Interleukins 17 and 10 in a sample of Egyptian relapsing remitting multiple sclerosis patients

Abstract Background Cytokines are major contributors in the immune disruption in multiple sclerosis (MS). Objective Evaluating the proinflammatory (IL-17A) and anti-inflammatory (IL-10) cytokines in relapsing-remitting (RR) MS patients at time of relapse and during remission. Subjects and method A c...

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Published in:Journal of the neurological sciences Vol. 369; pp. 36 - 38
Main Authors: Tawfik, Tarek Z., MD, Gad, Adel H., MD, Mehaney, Dina A., MD, El Nahrery, Eslam, MD, Shehata, Hatem S., MD, Hashem, Hebatalla, MD, Ghaffar, Nawal F. Abdel, Ms, Shalaby, Nevin Mohieldin, MD
Format: Journal Article
Language:English
Published: Netherlands Elsevier B.V 15-10-2016
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Summary:Abstract Background Cytokines are major contributors in the immune disruption in multiple sclerosis (MS). Objective Evaluating the proinflammatory (IL-17A) and anti-inflammatory (IL-10) cytokines in relapsing-remitting (RR) MS patients at time of relapse and during remission. Subjects and method A case-control study including 30 RRMS patients and 15 controls. Patients were recruited from the Kasr Al-Ainy MS research unit (KAMSU), Cairo University, Egypt. Levels of IL-17A and IL-10 were assessed in patients' sera, during relapse and 30 days after IV methylprednisolone, and in control subjects using enzyme linked immunosorbent assays (ELISA). Results IL-17 was higher in patients during relapse and remission phases when compared with controls (P = 0.001), whereas, IL-10 was higher in patients during remission but normal during relapse (P = 0.01; 0.86 respectively). IL-17 increased during relapses (P = 0.001) while IL-10 increased during remissions (P = 0.028). No significant correlations were found between both interleukins and age at onset; disease duration, number of relapses; or EDSS. Conclusion RRMS patients can have a regulatory imbalance between both pro-and antiinflammatory cytokines, which could be a target for treatment strategies rather than focusing on a single cytokine.
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ISSN:0022-510X
1878-5883
DOI:10.1016/j.jns.2016.07.034