CD4 and Parkinson disease: Second, the presentation of certain peptides on different MHC-II isotypes could alter the differentiation of CD4+ T cells into various subsets (i.e., Th1, Th2, Th17, or regulatory T cells).42 Evidence for such phenomena can be demonstrated in human autoimmune disease and humanized rodent models of autoimmunity.43 In this manner, antigen presentation via MHC-II on the surface of APCs to CD4+ T cells is a mechanism that could link the contribution of both genetic background and environmental exposure to susceptibility for developing PD.