To elucidate the role of antibodies in development of chronic non-remitting experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice, which is a well-established Th1-mediated autoimmune disease, and the involvement of activation-induced cytidine deaminase (AID) in Th1-mediated function, we have investigated the myelin oligodendrocyte glycoprotein (MOG)-induced EAE in mice deficient of AID, which is absolutely required for class switching and somatic hypermutation. Following immunization with MOG, AID(-/-) had completely same levels of clinical and pathological severity of EAE when compared with AID(+/-) and AID(+/+), although AID(-/-) did not produce IgG and anti-MOG IgG. Similar levels of T cell proliferation and a modest increase of anti-MOG IgM synthesis were found in spleen cells of AID(-/-) stimulated with MOG. These results indicate that antibodies are not involved in development of EAE in C57BL/6 mice.
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