In trans T cell tolerance exacerbates experimental allergic encephalomyelitis by interfering with protective antibody responses.

Abstract F 1 (SJL/J × C57BL/6) mice with MOG35–55-induced EAE recover from disease when treated with Ig-MOG carrying MOG35–55 peptide. However, Ig-PLP1, carrying PLP139–151, induced reduction of anti-MOG antibodies and exacerbated EAE. Herein, we show that Ig-PLP1 specifically reduces the frequency of B cells producing protective IgG2a/b anti-MOG antibodies. Surprisingly, these cells were marginal zone (MZ), rather than follicular (FO) or newly formed (NF), B cells and transfer of MZ B cells into sick mice nullified disease exacerbation by Ig-PLP1 in a complement dependent manner. These findings reveal a potential self-limiting regulatory mechanism involving auto-antibodies in MOG EAE.