先天性淋巴细胞
肾
局灶节段性肾小球硬化
免疫系统
免疫学
白细胞介素33
髓样
先天免疫系统
炎症
生物
急性肾损伤
肾小球硬化
肾脏疾病
医学
肾小球肾炎
病理
白细胞介素
内科学
细胞因子
内分泌学
蛋白尿
作者
Jan-Hendrik Riedel,Martina Becker,Kerstin Kopp,Mathis Düster,Silke R. Brix,Catherine Meyer-Schwesinger,Luis Kluth,Ann-Christin Gnirck,Madena Attar,Sonja Krohn,Boris Fehse,Rolf A.K. Stahl,Ulf Panzer,Jan‐Eric Turner
出处
期刊:Journal of The American Society of Nephrology
日期:2017-02-02
卷期号:28 (7): 2068-2080
被引量:96
标识
DOI:10.1681/asn.2016080877
摘要
Innate lymphoid cells (ILCs) have an important role in the immune system's response to different forms of infectious and noninfectious pathologies. In particular, IL-5– and IL-13–producing type 2 ILCs (ILC2s) have been implicated in repair mechanisms that restore tissue integrity after injury. However, the presence of renal ILCs in humans has not been reported. In this study, we show that ILC populations are present in the healthy human kidney. A detailed characterization of kidney-residing ILC populations revealed that IL-33 receptor–positive ILC2s are a major ILC subtype in the kidney of humans and mice. Short-term IL-33 treatment in mice led to sustained expansion of IL-33 receptor–positive kidney ILC2s and ameliorated adriamycin-induced glomerulosclerosis. Furthermore, the expansion of ILC2s modulated the inflammatory response in the diseased kidney in favor of an anti-inflammatory milieu with a reduction of pathogenic myeloid cell infiltration and a marked accumulation of eosinophils that was required for tissue protection. In summary, kidney-residing ILC2s can be effectively expanded in the mouse kidney by IL-33 treatment and are central regulators of renal repair mechanisms. The presence of ILC2s in the human kidney tissue identifies these cells as attractive therapeutic targets for CKD in humans.
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