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Genetic predisposition to MS through expression of specific human leukocyte antigen (HLA) alleles associated both with antigen presentation and other autoimmune diseases is also widely documented ( Evidence obtained both through clinical studies and pre-clinical research with the EAE model suggest adaptive peripheral immune activity is exerted mainly through CD4+ Th-1 and Th-17 lymphocytes, in a B-cell antigen-presentation dependent manner

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