title: IL-25 Elicits Innate Lymphoid Cells and Multipotent Progenitor Type 2 Cells That Reduce Renal Ischemic/Reperfusion Injury.
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.
authors.affiliation: Research Center for Immunology, Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, China;
authors.forename: Qingsong
authors.initials: Q
authors.lastname: Huang
authors.affiliation: Research Center for Immunology, Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, China;
authors.forename: Zhiguo
authors.initials: Z
authors.lastname: Niu
authors.affiliation: Department of Nephrology, Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, China;
authors.forename: Jing
authors.initials: J
authors.lastname: Tan
authors.affiliation: Department of Nephrology, First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China; and.
authors.forename: Jun
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of Nephrology, First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China; and.
authors.forename: Yun
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Nephrology, First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China; and.
authors.forename: Haijun
authors.initials: H
authors.lastname: Ma
authors.affiliation: Centre for Transplant and Renal Research, Westmead Millennium Institute, University of Sydney, Sydney, New South Wales, Australia.
authors.forename: Vincent W S
authors.initials: VW
authors.lastname: Lee
authors.affiliation: Research Center for Immunology, Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, China;
authors.forename: Shuming
authors.initials: S
authors.lastname: Sun
authors.affiliation: Research Center for Immunology, Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, China;
authors.forename: Xiangfeng
authors.initials: X
authors.lastname: Song
authors.affiliation: Department of Nephrology, First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China; and.
authors.forename: Minghao
authors.initials: M
authors.lastname: Guo
authors.affiliation: Centre for Transplant and Renal Research, Westmead Millennium Institute, University of Sydney, Sydney, New South Wales, Australia.
authors.forename: Yiping
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Research Center for Immunology, Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, China; Centre for Transplant and Renal Research, Westmead Millennium Institute, University of Sydney, Sydney, New South Wales, Australia qi.cao@sydney.edu.au.
authors.forename: Qi
authors.initials: Q
authors.lastname: Cao
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000276:immunology* / Q000517:prevention & control*; D019264:Adoptive Transfer; D000818:Animals; D002470:Cell Survival; D002478:Cells, Cultured; D007113:Immunity, Innate / Q000187:drug effects / Q000276:immunology; D007155:Immunologic Factors / Q000494:pharmacology / Q000627:therapeutic use*; D018793:Interleukin-13 / Q000378:metabolism; D020381:Interleukin-17 / Q000494:pharmacology / Q000627:therapeutic use*; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D007668:Kidney / Q000098:blood supply / Q000378:metabolism; D008214:Lymphocytes / Q000166:cytology / Q000187:drug effects*; D008264:Macrophages / Q000187:drug effects; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D039902:Multipotent Stem Cells / Q000166:cytology / Q000187:drug effects*; D015427:Reperfusion Injury / Q000150:complications / Q000276:immunology* / Q000517:prevention & control*; D018418:Th2 Cells / Q000276:immunology
chemical_list: D007155:Immunologic Factors; D018793:Interleukin-13; D020381:Interleukin-17; D015848:Interleukin-5; D015847:Interleukin-4
keywords: IL-25; injury; innate lymphoid cells; ischemia/reperfusion; multipotent progenitor type 2