirectionNeutral / Mixed
Key Limitations / NotesSubgroup heterogeneity; quality-sensitive results.
PMID35215468
DOI10.3390/nu14040818
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports cautious infection-prevention conclusion.
Reviews & meta-analysesR04 · 2022

Cho et al., 2022 treatment meta-analysis

Nutrients

What the study found

Small statistical signal overall was not clinically substantial and disappeared in high-quality RCTs.

Limits: Publication bias observed; treatment rather than prevention.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R04
IDR04
CitationCho et al., 2022 treatment meta-analysis
Year2022
JournalNutrients
Evidence ClassSystematic Review / Meta-analysis
Study DesignMeta-analysis of 18 RCTs
Research AreaARI treatment
Population / Model18 RCTs
N3648
Baseline 25(OH)DVarious
Vitamin D FormVitamin D
Dose / RegimenVarious
DurationVarious
ComparatorControl
Immune Endpoint(s)—
Clinical Endpoint(s)ARI treatment outcomes
Main FindingSmall statistical signal overall was not clinically substantial and disappeared in high-quality RCTs.
Key Statistical ResultOverall RR 1.07 (1.01–1.13); high-quality RR 1.02 (0.98–1.06)
Evidence DirectionNeutral / Not clinically effective
Key Limitations / NotesPublication bias observed; treatment rather than prevention.
PMID35334804
DOI10.3390/nu14061144
PubMed / Source URLPubMed ↗
ImmuneForward UseSupports distinction between mechanistic plausibility and clinical treatment efficacy.
Reviews & meta-analysesR05 · 2024

2024 dose-response ARI meta-analysis

Nutrition journal

What the study found

No significant overall preventive effect; some subgroup signals for daily dosing and seasonal windows.

Limits: Subgroup findings require caution given null overall result.

PubMed ↗DOI ↗Mixed findings
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R05
IDR05
Citation2024 dose-response ARI meta-analysis
Year2024
JournalNutrition journal
Evidence ClassSystematic Review / Meta-analysis
Study Design43-RCT dose-response/pairwise meta-analysis
Research AreaARI prevention
Population / Model43 RCTs
N49320
Baseline 25(OH)DVarious
Vitamin D FormVitamin D
Dose / RegimenMultiple
DurationMultiple
ComparatorControl
Immune Endpoint(s)—
Clinical Endpoint(s)ARI
Main FindingNo significant overall preventive effect; some subgroup signals for daily dosing and seasonal windows.
Key Statistical ResultOverall RR 0.99 (0.97–1.01)
Evidence DirectionNeutral / Mixed
Key Limitations / NotesSubgroup findings require caution given null overall result.
PMID39143549
DOI10.1186/s12937-024-00990-w
PubMed / Source URLPubMed ↗
ImmuneForward UseModern synthesis before 2025 update.
Reviews & meta-analysesR06 · 2025

Jolliffe et al., 2025

The lancet. Diabetes & endocrinology

What the study found

Updated evidence found no statistically significant overall reduction in ARI and no evidence of effect modification by age, baseline vitamin D status, dosing frequency, or dose size.

Limits: Most current major synthesis; funnel-plot asymmetry noted.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R06
IDR06
CitationJolliffe et al., 2025
Year2025
JournalThe lancet. Diabetes & endocrinology
Evidence ClassSystematic Review / Meta-analysis
Study DesignUpdated meta-analysis of stratified aggregate RCT data
Research AreaARI prevention
Population / Model40 placebo-controlled comparisons in primary analysis
N61589
Baseline 25(OH)DStratified
Vitamin D FormVitamin D
Dose / RegimenMultiple regimens
DurationMultiple
ComparatorPlacebo
Immune Endpoint(s)—
Clinical Endpoint(s)ARI
Main FindingUpdated evidence found no statistically significant overall reduction in ARI and no evidence of effect modification by age, baseline vitamin D status, dosing frequency, or dose size.
Key Statistical ResultOR 0.94 (0.88–1.00), P=0.057
Evidence DirectionNeutral / Not established
Key Limitations / NotesMost current major synthesis; funnel-plot asymmetry noted.
PMID39993397
DOI10.1016/S2213-8587(24)00348-6
PubMed / Source URLPubMed ↗
ImmuneForward UsePrimary current synthesis for overall ARI claim.
Reviews & meta-analysesR07 · 2025

Wang et al., 2025

BMC pediatrics

What the study found

No significant reduction in pediatric ARI incidence, hospitalization duration, recovery time, or mortality.

Limits: Pediatric-specific; substantial heterogeneity possible across trials.

