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IL-33–Mediated Expansion of Type 2 Innate Lymphoid Cells Protects from Progressive Glomerulosclerosis

IL-33–Mediated Expansion of Type 2 Innate Lymphoid Cells Protects from Progressive Glomerulosclerosis

Authors :
Mathis Düster
Kerstin Kopp
Ulf Panzer
Ann-Christin Gnirck
Jan-Eric Turner
Jan-Hendrik Riedel
Luis A. Kluth
Boris Fehse
Martina Becker
Silke R. Brix
Sonja Krohn
Rolf A.K. Stahl
Madena Attar
Catherine Meyer-Schwesinger
Source :
Journal of the American Society of Nephrology. 28:2068-2080
Publication Year :
2017
Publisher :
Ovid Technologies (Wolters Kluwer Health), 2017.

Abstract

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.

Details

ISSN :
15333450 and 10466673
Volume :
28
Database :
OpenAIRE
Journal :
Journal of the American Society of Nephrology
Accession number :
edsair.doi...........65615a8d5b0d4b9d3b941c50ef4b48ee
Full Text :
https://doi.org/10.1681/asn.2016080877