The Effects of Antibodies in Disease Progression of MOG-induced Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is an auto-inflammatory disease of the central nervous system (CNS), affecting over 400,000 people in the US. MS is primarily studied in the animal model experimental autoimmune encephalomyelitis (EAE). MS is a T cell mediated disease but there is mounting evidence for a role for B cells in MS. Previous studies have established that rMOG Induction depends on the presence of B cells, while induction using the MOG peptide covering amino acids 35-55 does not require B cells to cause disease. When plasma from the rMOG and MOG35-55 immunized WT mice was analyzed by ELISA there binding at MOG21-45, covering the encephalogenic epitope, and binding covering the MOG46-85 amino acids, which was not expected. This epitope was observed again in T cells when comparing the WT and B cell -/mice. WT T cells only bound MOG35-55 but T cells from B cell-/mice also bound MOG61-85. The same epitope observed in WT antibodies. This led to the conclusion that this was a cryptic epitope and seemed to produce an anti-inflammatory response. Mice coimmunized with both MOG35-55 and MOG61-85 similar results were observed as in rMOG immunization. Coimmunized mice had less severe disease than those immunized with just MOG35-55 giving further evidence that MOG61-85