IL-33 attenuates development and perpetuation of chronic intestinal inflammation

Groβ, Philipp; Doser, Kristina; Falk, Werner; Obermeier, Florian; Hofmann, Claudia

doi:10.1002/ibd.22900

Cited by 94 publications

(61 citation statements)

References 37 publications

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“…Overall, it is now well established that IL-33 is able to suppress inflammation by driving type 2 immunity and/or by boosting Treg activity, a phenomenon observed in our study but also in many murine models of human disease (6)(7)(8)10). For the first time, to our knowledge, we highlight the protective effect of repeated IL-33 injections in CIA and relate it to the emergence of type 2 immunity and to the expansion of a CD39 + Treg population.…”

Section: Discussionsupporting

confidence: 73%

In Vivo Expansion of Activated Foxp3+ Regulatory T Cells and Establishment of a Type 2 Immune Response upon IL-33 Treatment Protect against Experimental Arthritis

Biton

Athari

Thiolat

et al. 2016

The Journal of Immunology

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IL-33 is strongly involved in several inflammatory and autoimmune disorders with both pro- and anti-inflammatory properties. However, its contribution to chronic autoimmune inflammation, such as rheumatoid arthritis, is ill defined and probably requires tight regulation. In this study, we aimed at deciphering the complex role of IL-33 in a model of rheumatoid arthritis, namely, collagen-induced arthritis (CIA). We report that repeated injections of IL-33 during induction (early) and during development (late) of CIA strongly suppressed clinical and histological signs of arthritis. In contrast, a late IL-33 injection had no effect. The cellular mechanism involved in protection was related to an enhanced type 2 immune response, including the expansion of eosinophils, Th2 cells, and type 2 innate lymphoid cells, associated with an increase in type 2 cytokine levels in the serum of IL-33–treated mice. Moreover, our work strongly highlights the interplay between IL-33 and regulatory T cells (Tregs), demonstrated by the dramatic in vivo increase in Treg frequencies after IL-33 treatment of CIA. More importantly, Tregs from IL-33–treated mice displayed enhanced capacities to suppress IFN-γ production by effector T cells, suggesting that IL-33 not only favors Treg proliferation but also enhances their immunosuppressive properties. In concordance with these observations, we found that IL-33 induced the emergence of a CD39high Treg population in a ST2L-dependent manner. Our findings reveal a powerful anti-inflammatory mechanism by which IL-33 administration inhibits arthritis development.

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Section: Discussionsupporting

confidence: 73%

In Vivo Expansion of Activated Foxp3+ Regulatory T Cells and Establishment of a Type 2 Immune Response upon IL-33 Treatment Protect against Experimental Arthritis

Biton

Athari

Thiolat

et al. 2016

The Journal of Immunology

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“…15 IL-33 induces Th2 response and drives production of IL-5 and IL-13 by Th2 cells and ILC2. In the chronic dextran sulfate sodium (DSS)-induced colitis model, IL-33 promotes the recruitment of neutrophils for the bacterial clearance 16 and induces regulatory T-cell differentiation in the TGF-β-mediated pathway. 17 IL-37, a novel cytokine that is found to suppress innate immune response, could protect mice from colitis through decreasing the production of IL-1β and TNF and inducing expression of IL-10.…”

Section: Epithelial Barriermentioning

confidence: 99%

Regulatory immune cells in regulation of intestinal inflammatory response to microbiota

et al. 2015

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The intestinal lumen harbors nearly 100 trillion commensal bacteria that exert crucial function for health. An elaborate balance between immune responses and tolerance to intestinal microbiota is required to maintain intestinal homeostasis. This process depends on diverse regulatory mechanisms, including both innate and adaptive immunity. Dysregulation of the homeostasis between intestinal immune systems and microbiota has been shown to be associated with the development of inflammatory bowel diseases (IBD) in genetically susceptible populations. In this review, we discuss the recent progress reported in studies of distinct types of regulatory immune cells in the gut, including intestinal intraepithelial lymphocytes, Foxp3+ regulatory T cells, regulatory B cells, alternatively activated macrophages, dendritic cells, and innate lymphoid cells, and how dysfunction of this immune regulatory system contributes to intestinal diseases such as IBD. Moreover, we discuss the manipulation of these regulatory immune cells as a potential therapeutic method for management of intestinal inflammatory disorders.

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“…Genetic ablation of Il33 in mice of a mixed genetic background lowered clinical symptoms in the early phase of experimental colitis, but also delayed the resolution of inflammation (23). Administration of recombinant IL-33 was also shown to ameliorate colitis in Il33-sufficient (WT) mice, suggesting a protective role for IL-33 in colitis (24,25). By utilizing Il33 -/-mice generated on a congenic C57BL/6 background and employing cohousing strategies and littermate controls, we show that IL-33 protected from colitis and CAC.…”

Section: Introductionmentioning

confidence: 99%

IL-33 regulates the IgA-microbiota axis to restrain IL-1α–dependent colitis and tumorigenesis

Malik¹,

Sharma²,

Zhu³

et al. 2016

Journal of Clinical Investigation

149

144

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IL-33 attenuates development and perpetuation of chronic intestinal inflammation

Cited by 94 publications

References 37 publications

In Vivo Expansion of Activated Foxp3+ Regulatory T Cells and Establishment of a Type 2 Immune Response upon IL-33 Treatment Protect against Experimental Arthritis

In Vivo Expansion of Activated Foxp3+ Regulatory T Cells and Establishment of a Type 2 Immune Response upon IL-33 Treatment Protect against Experimental Arthritis

Regulatory immune cells in regulation of intestinal inflammatory response to microbiota

IL-33 regulates the IgA-microbiota axis to restrain IL-1α–dependent colitis and tumorigenesis

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