Evidence map›Paper›PMID 24781050›Full record

ArticleMucosal immunology2014

Differential effect of vitamin D on NOD2- and TLR-induced cytokines in Crohn's disease.

S Dionne, M R Calderon, J H White, B Memari, I Elimrani, B Adelson, C Piccirillo, E G Seidman

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In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Vitamin DFrontiers in immunology · 2026
    Review
  2. Article
  3. The Role of Vitamin D and Vitamin D Receptor in Sepsis.Current issues in molecular biology · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. High-dose vitamin DEuropean journal of nutrition · 2018
    Article
  10. World journal of gastroenterology · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. 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.

S DionneMcGill Center for IBD Research, Research Institute of the McGill University Health Center, McGill University, Montreal, Quebec, Canada.
M R CalderonDepartment of Physiology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
J H WhiteDepartment of Physiology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
B MemariDepartment of Physiology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
I ElimraniMcGill Center for IBD Research, Research Institute of the McGill University Health Center, McGill University, Montreal, Quebec, Canada.
B AdelsonMcGill Center for IBD Research, Research Institute of the McGill University Health Center, McGill University, Montreal, Quebec, Canada.
C PiccirilloMcGill Center for IBD Research, Research Institute of the McGill University Health Center, McGill University, Montreal, Quebec, Canada.
E G SeidmanMcGill Center for IBD Research, Research Institute of the McGill University Health Center, McGill University, Montreal, Quebec, Canada.
McGill University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence implicates defective innate immunity in the pathogenesis of Crohn's disease (CD). Ineffectual NOD2 (nucleotide-binding oligomerization domain 2) is the most common susceptibility gene contributing to CD. Vitamin D (vD), a potent modulator of innate and adaptive immunity, induces NOD2 gene expression and its downstream function. We hypothesized that the hormonal form of vD (1,25D) could beneficially modulate innate immune function in CD. Using peripheral mononuclear cells and monocyte-derived dendritic cells (Mo-DCs) from CD, it was found that 1,25D decreased Toll-like receptor (TLR)-induced cytokine production and enhanced cytokine levels induced by muramyl dipeptide (MDP), the NOD2 ligand. 1,25D increased the synergistic effect provided by NOD2 and TLR co-activation on interleukin (IL)-10, IL-23, and tumor necrosis factor-alpha (TNF-α). Whereas 1,25D inhibits Mo-DC TLR-induced cytokines, co-stimulation of NOD2 results in increased IL-10 and IL-23. IL-12p70 was completely abrogated by 1,25D. 1,25D similarly modulated cytokine production by immune cells in ulcerative colitis patients and healthy controls. Mo-DCs from CD patients heterozygous for NOD2 mutations had a response similar to those from patients without NOD2 mutations. Immune cells from patients homozygous for the 1007 fs mutation were unresponsive to MDP and 1,25D. Our in vitro data support 1,25D as a potential modulator of immunity. However, these results cannot be extrapolated to CD patients without further controlled studies.

Indexed as

CalcitriolCells, CulturedCrohn DiseaseCytokinesDendritic CellsFemaleHumansImmunologic FactorsMaleMutationNod2 Signaling Adaptor ProteinToll-Like ReceptorsVitaminsCalcitriolCytokinesImmunologic FactorsNOD2 protein, humanNod2 Signaling Adaptor ProteinToll-Like ReceptorsVitamins

Identifiers

PMID24781050
OpenAlexW2014717247

What OpenQuestion holds

Textmetadata
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.