TY - JOUR
T1 - Effect of MHC class I and CD8 cell deficiency on experimental autoimmune myasthenia gravis pathogenesis
AU - Shenoy, Mohan
AU - Kaul, Rashmi
AU - Goluszko, Elzbieta
AU - David, Chella
AU - Christadoss, Premkumar
PY - 1994/12/1
Y1 - 1994/12/1
N2 - 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.
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 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.
UR - http://www.scopus.com/inward/record.url?scp=0028062801&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028062801&partnerID=8YFLogxK
M3 - Article
C2 - 7963585
AN - SCOPUS:0028062801
SN - 0022-1767
VL - 153
SP - 5330
EP - 5335
JO - Journal of Immunology
JF - Journal of Immunology
IS - 11
ER -