Propagation and regulation of systemic autoimmunity by gammadelta T cells.
Propagation and regulation of systemic autoimmunity by gammadelta T cells.
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DOI：
10.4049/jimmunol.157.12.5689
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发表时间：
1996-12
影响因子：
4.4
通讯作者：
S. Peng;M. Madaio;A. Hayday;J. Craft
中科院分区：
文献类型：
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作者：
S. Peng;M. Madaio;A. Hayday;J. Craft
虽然许多研究已经证明了α T细胞在小鼠狼疮中的致病作用，但很少有工作涉及γ δ T细胞。在这里，通过产生缺乏α-T细胞和/或γ-δ T细胞的狼疮易感小鼠，研究了α-T细胞和γ-δ T细胞在全身性自身免疫发病机制中的作用。与T细胞完整的小鼠相比，缺乏γ δ T细胞的小鼠出现了加重的疾病表型，包括增加的高丙种球蛋白血症和自身抗体产生，更严重的肾脏疾病和死亡率增加，与常规CD 4 + α T细胞的多克隆扩增相关。相反，α-T细胞缺陷的动物发展为部分狼疮综合征，其特征是同种型特异性高丙种球蛋白血症，不完全渗透的自身抗体和轻度免疫复合物肾病，所有这些都是由γ-δ T细胞依赖性帮助驱动的。这些数据表明，γ δ T细胞参与调节和小鼠狼疮的传播。
Although many studies have demonstrated a pathogenic role for alphabeta T cells in murine lupus, little work has addressed gammadelta T cells. Here, the roles of alphabeta and gammadelta T cells in the pathogenesis of systemic autoimmunity were investigated by generating lupus-prone mice deficient in alphabeta T cells and/or gammadelta T cells. Mice deficient in gammadelta T cells developed an exacerbated disease phenotype compared with that of T cell-intact mice, consisting of augmented hypergammaglobulinemia and autoantibody production, more severe renal disease, and increased mortality, associated with a polyclonal expansion of conventional CD4+ alphabeta T cells. Conversely, alphabeta T cell-deficient animals developed a partial lupus syndrome, characterized by isotype-specific hypergammaglobulinemia, incompletely penetrant autoantibodies, and mild immune complex renal disease, all of which were driven by gammadelta T cell-dependent help. These data indicate that gammadelta T cells participate in both the regulation and the propagation of murine lupus.