Document Type: Original Article
Immunology Department, Medicine Faculty
Neuroscience Research Center, Tabriz University of Medical Sciences,Tabriz, Iran
Institute for Cancer Research, Shiraz University of Medical Sciences, Shiraz, Iran
Bakground: Multiple sclerosis (MS) is a CD4+ T cell-mediated autoimmune disease affecting the central nervous system (CNS). It was previously believed that Th1 cells were pathogenic T cells in experimental autoimmune encephalomyelitis (EAE). However, the functional role of Th1 cells in EAE has been reconsidered upon the discovery of IL-17- producing T cells which are consider as dominant effectors for inducing autoimmune tissue inflammation.
Objective: The objective of this study was to assess the role of IL-17A and IL-17F in MS pathogenesis.
Methods: We evaluated mRNA expression of IL-17A and IL-17F in thirty-five Iranian patients with relapsing–remitting MS (RRMS) and twenty-five healthy controls by Quantitative Real Time PCR.
Results: The results of this study showed a twenty-fold increase in the expression of IL-17A mRNA in MS patients compared to the control group (p < 0.0001 ). IL-17F mRNA expression in MS patients was thirty three-times greater than control group (p = 0.0008). IL-17A mRNA expression in periphery was positively correlated with expression of IL-17F transcripts in MS patients and controls (p < 0.01 and p < 0.05, respectively).
Conclusion: These results indicate the critical role of Th17- mediated cytokines in development of MS which classically has been considered as a Th1-mediated disorder. The results of this study showed, for the first time, the importance of IL-17F in MS immunopathogenesis.