| First Author | Poussin MA | Year | 2003 |
| Journal | J Neuroimmunol | Volume | 134 |
| Issue | 1-2 | Pages | 104-10 |
| PubMed ID | 12507777 | Mgi Jnum | J:100123 |
| Mgi Id | MGI:3586996 | Doi | 10.1016/s0165-5728(02)00425-3 |
| Citation | Poussin MA, et al. (2003) Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-gamma release by acetylcholine receptor-specific T cells. J Neuroimmunol 134(1-2):104-10 |
| abstractText | 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. |
