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

Huang, Qingsong; Niu, Zhiguo; Jinquan, Tan; Yang, Jing; Liu, Yun; Ma, Haijun; Lee, Vincent; Sun, Shuming; Song, Xiangfeng; Guο, Minghao; Wang, Yiping; Cao, Qi

doi:10.1681/asn.2014050479

Cited by 75 publications

(91 citation statements)

References 45 publications

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“…IL-25 also sustains homeostasis and activation of IL-13-producing ILC2 and type II natural killer T (NKT) cells in adipose tissue (17). Increasing adipose tissue levels of IL-13-producing ILC2 and type II NKT cells by adoptive transfer or IL-25 administration can increase adipose eosinophil and M2-like macrophage levels (17,18). Thus, a newly defined ILC2-eosinophil-M2 axis maintains adipose tissue metabolic homeostasis.…”

Section: Maintenance Of Normal Adipose Tissue Functionmentioning

confidence: 99%

Obesity, Inflammation, and Cancer

Deng

Lyon

Bergin

et al. 2016

Annu. Rev. Pathol. Mech. Dis.

646

522

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Obesity, a worldwide epidemic, confers increased risk for multiple serious conditions, including cancer, and is increasingly recognized as a growing cause of preventable cancer risk. Chronic inflammation, a well-known mediator of cancer, is a central characteristic of obesity, leading to many of its complications, and obesity-induced inflammation confers additional cancer risk beyond obesity itself. Multiple mechanisms facilitate this strong association between cancer and obesity. Adipose tissue is an important endocrine organ, secreting several hormones, including leptin and adiponectin, and chemokines that can regulate tumor behavior, inflammation, and the tumor microenvironment. Excessive adipose expansion during obesity causes adipose dysfunction and inflammation to increase systemic levels of proinflammatory factors. Cells from adipose tissue, such as cancer-associated adipocytes and adipose-derived stem cells, enter the cancer microenvironment to enhance protumoral effects. Dysregulated metabolism that stems from obesity, including insulin resistance, hyperglycemia, and dyslipidemia, can further impact tumor growth and development. This review describes how adipose tissue becomes inflamed in obesity, summarizes ways these mechanisms impact cancer development, and discusses their role in four adipose-associated cancers that demonstrate elevated incidence or mortality in obesity.

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Section: Maintenance Of Normal Adipose Tissue Functionmentioning

confidence: 99%

Obesity, Inflammation, and Cancer

Deng

Lyon

Bergin

et al. 2016

Annu. Rev. Pathol. Mech. Dis.

646

522

View full text Add to dashboard Cite

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“…The M2 phenotype can be induced ex vivo or in vivo via IL‐10 and transforming growth factor (TGF)‐β stimulation for treating kidney diseases . The type 2 innate lymphoid cells (ILC2s), which are a recently described innate immune cell population that can be activated by IL‐33 or IL‐25, also contribute to M2 polarization of macrophages through secretion of various type 2 cytokines, such as IL‐4 and IL‐13 …”

Section: Introductionmentioning

confidence: 99%

Peritoneal M2 macrophage transplantation as a potential cell therapy for enhancing renal repair in acute kidney injury

Mao

Wang

Zhang

et al. 2020

J Cellular Molecular Medi

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Acute kidney injury (AKI) is a clinical condition that is associated with high morbidity and mortality. Inflammation is reported to play a key role in AKI. Although the M2 macrophages exhibit antimicrobial and anti‐inflammatory activities, their therapeutic potential has not been evaluated for AKI. This study aimed to investigate the protective effect of peritoneal M2 macrophage transplantation on AKI in mice. The macrophages were isolated from peritoneal dialysates of mice. The macrophages were induced to undergo M2 polarization using interleukin (IL)‐4/IL‐13. AKI was induced in mice by restoring the blood supply after bilateral renal artery occlusion for 30 minutes. The macrophages were injected into the renal cortex of mice. The changes in renal function, inflammation and tubular proliferation were measured. The M2 macrophages were co‐cultured with the mouse primary proximal tubular epithelial cells (PTECs) under hypoxia/reoxygenation conditions in vitro. The PTEC apoptosis and proliferation were analysed. The peritoneal M2 macrophages effectively alleviated the renal injury and inflammatory response in mice with ischaemia‐reperfusion injury (IRI) and promoted the PTEC proliferation in vivo and in vitro. These results indicated that the peritoneal M2 macrophages ameliorated AKI by decreasing inflammatory response and promoting PTEC proliferation. Hence, the peritoneal M2 macrophage transplantation can serve as a potential cell therapy for renal diseases.

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“…In the seminal study reported by Huang et al , it was demonstrated that IL‐25–dependent inflammatory ILC2s also express high levels of GATA‐3 (more than that expressed by natural ILC2s), and that they express an intermediate amount of retinoic acid receptor–related orphan nuclear receptor γt (RORγt) (a smaller amount than that expressed by ILC3s, but significantly distinct from the amount expressed by natural ILC2s). The exact contribution of these different transcription factors in modulating ILC2 expansion needs to be better clarified in future studies.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, IL‐25 regulates the development of autoimmune inflammation mediated by IL‐17–producing T cells . Furthermore, IL‐25/IL‐17RB activation promotes Th2 responses by increasing the frequency of M2‐type macrophages and the differentiation of both natural and inflammatory group 2 innate lymphoid cells (ILC2s) . Despite these pivotal functions in modulating immune responses, the roles of the IL‐25/IL‐17RB axis and of ILC2s in the pathogenesis of experimental SS and primary SS, as well as in primary SS–associated lymphoma, have not yet been investigated.…”

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confidence: 99%