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Copolymer-I binds to specialized molecules on cells whose function is to then trigger T cells. The cells are called antigen presenting cells and the molecules that copolymer-I binds are called MHC class II molecules. With copolymer-I bound to its surface, the antigen presenting cells trigger human T cells to become cells with anti-inflammatory properties. The T cells then migrate to the brain, where they suppress the brain inflammation that causes MS by releasing anti-inflammatory substances such as IL-10 and TGF-beta. Copolymer-I is not simply an MBP analog, as originally described by Sela and Arnon. Although it may have some cross-reactivity with MBP, it has much broader properties. Human T cells from all individuals can be stimulated by copolymer-I, and after stimulation they shift from Th1 to Th2/Th3 type cells, which act as suppressor or regulatory cells. When they enter the brain, they suppress inflammation via bystander suppression....
Thus, the copolymer designed to cause EAE in mice ultimately worked in MS because of unique interactions with human T cells that weren't known when the molecule was synthesized.
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