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
Copyright policy )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 alpha 146-162, whereas the response to the epitope alpha 111-126 remained intact. Calcium mobilization after stimulation of AChR-immune T cells with AChR or alpha 146-162 peptide, but not alpha 111-126 peptide, was decreased in bm12 compared to C57BL/6. Thus, the reduced incidence of clinical EAMG in bm12 is linked to lower IFN-gamma and IL-10 release, and intracellular calcium mobilization by alpha 146-162-specific T cells.
- University of Pennsylvania United States
- The University of Texas Medical Branch at Galveston United States
- National Institutes of Health United States
- National Cancer Institute United States
- University Medical Center United States
Intracellular Fluid, T-Lymphocytes, Histocompatibility Antigens Class II, Down-Regulation, Immunity, Innate, Peptide Fragments, Interleukin-10, Myasthenia Gravis, Autoimmune, Experimental, Mice, Inbred C57BL, Epitopes, Interferon-gamma, Mice, Mutation, Immune Tolerance, Animals, Calcium, Receptors, Cholinergic, Calcium Signaling, Spleen, Signal Transduction
Intracellular Fluid, T-Lymphocytes, Histocompatibility Antigens Class II, Down-Regulation, Immunity, Innate, Peptide Fragments, Interleukin-10, Myasthenia Gravis, Autoimmune, Experimental, Mice, Inbred C57BL, Epitopes, Interferon-gamma, Mice, Mutation, Immune Tolerance, Animals, Calcium, Receptors, Cholinergic, Calcium Signaling, Spleen, Signal Transduction
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