New roles revealed for T cells and DCs in glomerulonephritis.
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).
Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Alfred H J
AH
Kim
Mary A
MA
Markiewicz
Andrey S
AS
Shaw
D000818:Animals; D017951:Antigen Presentation / Q000276:immunology; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology / Q000473:pathology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000637:transplantation; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000637:transplantation; D003713:Dendritic Cells / Q000276:immunology*; D004195:Disease Models, Animal; D005921:Glomerulonephritis / Q000276:immunology* / Q000473:pathology*; D007668:Kidney / Q000276:immunology / Q000473:pathology; D008198:Lymph Nodes / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008822:Mice, Transgenic; D010047:Ovalbumin / Q000235:genetics / Q000276:immunology; D050199:Podocytes / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology* / Q000637:transplantation
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