Evidence map›Paper›PMID 25230725›Full record

ArticleBMC immunology2014

Vitamin D-binding protein controls T cell responses to vitamin D.

Martin Kongsbak, Marina Rode von Essen, Trine Bøegh Levring, Peter Schjerling, Anders Woetmann, Niels Ødum, Charlotte Menné Bonefeld, Carsten Geisler

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 112 citations in OpenAlex.

  1. Trial
  2. Effects of vitamin D supplements on frequency of CD4European journal of clinical nutrition · 2019
    Trial
  3. Review
  4. The Role of Vitamin D and Vitamin D Receptor in Sepsis.Current issues in molecular biology · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Observational
  12. Review
  13. Vitamin D in Neurological Diseases.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Free vitamin DEuropean journal of neurology · 2022
    Article
  18. Article
  19. Article
  20. Article
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

8 authors at 1 institution in 1 country.

Martin Kongsbak
Marina Rode von Essen
Trine Bøegh Levring
Peter Schjerling
Anders Woetmann
Niels Ødum
Charlotte Menné Bonefeld
Carsten Geisler
University of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn vitro studies have shown that the active form of vitamin D3, 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3), can regulate differentiation of CD4+ T cells by inhibiting Th1 and Th17 cell differentiation and promoting Th2 and Treg cell differentiation. However, the serum concentration of 1,25(OH)2D3 is far below the effective concentration of 1,25(OH)2D3 found in in vitro studies, and it has been suggested that 1,25(OH)2D3 must be produced locally from the inactive precursor 25-hydroxyvitamin D3 (25(OH)D3) to affect ongoing immune responses in vivo. Although it has been reported that activated T cells express the 25(OH)D-1α-hydroxylase CYP27B1 that converts 25(OH)D3 to 1,25(OH)2D3, it is still controversial whether activated T cells have the capacity to produce sufficient amounts of 1,25(OH)2D3 to affect vitamin D-responsive genes. Furthermore, it is not known how the vitamin D-binding protein (DBP) found in high concentrations in serum affects T cell responses to 25(OH)D3.

resultsWe found that activated T cells express CYP27B1 and have the capacity to produce sufficient 1,25(OH)2D3 to affect vitamin D-responsive genes when cultured with physiological concentrations of 25(OH)D3 in serum-free medium. However, if the medium was supplemented with serum or purified DBP, DBP strictly inhibited the production of 1,25(OH)2D3 and 25(OH)D3-induced T cell responses. In contrast, DBP did not inhibit the effect of exogenous 1,25(OH)2D3. Actin, arachidonic acid and albumin did not affect the sequestration of 25(OH)D3 by DBP, whereas carbonylation of DBP did.

conclusionsActivated T cells express CYP27B1 and can convert 25(OH)D3 to 1,25(OH)2D3 in sufficiently high concentrations to affect vitamin D-responsive genes when cultured in serum-free medium. However, DBP sequesters 25(OH)D3 and inhibits the production of 1,25(OH)2D3 in T cells. To fully exploit the immune-regulatory potential of vitamin D, future studies of the mechanisms that enable the immune system to exploit 25(OH)D3 and convert it to 1,25(OH)2D3 in vivo are required.

Indexed as

25-Hydroxyvitamin D3 1-alpha-HydroxylaseActinsADP-ribosyl Cyclase 1AlbuminsArachidonic AcidBiological AvailabilityCalcifediolFlow CytometryGene Expression RegulationHumansLymphocyte ActivationPinocytosisProtein CarbonylationSerumT-LymphocytesVitamin D25-Hydroxyvitamin D3 1-alpha-HydroxylaseActinsADP-ribosyl Cyclase 1AlbuminsArachidonic AcidCalcifedioldihydroxy-vitamin D3Vitamin DVitamin D-Binding Protein

Identifiers

PMID25230725
PMCPMC4177161
OpenAlexW2146606039

What OpenQuestion holds

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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.