IL-25 Elicits Innate Lymphoid Cells and Multipotent Progenitor Type 2 Cells That Reduce Renal Ischemic/Reperfusion Injury.

IL-25 Elicits Innate Lymphoid Cells and Multipotent Progenitor Type 2 Cells That Reduce Renal Ischemic/Reperfusion Injury.

J Am Soc Nephrol. 2015 Jan 2;

Authors: Huang Q, Niu Z, Tan J, Yang J, Liu Y, Ma H, Lee VW, Sun S, Song X, Guo M, Wang Y, Cao Q

Abstract
IL-25 is an important immune regulator that can promote Th2 immune response-dependent immunity, inflammation, and tissue repair in asthma, intestinal infection, and autoimmune diseases. In this study, we examined the effects of IL-25 in renal ischemic/reperfusion injury (IRI). Treating IRI mice with IL-25 significantly improved renal function and reduced renal injury. Furthermore, IL-25 treatment increased the levels of IL-4, IL-5, and IL-13 in serum and kidney and promoted induction of alternatively activated (M2) macrophages in kidney. Notably, IL-25 treatment also increased the frequency of type 2 innate lymphoid cells (ILC2s) and multipotent progenitor type 2 (MPP(type2)) cells in kidney. IL-25-responsive ILC2 and MPP(type2) cells produced greater amounts of Th2 cytokines that associated with the induction of M2 macrophages and suppression of classically activated (M1) macrophages in vitro. Finally, adoptive transfer of ILC2s or MPP(type2) cells not only reduced renal functional and histologic injury in IRI mice but also induced M2 macrophages in kidney. In conclusion, our data identify a mechanism whereby IL-25-elicited ILC2 and MPP(type2) cells regulate macrophage phenotype in kidney and prevent renal IRI.

PMID: 25556172 [PubMed – as supplied by publisher]

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Group 2 innate lymphoid cells in lung inflammation.

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Group 2 innate lymphoid cells in lung inflammation.

Immunology. 2013 Jul 19;

Authors: Li BW, Hendriks RW

Abstract
Although allergic asthma is a heterogeneous disease, allergen-specific T helper 2 (Th2) cells producing the key cytokines involved in type 2 inflammation, IL-4, IL-5 and IL-13, are thought to play a major role in asthma pathogenesis. This model is challenged by the recent discovery of group 2 innate lymphoid cells (ILC2) that represent a critical innate source of type 2 cytokines. These ILC2 are activated by epithelial cell-derived cytokines, including IL-25 and IL-33, which have been implicated in the initiation of asthma. In this review, we will discuss recent studies supporting a significant role for ILC2 in lung inflammation, with special attention to allergen-induced asthma. This article is protected by copyright. All rights reserved.

PMID: 23866009 [PubMed – as supplied by publisher]

View full post on pubmed: asthma