IL-33-induced alternatively activated macrophage attenuates the development of TNBS-induced colitis

Tu, Lei; Chen, Jie; Xu, Dandan; Xie, Zhongming; Yu, Bing; Ying, Tao; Shi, Guixiu; Duan, Lihua

doi:10.18632/oncotarget.15984

Cited by 37 publications

(33 citation statements)

References 35 publications

(49 reference statements)

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“…In other studies, IL-33 was protective in colitis by inducing polarization of macrophages to M2 macrophages, which are typically associated with T H 2 cytokines and promote resolution of inflammation [131, 132]. In one study, these M2 macrophages, which they termed alternatively activated macrophages, were isolated from IL-33-treated mice and transferred to mice with TNBS-induced colitis [131].…”

Section: Il-33/st2 Signaling Axis In Inflammatory Bowel Diseasementioning

confidence: 99%

Section: Il-33/st2 Signaling Axis In Inflammatory Bowel Diseasementioning

confidence: 99%

“…In one study, these M2 macrophages, which they termed alternatively activated macrophages, were isolated from IL-33-treated mice and transferred to mice with TNBS-induced colitis [131]. This conferred protection to recipient mice, in which there was a significant decrease in intestinal disease and inflammatory markers [131]. A similar finding was found in which peritoneal injection of IL-33 in experimental colitis induced M2 macrophage polarization, which subsequently resulted in goblet cell differentiation and attenuated inflammation [132].…”

Section: Il-33/st2 Signaling Axis In Inflammatory Bowel Diseasementioning

confidence: 99%

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IL-33 and the intestine: The good, the bad, and the inflammatory

et al. 2017

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Interleukin-33 (IL-33) is a member of the IL-1 cytokine family that has been widely studied since its discovery in 2005 for its dichotomous functions in homeostasis and inflammation. IL-33, along with its receptor suppression of tumorigenicity 2 (ST2), has been shown to modulate both the innate and adaptive immune system. Originally, the IL-33/ST2 signaling axis was studied in the context of inducing type 2 immune responses with the expression of ST2 by T helper 2 (TH2) cells. However, the role of IL-33 is not limited to TH2 responses. Rather, IL-33 is a potent activator of TH1 cells, group 2 innate lymphoid cells (ILC2s), regulatory T (Treg) cells, and CD8+ T cells. The intestine is uniquely important in this discussion, as the intestinal epithelium is distinctively positioned to interact with both pathogens and the immune cells housed in the mucosa. In the intestine, IL-33 is expressed by the pericryptal fibroblasts and its expression is increased particularly in disease states. Moreover, IL-33/ST2 signaling aberrancy is implicated in the pathogenesis of inflammatory bowel disease (IBD). Accordingly, for this review, we will focus on the role of IL-33 in the regulation of intestinal immunity, involvement in intestinal disease, and implication in potential therapeutics.

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Section: Il-33/st2 Signaling Axis In Inflammatory Bowel Diseasementioning

confidence: 99%

Section: Il-33/st2 Signaling Axis In Inflammatory Bowel Diseasementioning

confidence: 99%

Section: Il-33/st2 Signaling Axis In Inflammatory Bowel Diseasementioning

confidence: 99%

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IL-33 and the intestine: The good, the bad, and the inflammatory

et al. 2017

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“…IL-33 preferentially activates type 2 immune responses; it promotes M2 macrophage polarization, activates ILC2s and Th2 cells [20,21], and functions as a disease-sensitizing mediator in the pathogenesis of allergic disorders, including respiratory allergies (asthma and allergic rhinitis) and skin allergies (atopic dermatitis) [2]. …”

Section: Il-33 and St2 Signallingmentioning

confidence: 99%

“…In mouse models of experimental colitis induced by dextran sulphate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS), deficiency of the IL33 or IL1RL1 genes leads to amelioration of the disease, compared to its outcome in wild-type control mice, and treatment with an ST2 blocking antibody ameliorates experimental colitis by enhancing mucosal healing in mice [58]. However, other studies have shown that administration of recombinant IL-33 ameliorates TNBS-induced inflammatory bowel disease (IBD) in mice [20,59]. Intriguingly, treatment with IL-33 at the onset of DSS-induced colitis exacerbates the disease severity, whereas treatment with IL-33 during the recovery phases ameliorates DSS-induced colitis.…”

Section: Gastrointestinal Diseasesmentioning

confidence: 99%

Therapeutic Strategies for Targeting IL-33/ST2 Signalling for the Treatment of Inflammatory Diseases

Chen

Tsai

Yang

et al. 2018

Cell Physiol Biochem

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Interleukin (IL)-33, a member of the IL-1 family of cytokines, is involved in innate and adaptive immune responses via interaction with its receptor, ST2. Activation of ST2 signalling by IL-33 triggers pleiotropic immune functions in multiple ST2-expressing immune cells, including macrophages, neutrophils, eosinophils, basophils, mast cells, type 2 helper T cells, regulatory T cells, and group 2 innate lymphoid cells. IL-33-mediated effector functions contribute to the tissue inflammatory and reparative responses in various organs including lung, skin, kidney, central nerve system, cardiovascular system, and gastrointestinal system. Endogenous IL-33/ ST2 signaling exhibits diverse immune regulatory functions during progression of different diseases. IL-33 likely functions as a disease sensitizer and plays pathological roles in inflamed tissues in allergic disorders that involve hyperreactive immune responses in the context of skin and pulmonary allergy. However, IL-33 also mediates tissue-protective functions during the recovery phase following tissue injury in the central nerve system and gastrointestinal system. Modulation of the IL-33/ST2 axis, therefore, represents a promising strategy for treating immune disorders that involve dysregulation of the cytokine signalling. In the past two decades, therapeutic strategies blocking IL-33/ST2 have been extensively studied for the treatment of diseases in animal models. In this review, the current progress on the development of therapeutic biologics for targeting IL-33/ST2 signalling in inflammatory diseases is summarized.

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Current perspectives on the interleukin‐1 family as targets for inflammatory disease

et al. 2019

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Since the first description of interleukin-1 (IL-1) and the genesis of the field of cytokine biology, the understanding of how IL-1 and related cytokines play central orchestrating roles in the inflammatory response has been an area of intense investigation. As a consequence of these endeavours, specific strategies have been developed to target the function of the IL-1 family in human disease realizing significant impacts for patients. While the most significant advances to date have been associated with inhibition of the prototypical family members IL-1α/β, approaches to target more recently identified family members such as IL-18, IL-33 and the IL-36 subfamily are now beginning to come to fruition. This review summarizes current knowledge surrounding the roles of the IL-1 family in human disease and describes the rationale and strategies which have been developed to target these cytokines to inhibit the pathogenesis of a wide range of diseases in which inflammation plays a centrally important role.Keywords: Canakinumab r Inflammation r Inflammatory disease r Interleukin-1 family r Therapy

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IL-33-induced alternatively activated macrophage attenuates the development of TNBS-induced colitis

Cited by 37 publications

References 35 publications

IL-33 and the intestine: The good, the bad, and the inflammatory

IL-33 and the intestine: The good, the bad, and the inflammatory

Therapeutic Strategies for Targeting IL-33/ST2 Signalling for the Treatment of Inflammatory Diseases

Current perspectives on the interleukin‐1 family as targets for inflammatory disease

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