RT Journal Article
SR Electronic
T1 Effect of MHC class I and CD8 cell deficiency on experimental autoimmune myasthenia gravis pathogenesis.
JF The Journal of Immunology
JO J. Immunol.
FD American Association of Immunologists
SP 5330
OP 5335
VO 153
IS 11
A1 Shenoy, M
A1 Kaul, R
A1 Goluszko, E
A1 David, C
A1 Christadoss, P
YR 1994
UL http://www.jimmunol.org/content/153/11/5330.abstract
AB 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 beta 2 microglobulin (beta 2-m) gene-disrupted (beta 2 m-/-) C57BL10 (B10) mice, deficient in class I gene expression and CD8+ cells, and heterozygous (beta 2-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, beta 2-m-/- mice developed EAMG. Moreover, the incidence of EAMG in the beta 2-m-/- mice was higher than that of beta 2-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.