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Vitamin D deficiency and the pathogenesis of Crohn's disease
被引:58
作者:
White, John H.
[1
,2
]
机构:
[1] McGill Univ, Dept Physiol, Montreal, PQ, Canada
[2] McGill Univ, Dept Med, Montreal, PQ, Canada
关键词:
Crohn's disease;
1;
alpha;
25-dihydroxyvitamin D-3;
Vitamin D receptor;
Innate immunity;
Autophagy;
Vitamin D deficiency;
Intervention trials;
INFLAMMATORY-BOWEL-DISEASE;
GENOME-WIDE ASSOCIATION;
D-RECEPTOR;
SUSCEPTIBILITY LOCI;
REDUCED RISK;
AUTOPHAGY;
GENE;
NOD2;
VARIANTS;
EPIDEMIOLOGY;
D O I:
10.1016/j.jsbmb.2016.12.015
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Vitamin D has emerged as a key regulator of innate immune responses to pathogen threat. The hormonal form of vitamin D signals through a nuclear receptor transcription factor and regulates gene transcription. Several papers have shown that vitamin D signaling is active both upstream and downstream of pattern recognition receptors, vanguards of innate immune responses. Crohn's disease (CD) is a relapsing-recurring inflammatory bowel disease (IBD) that arises from dysregulated intestinal innate immunity. Indeed, genetic studies have identified several CD susceptibility markers linked to mechanisms of innate immune responses to infection. Interest in links between vitamin D deficiency and CD has grown substantially, particularly in the last five years. While a number of studies have consistently revealed an association between CD and vitamin D deficiency, recent experimental work has uncovered a compelling mechanistic basis for the contribution of vitamin D deficiency to the pathogenesis of the disease. Moreover, a number of intervention trials have provided generally solid evidence that robust vitamin D supplementation may be of therapeutic benefit to patients with CD. This review summarizes these laboratory and clinical findings. (C) 2016 Elsevier Ltd. All rights reserved.
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页码:23 / 28
页数:6
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