TY - JOUR
T1 - 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
AU - Poussin, Mathilde A.
AU - Fuller, Claudette L.
AU - Goluszko, Elzbieta
AU - Reyes, Victor E.
AU - Braciale, Vivian L.
AU - Christadoss, Premkumar
N1 - Funding Information:
This work was supported by grants from the Myasthenia Gravis Foundation of America, the Muscular Dystrophy Association and the Association Française contre les Myopathies. Mathilde A. Poussin was successively an Association Française contre les Myopathies, Myasthenia Gravis Foundation of America, a McLaughlin Fellowship Fund postdoctoral fellow, and a Muscular Dystrophy Association development grant recipient. The authors are grateful to Mardelle Susman, MA for critically editing this manuscript.
PY - 2003/1
Y1 - 2003/1
N2 - 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.
AB - 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.
KW - Antigen presentation
KW - Autoimmunity
KW - Class II MHC
KW - Cytokines
KW - Mouse model
KW - Myasthenia gravis
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U2 - 10.1016/S0165-5728(02)00425-3
DO - 10.1016/S0165-5728(02)00425-3
M3 - Article
C2 - 12507777
AN - SCOPUS:0037222961
SN - 0165-5728
VL - 134
SP - 104
EP - 110
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -