Peng S L, Madaio M P, Hayday A C, Craft J
Department of Biology, Yale University, New Haven, CT 06510, USA.
J Immunol. 1996 Dec 15;157(12):5689-98.
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.
尽管许多研究已证明αβ T细胞在小鼠狼疮中具有致病作用，但针对γδ T细胞的研究却很少。在此，通过构建缺乏αβ T细胞和/或γδ T细胞的狼疮易感小鼠，研究了αβ和γδ T细胞在系统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γδ T细胞的小鼠病情加重，表现为高球蛋白血症和自身抗体产生增加、更严重的肾脏疾病以及死亡率上升，这与传统CD4⁺αβ T细胞的多克隆扩增有关。相反，缺乏αβ T细胞的动物出现部分狼疮综合征，其特征为同种型特异性高球蛋白血症、不完全显性的自身抗体以及轻度免疫复合物肾病，所有这些均由γδ T细胞依赖性辅助驱动。这些数据表明，γδ T细胞参与了小鼠狼疮的调节和传播。
