Abstract
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 (microMT) and wild type C57BL/6 mice with AChR in complete Freund's adjuvant. The ability of AChR-primed lymph node cells to proliferate and secrete IFN-gamma in response to AChR and its dominant peptide alpha 146-162 were intact in microMT as in wild type mice. Similar levels of mRNA for IFN-gamma, IL-4 and IL-10 in AChR-reactive lymph node cells were detected in microMT and wild type mice. However, microMT 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.
Published Version
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