EXPERIMENTAL AUTOIMMUNE MYASTHENIA-GRAVIS INDUCTION IN B-CELL-DEFICIENT MICE

Experimental autoimmune myasthenia gravis (EAMG) is an animal model fo r human myasthenia gravis (MG), Autoantibody-induced functional loss o f nicotinic acetylcholine receptor (AChR) at the postsynaptic membrane is an important pathogenic feature of both MG and EAMG, To evaluate t he extent at which the humoral immune response against AChR operates i n the pathogenesis of EAMG, we immunized B cell knockout (mu MT) and w ild-type C57BL/6 mice with AChR and complete Freund's adjuvant, The ab ility of AChR-primed lymph node cells to proliferate and secrete IFN-g amma in response to AChR and its dominant peptide alpha 145-162 were i ntact in mu MT mice as in wild-type mice. Similar amounts of mRNA for IFN-gamma, IL-4 and IL-10 in AChR-reactive lymph node cells were detec ted in mu MT and wild-type mice. However, mu MT mice had no detectable anti-AChR antibodies and remained completely free from clinical EAMG. We conclude that B cells are critically required for the genesis of c linical EAMG, but not for AChR-specific T cell priming.