Effect of MHC class I and CD8 cell deficiency on experimental autoimmune myasthenia gravis pathogenesis.
Effect of MHC class I and CD8 cell deficiency on experimental autoimmune myasthenia gravis pathogenesis.
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DOI：
10.4049/jimmunol.153.11.5330
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发表时间：
1994-12
影响因子：
4.4
通讯作者：
M. Shenoy;R. Kaul;E. Goluszko;C. David;P. Christadoss;P. Christadoss
中科院分区：
文献类型：
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作者：
M. Shenoy;R. Kaul;E. Goluszko;C. David;P. Christadoss;P. Christadoss
MHC I类分子和CD 8+细胞缺乏可以预防小鼠的系统性红斑狼疮样疾病，或者增强非肥胖糖尿病小鼠的I型糖尿病。为了研究MHC I类和I类限制性CD 8 + T细胞在经典Ab介导的疾病实验性自身免疫性重症肌无力（EAMG）诱导中的参与，我们免疫了β 2微球蛋白（β 2 MG）。（β 2-m）基因破坏（β 2 m-/-）C57 BL 10（B10）小鼠，I类基因表达和CD 8+细胞缺陷，和杂合子（β 2-m+/-）B10小鼠，其在CFA中具有I类分子的正常表达和足够的具有电鳐乙酰胆碱受体的CD 8+细胞，并评估它们的EAMG的临床和免疫病理学表现。尽管MHC I类和CD 8+细胞缺乏，β 2-m-/-小鼠发展EAMG。此外，β 2-m-/-小鼠中EAMG的发生率高于具有正常I类表达和CD 8+细胞频率的β 2-m+/-杂合子小鼠。这一发现提供了直接的遗传学证据，反对C57 BL 10小鼠中MHCI类分子和I类限制性CD 8 + T细胞在EAMG发病机制中的致病效应作用。
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.