The role of B-cells in experimental myasthenia gravis in mice

Myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG) are caused by auto-antibodies against the nicotinic acetylcholine receptor (AChR) at the postsynaptic membrane. To evaluate the extent to which the humoral immune response against AChR operates in the pathogenesis of EAMG, we immunized B-cell knockout (μMT) and wild type C57BL/6 mice with AChR in complete Freundʹs adjuvant. The ability of AChR-primed lymph node cells to proliferate and secrete IFN-γ in response to AChR and its dominant peptide α 146–162 were intact in μMT as in wild type mice. Similar levels of mRNA for IFN-γ, IL-4 and IL-10 in AChR-reactive lymph node cells were detected in μMT and wild type mice. However, μMT mice had no detectable anti-AChR antibodies and never developed clinical EAMG. We conclude that B-cells are critically required for the genesis of clinical EAMG, but not for AChR-specific T-cell priming.