Potentiating Tissue-Resident Type 2 Innate Lymphoid Cells by IL-33 to Prevent Renal Ischemia-Reperfusion Injury

Cao, Qi; Wang, Yiping; Niu, Zhiguo; Wang, Chengshi; Wang, Ruifeng; Zhang, Zhiqiang; Chen, Titi; Wang, Xin Maggie; Li, Qing; Lee, Vincent; Huang, Qingsong; Jinquan, Tan; Guο, Minghao; Wang, Yuan Min; Zheng, Guoping; Yu, Di; Alexander, Stephen I.; Wang, Hui; Harris, David C.H.

doi:10.1681/asn.2017070774

Cited by 98 publications

(176 citation statements)

References 56 publications

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“…In other studies, treatment with murine IL‐33, or recombinant human IL‐33 in humanized mice, prior to injury, induced similar protective effects, although only the day following injury was assessed . Loss of function studies were also performed by depletion of ILC2s in T/B cell‐deficient ( Rag1 −/− ) mice by treatment with anti‐CD90 . These studies demonstrated that the protective effects of IL‐33 were significantly diminished in the absence of ILC2s .…”

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 90%

“…These studies demonstrated that the protective effects of IL‐33 were significantly diminished in the absence of ILC2s . However, these mice were also depleted of other CD90 expressing cells including T reg cells, which may also be critical for this renoprotection . Furthermore, a complex bidirectional relationship exists between ILC2s and T reg .…”

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 97%

“…However, these mice were also depleted of other CD90 expressing cells including T reg cells, which may also be critical for this renoprotection . Furthermore, a complex bidirectional relationship exists between ILC2s and T reg . This concept is supported by studies examining the IL233 hybrid cytokine .…”

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 98%

“…IL‐33 treatment or transfer of IL‐33‐stimulated ILC2s was sufficient to significantly reduce SCr, tubular injury and increase survival to 100% out to 28 days post injury . In other studies, treatment with murine IL‐33, or recombinant human IL‐33 in humanized mice, prior to injury, induced similar protective effects, although only the day following injury was assessed . Loss of function studies were also performed by depletion of ILC2s in T/B cell‐deficient ( Rag1 −/− ) mice by treatment with anti‐CD90 .…”

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 99%

“…Most recently, the therapeutic potential of ILC2s in IRI has been further elucidated [63]. IL-33 treatment or transfer of IL-33-stimulated ILC2s was sufficient to significantly reduce SCr, tubular injury and increase survival to 100% out to 28 days post injury [63].…”

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 99%

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Emerging therapeutic potential of group 2 innate lymphoid cells in acute kidney injury

Cameron

Jiang

Loering

et al. 2019

The Journal of Pathology

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Acute kidney injury (AKI) remains a global challenge and, despite the availability of dialysis and transplantation, can be fatal. Those that survive an AKI are at increased risk of developing chronic kidney disease and end stage renal failure. Understanding the fundamental mechanisms underpinning the pathophysiology of AKI is critical for developing novel strategies for diagnosis and treatment. A growing body of evidence indicates that amplifying type 2 immunity may have therapeutic potential in kidney injury and disease. Of particular interest are the recently described subset of innate immune cells, termed group 2 innate lymphoid cells (ILCs). Group 2 ILCs are crucial tissue‐resident immune cells that maintain homeostasis and regulate tissue repair at multiple organ sites, including the kidney. They are critical mediators of type 2 immune responses following infection and injury. The existing literature suggests that activation of group 2 ILCs and production of a local type 2 immune milieu is protective against renal injury and associated pathology. In this review, we describe the emerging role for group 2 ILCs in renal homeostasis and repair. We provide an in‐depth discussion of the most recent literature that use preclinical models of AKI and assess the therapeutic effect of modulating group 2 ILC function. We debate the potential for targeting these cells as novel cellular therapies in AKI and discuss the implications for future studies and translation. Copyright © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 90%

