Th1 and Th17 Cells Induce Proliferative Glomerulonephritis

Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cell...

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Veröffentlicht in:	Journal of the American Society of Nephrology 2009-12, Vol.20 (12), p.2518-2524
Hauptverfasser:	SUMMERS, Shaun A, STEINMETZ, Oliver M, MING LI, KAUSMAN, Joshua Y, SEMPLE, Timothy, EDGTTON, Kristy L, BORZA, Dorin-Bogdan, BRALEY, Hal, HOLDSWORTH, Stephen R, KITCHING, A. Richard
Format:	Artikel
Sprache:	eng
Schlagworte:	Adaptive Immunity Adoptive Transfer Animals Biological and medical sciences Brief Communications Chemokines - genetics Chemokines - metabolism Disease Models, Animal Genes, RAG-1 Glomerulonephritis Glomerulonephritis, Membranoproliferative - etiology Glomerulonephritis, Membranoproliferative - genetics Glomerulonephritis, Membranoproliferative - immunology Immunoglobulin G - metabolism Interleukin-17 - metabolism Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Ovalbumin - immunology RNA, Messenger - genetics RNA, Messenger - metabolism T-Lymphocyte Subsets - immunology T-Lymphocytes, Helper-Inducer - immunology Th1 Cells - immunology
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