MHC class I and CD8+ cell deficiency have either prevented systemic lupus erythematosus-like disease in mice or enhanced type I diabetes in nonobese diabetic mice. To study the involvement of MHC class I and class I-restricted CD8+ T cells in the induction of a classical Ab-mediated disease, experimental autoimmune myasthenia gravis (EAMG), we immunized β2 microglobulin (β2-m) gene-disrupted (β2 m(-/-)) C57BL10 (B10) mice, deficient in class I gene expression and CD8+ cells, and heterozygous (β2- m(+/-)) B10 mice with normal expression of class I molecules and sufficient CD8+ cells with Torpedo acetylcholine receptor in CFA, and assessed them for clinical and immunopathologic manifestations of EAMG. Despite MHC class I and CD8+ cell deficiency, β2-m(-/-) mice developed EAMG. Moreover, the incidence of EAMG in the β2-m(-/-) mice was higher than that of β2-m(+/- ) heterozygous mice with normal class I expression and frequency of CD8+ cells. The finding provided direct genetic evidence against a pathogenic effector role in C57BL10 mice for MHC class I molecule and class I-restricted CD8+ T cells in EAMG pathogenesis.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Immunology|
|State||Published - Dec 1 1994|
ASJC Scopus subject areas
- Immunology and Allergy