Vitamin D supplementation could limit T helper-17 response in multiple sclerosis

Objectives Low vitamin D and high response of T helper-17 (Th17) are two main risk factors in multiple sclerosis (MS). The purpose of the present study was to investigate whether vitamin D supplementation can reduce Th17 responses and interleukin-17A (IL-17A) production. Methods Serum samples of 17...

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Veröffentlicht in:Clinical & experimental neuroimmunology 2014-10, Vol.5 (3), p.336-339
Hauptverfasser: Najafipoor, Adeleh, Roghanian, Rasoul, Rahimi, Maryam, Zarkesh-Esfahani, Sayyed Hamid, Shayegannejad, Vahid
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Sprache:eng
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Zusammenfassung:Objectives Low vitamin D and high response of T helper-17 (Th17) are two main risk factors in multiple sclerosis (MS). The purpose of the present study was to investigate whether vitamin D supplementation can reduce Th17 responses and interleukin-17A (IL-17A) production. Methods Serum samples of 17 relapsing-remitting MS patients were collected at onset of disease. They were supplemented with 50 000 IU/week vitamin D3 for 6 months. After 6 months, sampling was repeated from the patients. The serum level of 25-hydroxyvitamin D and IL-17A were measured at baseline, and after 6 months using commercially available enzyme-linked immunosorbent assay. Statistical analyses were carried out by Wilcoxon test and Spearman's rho correlation coefficient. Results The levels of 25-hydroxyvitamin D were generally deficient (29.4%) and insufficient (47%) in the patients at baseline. The initial IL-17A levels (mean 3.9, standard error 0.28) were significantly decreased after vitamin D supplementation (mean 2.2, standard error 0.18, P < 0.0001). Furthermore, a positive correlation was seen between pre-supplementation IL-17A levels and reduction after supplementation (Spearman's rho = 0.61, P = 0.008). Conclusion In the present study, it was shown that vitamin D supplementation could reduce the level of IL-17A in MS patients, and there was an association between these two risk factors in MS disease. [PUBLICATION ABSTRACT]
ISSN:1759-1961
1759-1961
DOI:10.1111/cen3.12139