Kim Alfred H J, Markiewicz Mary A, Shaw Andrey S
Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
J Clin Invest. 2009 May;119(5):1074-6. doi: 10.1172/jci39071.
Little is known about the potential role of T cells in the inflammatory renal disease glomerulonephritis (GN). GN has been historically viewed as a product of immune complex-mediated complement activation, and the presence of autoantibodies made identifying T cell-specific effector contributions difficult to elucidate. In this issue of the JCI, Heymann et al. generate what they believe to be a novel, transgenic murine model of GN, demonstrating a direct role for CD8+ T cells, activated CD4+ T cells, and DCs in the pathogenesis of GN (see the related article beginning on page 1286).
关于T细胞在炎性肾脏疾病肾小球肾炎(GN)中的潜在作用,人们了解甚少。从历史上看,GN一直被视为免疫复合物介导的补体激活的产物,并且自身抗体的存在使得难以阐明T细胞特异性效应作用。在本期《临床研究杂志》中,海曼等人构建了他们认为是新型的GN转基因小鼠模型,证明了CD8 + T细胞、活化的CD4 + T细胞和树突状细胞在GN发病机制中的直接作用(见第1286页开始的相关文章)。