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).

Original languageEnglish
Pages (from-to)1074-1076
Number of pages3
JournalThe Journal of clinical investigation
Issue number5
StatePublished - May 2009


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