Document Detail


Vitamin d deficiency and connective tissue disease.
MedLine Citation:
PMID:  21419275     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Recently, the evidence linking vitamin D status as a potential environmental factor affecting autoimmune disease prevalence continues to accumulate. Beyond that the traditional known metabolic activities, vitamin D has been shown to modulate the immune system and has anti-inflammatory properties. The immune-regulatory role of vitamin D affects both the innate and adaptive immune responses contributing to the immune-tolerance of self-structures. Vitamin D deficiency skews the immunologic response towards loss of tolerance. Serum levels of vitamin D have been found to be significantly lower in several autoimmune or immune-mediated diseases than in the healthy population. Experimental animal models and clinical studies show that 1,25-dihydroxyvitamin D3 or vitamin D receptor (VDR) agonists can either prevent or suppress symptoms of type 1 diabetes, experimental autoimmune encephalomyelitis, rheumatoid arthritis, systemic lupus erthyematosus and inflammatory bowel disease. The heading aims at reviewing the complex immune-regulatory role of vitamin D from the cellular and humoral level through animal models of autoimmune rheumatic diseases and representing the known contribution of vitamin D in the pathogenesis of connective tissue diseases. Increased vitamin D intakes might reduce the incidence and severity of autoimmune disorders besides reducing the rate of osteoporotic bone fracture.
Authors:
Eva Zold; Zsolt Barta; Edit Bodolay
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Vitamins and hormones     Volume:  86     ISSN:  0083-6729     ISO Abbreviation:  Vitam. Horm.     Publication Date:  2011  
Date Detail:
Created Date:  2011-03-22     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0413601     Medline TA:  Vitam Horm     Country:  United States    
Other Details:
Languages:  eng     Pagination:  261-86     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
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