The Th17 immune response in renal inflammation

Jan-Eric Turner, Hans-Joachim Paust, Oliver Steinmetz, Ulf Panzer

Research output: Contribution to journalArticleResearchpeer-review

106 Citations (Scopus)

Abstract

The discovery of interleukin (IL)-17-producing CD4(+) T (Th17) cells as a unique T-helper cell lineage has revised our understanding of T-cell-mediated tissue injury. Recent data from studies in humans and mice indicate that autoimmune diseases such as multiple sclerosis and rheumatoid arthritis, classically believed to be Th1-mediated, are predominantly driven by a Th17 immune response. IL-17 (IL-17A), IL-17F, IL-21, IL-22, and possibly also IL-9 produced by Th17 cells promote inflammation by directly causing tissue injury and enhancing secretion of pro-inflammatory cytokines and chemokines by resident cells. This results in augmented infiltration of leukocytes, in particular neutrophils, to the affected tissue where they induce organ inflammation and injury. Recent studies have highlighted the potential importance of the Th17 immune response also in renal inflammatory disease. This includes the identification and characterization of IL-17-producing T cells in nephritic kidneys of mice and humans, as well as evidence for the contribution of IL-17 and the IL-23/Th17 axis to renal tissue injury in glomerulonephritis. In this review, we will briefly summarize general characteristics of Th17 cells and discuss in detail the potential role of the Th17 immune response in human and experimental renal inflammation with a special focus on glomerulonephritis.
Original languageEnglish
Pages (from-to)1070 - 1075
Number of pages6
JournalKidney International
Volume77
Issue number12
DOIs
Publication statusPublished - 2010

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