PubMed ↗DOI ↗No significant benefit
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R07
IDR07
CitationWang et al., 2025
Year2025
JournalBMC pediatrics
Evidence ClassSystematic Review / Meta-analysis
Study DesignPediatric RCT systematic review/meta-analysis
Research AreaPediatric ARI
Population / Model17 pediatric RCTs
N18372
Baseline 25(OH)DVarious
Vitamin D FormVitamin D
Dose / RegimenVarious
DurationVarious
ComparatorPlacebo/no treatment
Immune Endpoint(s)—
Clinical Endpoint(s)ARI incidence, hospitalization, recovery, mortality
Main FindingNo significant reduction in pediatric ARI incidence, hospitalization duration, recovery time, or mortality.
Key Statistical ResultARI RR 0.82 (0.64–1.06)
Evidence DirectionNeutral
Key Limitations / NotesPediatric-specific; substantial heterogeneity possible across trials.
PMID41387808
DOI10.1186/s12887-025-06361-6
PubMed / Source URLPubMed ↗
ImmuneForward UseCurrent pediatric synthesis.
Reviews & meta-analysesR08 · 2011

Hewison, 2011

Vitamins and hormones

What the study found

Review describes intracrine/paracrine vitamin D signaling in innate and adaptive immunity.

Limits: Review, not primary clinical evidence.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R08
IDR08
CitationHewison, 2011
Year2011
JournalVitamins and hormones
Evidence ClassMajor Review
Study DesignNarrative mechanistic review
Research AreaInnate & adaptive immunity
Population / ModelHuman/experimental literature
N—
Baseline 25(OH)D—
Vitamin D FormVitamin D metabolites
Dose / Regimen—
Duration—
Comparator—
Immune Endpoint(s)CYP27B1/VDR, antimicrobial activity, antigen presentation, T/B-cell function
Clinical Endpoint(s)—
Main FindingReview describes intracrine/paracrine vitamin D signaling in innate and adaptive immunity.
Key Statistical Result—
Evidence DirectionMechanistic Review
Key Limitations / NotesReview, not primary clinical evidence.
PMID21419266
DOI10.1016/B978-0-12-386960-9.00002-2
PubMed / Source URLPubMed ↗
ImmuneForward UseCore mechanistic background.
Reviews & meta-analysesR09 · 2013

Kongsbak et al., 2013

Frontiers in immunology

What the study found

Summarizes VDR regulation and its role in T-cell development and effector function.

Limits: Review; use primary studies for specific clinical claims.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R09
IDR09
CitationKongsbak et al., 2013
Year2013
JournalFrontiers in immunology
Evidence ClassMajor Review
Study DesignNarrative review
Research AreaT-cell biology
Population / ModelT-cell / mechanistic literature
N—
Baseline 25(OH)D—
Vitamin D Form1,25(OH)2D3 / VDR
Dose / Regimen—
Duration—
Comparator—
Immune Endpoint(s)VDR expression, T-cell development, differentiation, effector function
Clinical Endpoint(s)—
Main FindingSummarizes VDR regulation and its role in T-cell development and effector function.
Key Statistical Result—
Evidence DirectionMechanistic Review
Key Limitations / NotesReview; use primary studies for specific clinical claims.
PMID23785369
DOI10.3389/fimmu.2013.00148
PubMed / Source URLPubMed ↗
ImmuneForward UseT-cell mechanism background.
Reviews & meta-analysesR10 · 2010

Kamen & Tangpricha, 2010

Journal of molecular medicine (Berlin, Germany)

What the study found

Summarizes immunomodulatory effects including antimicrobial peptide induction and adaptive immune regulation.

Limits: Review-level evidence.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R10
IDR10
CitationKamen & Tangpricha, 2010
Year2010
JournalJournal of molecular medicine (Berlin, Germany)
Evidence ClassMajor Review
Study DesignNarrative review
Research AreaInnate/adaptive immunity
Population / ModelHuman/experimental literature
N—
Baseline 25(OH)D—
Vitamin D FormVitamin D
Dose / Regimen—
Duration—
Comparator—
Immune Endpoint(s)Macrophages, antimicrobial peptides, dendritic cells, T/B cells
Clinical Endpoint(s)—
Main FindingSummarizes immunomodulatory effects including antimicrobial peptide induction and adaptive immune regulation.
Key Statistical Result—
Evidence DirectionMechanistic Review
Key Limitations / NotesReview-level evidence.
PMID20119827
DOI10.1007/s00109-010-0590-9
PubMed / Source URLPubMed ↗
ImmuneForward UseGeneral immune mechanism background.
Reviews & meta-analysesR11 · 2024

Carlberg & Velleuer, 2024

Nutrients

What the study found

Proposes a central role for VDR-dependent immune-cell programming in immunocompetence and aging.

