Peng S L, Madaio M P, Hughes D P, Crispe I N, Owen M J, Wen L, Hayday A C, Craft J
Department of Biology, Yale University, New Haven, CT 06510, USA.
J Immunol. 1996 May 15;156(10):4041-9.
To investigate the possibility that non-alpha beta T cell-dependent mechanisms can induce systemic autoimmune disease, and to address the roles of alpha beta T cells in murine lupus, we analyzed lupus-prone MRL mice congenitally deficient in alpha beta T cells. Surprisingly, TCR-alpha-/- MRL mice developed several characteristics of human systemic lupus erythematosus, including hypergammaglobulinemia, autoantibodies against DNA and small nuclear ribonucleoproteins, and immune deposits in kidneys. These results, which contrast with past studies concluding that MRL autoimmunity requires CD4+ alpha beta T cells, demonstrate that non-alpha beta T cell-dependent mechanisms are capable of inducing lupus phenomena, and further suggest that MRL disease may consist of both alpha beta T cell-independent and alpha beta T cell-dependent mechanisms.
为了研究非αβ T细胞依赖性机制诱导系统性自身免疫疾病的可能性，并探讨αβ T细胞在小鼠狼疮中的作用，我们分析了先天性缺乏αβ T细胞的狼疮易感MRL小鼠。令人惊讶的是，TCR-α-/- MRL小鼠出现了人类系统性红斑狼疮的若干特征，包括高球蛋白血症、针对DNA和小核核糖核蛋白的自身抗体以及肾脏中的免疫沉积物。这些结果与过去认为MRL自身免疫需要CD4+αβ T细胞的研究结果形成对比，表明非αβ T细胞依赖性机制能够诱导狼疮现象，并进一步表明MRL疾病可能由αβ T细胞非依赖性和αβ T细胞依赖性机制共同组成。
