association of new putative epitopes of myelin proteolipid protein (58-74) with pathogenesis of multiple sclerosis

multiple sclerosis (ms) is an autoimmune disease in which auto-reactive t cells react with self-antigens expressed in the central nervous system (cns). the main cause of ms is unknown. nonetheless, the most probable theory is based on molecular mimicry, which suggests that some infections can activate t cells against brain auto-antigens like myelin proteolipid protein (plp) and initiate the disease cascade. this study is conducted to evaluate the activatory effects of plp 58-74 on t lymphocytes and humoral immunity. plp 58-74 was considered as an immunodominant epitope candidate of plp using bioinformatics tools. patients and healthy individuals’ peripheral blood mononuclear cells (pbmcs) were treated with plp 58-74 and its proliferative effects were evaluated through assessing proliferating cell nuclear antigen (pcna) gene expression changes by real time pcr and immunocytochemistry assay. finally, the rate of cd4 + and cd8 + t cells were assessed by flowcytometry. elisa was also performed to measure anti plp 58-74 antibody in patients’ serum. plp 58-74 induced proliferation in patients’ pbmcs while it did not influence pbmcs of healthy individuals. cd4 + t cells were the main activated cells in reaction to plp 58-74 which increased from 22% to 39.91%. in addition, immune assay showed threefold increase in specific anti plp 58-74 igg in patients compared to healthy controls. results showed that plp 58-74 can stimulate cd4 + t cells and humoral immunity. therefore it seems that the epitopes of some microorganisms mimicking plp such as plp 58-74 might have a potential role in the initiation of ms.