Limits: Conceptual review; does not establish that supplementation reverses immunosenescence.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · R11
IDR11
CitationCarlberg & Velleuer, 2024
Year2024
JournalNutrients
Evidence ClassMajor Review
Study DesignNarrative mechanistic review
Research AreaImmune aging
Population / ModelHuman immune aging / molecular literature
N—
Baseline 25(OH)D—
Vitamin D FormVitamin D3 / 1,25(OH)2D3 / VDR
Dose / Regimen—
Duration—
Comparator—
Immune Endpoint(s)VDR epigenome/transcriptome, myeloid cells, immunocompetence
Clinical Endpoint(s)Healthy aging / disease context
Main FindingProposes a central role for VDR-dependent immune-cell programming in immunocompetence and aging.
Key Statistical Result—
Evidence DirectionMechanistic / Aging Review
Key Limitations / NotesConceptual review; does not establish that supplementation reverses immunosenescence.
PMID38337682
DOI10.3390/nu16030398
PubMed / Source URLPubMed ↗
ImmuneForward UseImmune-aging context; supports mechanistic discussion, not rejuvenation claims.
Human cell experimentsM01 · 2006 · Added source

Liu et al., 2006

Science

What the study found

TLR activation induced a vitamin-D-dependent antimicrobial pathway in human macrophages.

Limits: Cell experiments establish a pathway, not that supplements prevent tuberculosis or respiratory infections in people.

PubMed ↗DOI ↗Mechanism / biomarker
View all 24 fields

Normalized source record. Bibliographic metadata were checked against PubMed. Remaining extraction gaps are stated rather than filled by inference.

Complete study record · M01
IDM01
CitationLiu et al., 2006
Year2006
JournalScience
Evidence ClassHuman cell / mechanistic study
Study DesignLaboratory experiments in human macrophages
Research AreaAntimicrobial pathways
Population / ModelHuman macrophages; ex vivo / in vitro
NNot a clinical trial
Baseline 25(OH)DSerum-dependent experiments
Vitamin D FormVitamin D metabolites
Dose / RegimenLaboratory conditions
DurationLaboratory experiments
ComparatorExperimental control conditions
Immune Endpoint(s)TLR activation, VDR, CYP27B1, cathelicidin and intracellular mycobacterial killing
Clinical Endpoint(s)No clinical infection-prevention endpoint
Main FindingTLR activation induced a vitamin-D-dependent antimicrobial pathway in human macrophages.
Key Statistical ResultMechanistic experiments; not a supplementation trial.
Evidence DirectionMechanistically Positive
Key Limitations / NotesCell experiments establish a pathway, not that supplements prevent tuberculosis or respiratory infections in people.
PMID16497887
DOI10.1126/science.1123933
PubMed / Source URLPubMed ↗
ImmuneForward UsePrimary human-cell evidence underlying the mechanism explanation.

Methods, Verification and Corrections

Starting material: the supplied September 2026 workbook and two Vitamin D documents. This is a curated PubMed-centered collection with targeted additions, not a registered systematic review. Editorial check: 27 October 2026.

  • All 44 supplied PubMed identifiers were checked against PubMed bibliographic records. Available abstracts informed the review. This does not imply independent full-text extraction of every numerical field.
  • H11: restored the missing clinical-endpoint field and realigned trailing columns; clarified that the activation measure decreased. A typographically inconsistent abstract confidence interval is not reproduced.
  • R10: the supplied PMID identifies Kamen & Tangpricha (2010), not Aranow (2011). The guide cites the actual Aranow review separately (PMID 21527855). Journals and available DOIs were normalized to PubMed.
  • H17 and H19: completed key trial details from the primary abstracts. Remaining extraction gaps are retained and can be filtered.
  • H20 includes the Rastgoo corrigendum, which corrects 50,000 to 5,000 IU in a table legend. H21, H22 and M01 are targeted additions, not claims that a new exhaustive search was performed.

The original workbook is available unchanged. The reviewed CSV reflects the corrections and additions. The French page provides translated findings and limitations while preserving complete source records in English for traceability.

Download and Keep Exploring

Reviewed evidence CSV ↓48 records · all 24 fields · source language EnglishOriginal workbook ↓Unchanged source · 44 records · 2 sheetsReturn to the Vitamin D guide →Mechanisms, human trials, ImmAge and safety