Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells

Class II MHC mutant bm12 mice have an increased resistance to experimental autoimmune myasthenia gravis (EAMG) compared to C57BL/6 mice. In vitro, this relative resistance was mainly associated with a reduced cytokine response to acetylcholine receptor (AChR) and its dominant pathogenic peptide α146–162, whereas the response to the epitope α111–126 remained intact. Calcium mobilization after stimulation of AChR-immune T cells with AChR or α146–162 peptide, but not α111–126 peptide, was decreased in bm12 compared to C57BL/6. Thus, the reduced incidence of clinical EAMG in bm12 is linked to lower IFN-γ and IL-10 release, and intracellular calcium mobilization by α146–162-specific T cells.