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 97%

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 98%

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 99%

Section: Ilc2s As a Potential Cellular Therapy In Renal Injurymentioning

confidence: 99%

See 3 more Smart Citations

Emerging therapeutic potential of group 2 innate lymphoid cells in acute kidney injury

Cameron

Jiang

Loering

et al. 2019

The Journal of Pathology

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Biodegradable and Antioxidant DNA Hydrogel as a Cytokine Delivery System for Diabetic Wound Healing

Wang

Gou

et al. 2022

Adv Healthcare Materials

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Impaired diabetic wound healing is associated with the persistence of chronic inflammation and excessive oxidative stress, which has become one of the most serious clinical challenges. Wound dressings with anti-inflammatory and reactive oxygen species (ROS)-scavenging properties are desirable for diabetic wound treatment. In this study, a shape-adaptable, biodegradable, biocompatible, antioxidant, and immunomodulatory interleukin-33 (IL-33)-cytogel is developed by encapsulating IL-33 into physically cross-linked DNA hydrogels and used as wound dressings to promote diabetic wound healing. The porous microstructures and biodegradable properties of the IL-33-cytogel ensure the local sustained-release of IL-33 in the wound area, where the sustained-release of IL-33 is maintained for at least 7 days. IL-33-cytogel can induce local accumulation of group 2 innate lymphoid cells (ILC2s) and regulatory T cells (Tregs), as well as M1-to-M2 transition at the wound sites. Additionally, the antioxidant and biocompatible characteristics of DNA hydrogels promote the scavenging of intracellular ROS without affecting cell viability. As a result, local inflammation in the diabetic wound area is resolved upon IL-33-cytogel treatment, which is accompanied by improved granulation tissue regeneration and accelerated wound closure. This study demonstrates a promising strategy in tissue engineering and regenerative medicine by incorporating DNA hydrogels and cytokine immunotherapy for promoting diabetic wound healing.

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Ultrasmall Nanoparticles Regulate Immune Microenvironment by Activating IL‐33/ST2 to Alleviate Renal Ischemia‐Reperfusion Injury

Xu,

Xing,

Yuan

et al. 2024

Adv Healthcare Materials

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Renal ischemia‐reperfusion injury (IRI) is a common disease with high morbidity and mortality. Renal IRI can cause the disorder of immune microenvironment and reprograming the immune microenvironment to alleviate excessive inflammatory response is crucial for its treatment. Cytokine IL‐33 can improve the immune inflammatory microenvironment by modulating both innate and adaptive immune cells, and serve as an important target for modulating immune microenvironment of renal IRI. Herein, we report that bilobetin‐functionalized ultra‐small Cu2‐xSe nanoparticles (i.e., CSPB NPs) can activate the PKA/p‐CREB/IL‐33/ST2 signaling pathway to regulate innate and adaptive immune cells for reprograming the immune microenvironment of IRI‐induced acute kidney injury (AKI). The biocompatible CSPB NPs can promote the polarization of M1‐like macrophages into M2‐like macrophages, and the expansion of ILC2 and Treg cells by activating IL‐33/ST2 to modulate the excessive immune inflammatory response of renal IRI. More importantly, they can rapidly accumulate at the injured kidney to significantly alleviate IRI. This work demonstrates that modulating the expression of cytokines to reprogram immune microenvironment has great potential in the treatment of renal IRI and other ischemic diseases.This article is protected by copyright. All rights reserved

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Potentiating Tissue-Resident Type 2 Innate Lymphoid Cells by IL-33 to Prevent Renal Ischemia-Reperfusion Injury

Cited by 98 publications

References 56 publications

Emerging therapeutic potential of group 2 innate lymphoid cells in acute kidney injury

Emerging therapeutic potential of group 2 innate lymphoid cells in acute kidney injury

Biodegradable and Antioxidant DNA Hydrogel as a Cytokine Delivery System for Diabetic Wound Healing

Ultrasmall Nanoparticles Regulate Immune Microenvironment by Activating IL‐33/ST2 to Alleviate Renal Ischemia‐Reperfusion Injury

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