Evidence map›Paper›PMID 25852682›Full record

ReviewFrontiers in immunology2015

Vitamin D Actions on CD4(+) T Cells in Autoimmune Disease.

Colleen Elizabeth Hayes, Shane L Hubler, Jerott R Moore, Lauren E Barta, Corinne E Praska, Faye E Nashold

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
9.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 116 citations in OpenAlex.

  1. Trial
  2. Sixteen-Week Vitamin DNutrients · 2022
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  5. Effects of vitamin D supplements on frequency of CD4European journal of clinical nutrition · 2019
    Trial
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  7. Observational
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  12. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Colleen Elizabeth HayesDepartment of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison , Madison, WI , USA.
Shane L HublerDepartment of Statistics, College of Letters and Sciences, University of Wisconsin-Madison , Madison, WI , USA.
Jerott R MooreDepartment of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison , Madison, WI , USA.
Lauren E BartaDepartment of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison , Madison, WI , USA.
Corinne E PraskaDepartment of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison , Madison, WI , USA.
Faye E NasholdDepartment of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison , Madison, WI , USA.
University of Wisconsin–Madison · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review summarizes and integrates research on vitamin D and CD4(+) T-lymphocyte biology to develop new mechanistic insights into the molecular etiology of autoimmune disease. A deep understanding of molecular mechanisms relevant to gene-environment interactions is needed to deliver etiology-based autoimmune disease prevention and treatment strategies. Evidence linking sunlight, vitamin D, and the risk of multiple sclerosis and type 1 diabetes is summarized to develop the thesis that vitamin D is the environmental factor that most strongly influences autoimmune disease development. Evidence for CD4(+) T-cell involvement in autoimmune disease pathogenesis and for paracrine calcitriol signaling to CD4(+) T lymphocytes is summarized to support the thesis that calcitriol is sunlight's main protective signal transducer in autoimmune disease risk. Animal modeling and human mechanistic data are summarized to support the view that vitamin D probably influences thymic negative selection, effector Th1 and Th17 pathogenesis and responsiveness to extrinsic cell death signals, FoxP3(+)CD4(+) T-regulatory cell and CD4(+) T-regulatory cell type 1 (Tr1) cell functions, and a Th1-Tr1 switch. The proposed Th1-Tr1 switch appears to bridge two stable, self-reinforcing immune states, pro- and anti-inflammatory, each with a characteristic gene regulatory network. The bi-stable switch would enable T cells to integrate signals from pathogens, hormones, cell-cell interactions, and soluble mediators and respond in a biologically appropriate manner. Finally, unanswered questions and potentially informative future research directions are highlighted to speed delivery of etiology-based strategies to reduce autoimmune disease.

Indexed as

autoimmune diseasesCD4-positive T lymphocytesmultiple sclerosistype 1 diabetesvitamin D

Identifiers

PMID25852682
PMCPMC4364365
OpenAlexW2094080536

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.