期刊
JOURNAL OF PATHOLOGY
卷 235, 期 1, 页码 79-89出版社
WILEY
DOI: 10.1002/path.4430
关键词
IL-17A; RANTES; renal fibrosis; inflammation; obstructive nephropathy
资金
- National Natural Science Foundation of China [31090363, 81230006, 91339000, 81100144]
- Chinese Ministry of Science and Technology [2012CB945104]
- Beijing Collaborative Innovative Research Centre for Cardiovascular Diseases [PXM2014_014226_000002]
IL-17A-producing T lymphocytes play a crucial role in inflammatory kidney diseases, but their role in renal fibrosis remains to be explored. Here, we demonstrated that up-regulation of IL-17A was associated with the development of obstructive kidney injury. The primary source of IL-17A production in obstructed kidneys was infiltrating T lymphocytes and CD4(+) T cells. IL-17A-deficient mice were protected from myofibroblast activation and extracellular matrix deposition, leading to reduced kidney fibrosis in response to obstructive injury. Mechanistically, IL-17A deficiency suppressed the expression of the chemokine RANTES in infiltrated CD3(+) T cells and peritubular inflammation following renal obstruction. Administration of RANTES-neutralizing antibody significantly reduced the accumulation of T cells and macrophages, and of collagen deposition in obstructed kidneys. Taken together, our results indicate that IL-17A contributes significantly to the pathogenesis of renal fibrosis by regulating RANTES-mediated inflammatory cell infiltration. Copyright (c) 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd
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