Effect of MHC class I and CD8 cell deficiency on experimental autoimmune myasthenia gravis pathogenesis

Mohan Shenoy, Rashmi Kaul, Elzbieta Goluszko, Chella David, Premkumar Christadoss

Research output: Contribution to journalArticle

27 Scopus citations


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 languageEnglish
Pages (from-to)5330-5335
Number of pages6
JournalJournal of Immunology
Issue number11
StatePublished - 1 Dec 1994


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