IL-13 receptor α 2: A regulator of IL-13 and IL-4 signal transduction in primary human fibroblasts

Andrews, Allison-Lynn; Nasir, Tosia; Bucchieri, Fabio; Holloway, John W.; Holgate, Stephen T.; Davies, Donna E.

doi:10.1016/j.jaci.2006.06.041

Cited by 86 publications

(77 citation statements)

References 37 publications

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“…Our results suggest that the type I IL-4 receptor is not required for IL-33-induced fibrosis. IL-13 can signal through the type II IL-4 receptor and IL-13Ra2, which both can contribute to the development of fibrosis (53)(54)(55). Future studies will examine the requirement for specific IL-13 receptors in the development of IL-33-induced fibrosis.…”

Section: Discussionmentioning

confidence: 99%

IL-33 Induces IL-13–Dependent Cutaneous Fibrosis

Rankin¹,

Mumm²,

Murphy³

et al. 2009

The Journal of Immunology

201

156

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IL-33 is constitutively expressed in epithelial barrier tissues, such as skin. Although increased expression of IL-33/IL-33R has been correlated with fibrotic disorders, such as scleroderma and progressive systemic sclerosis, the direct consequences of IL-33 release in skin has not been reported. To determine the effects of dysregulated IL-33 signaling in skin, we administered IL-33 s.c. and monitored its effects at the injection site. Administration of IL-33 resulted in IL-33R–dependent accumulation of eosinophils, CD3+ lymphocytes, F4/80+ mononuclear cells, increased expression of IL-13 mRNA, and the development of cutaneous fibrosis. Consistent with extensive cutaneous tissue remodeling, IL-33 resulted in significant modulation of a number of extracellular matrix-associated genes, including collagen VI, collagen III, and tissue inhibitor of metalloproteases-1. We establish that IL-33–induced fibrosis requires IL-13 using IL-13 knockout mice and eosinophils using ΔdblGATA mice. We show that bone marrow-derived eosinophils secrete IL-13 in response to IL-33 stimulation, suggesting that eosinophil-derived IL-13 may promote IL-33–induced cutaneous fibrosis. Collectively, our results identify IL-33 as a previously unrecognized profibrotic mediator in skin and highlight the cellular and molecular pathways by which this pathology develops.

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Section: Discussionmentioning

confidence: 99%

IL-33 Induces IL-13–Dependent Cutaneous Fibrosis

Rankin¹,

Mumm²,

Murphy³

et al. 2009

The Journal of Immunology

201

156

View full text Add to dashboard Cite

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“…20,21 This may be a result of the antibody causing steric hindrance around IL-13Ra2, blocking its interaction with IL-4Ra, but it remains unclear whether IL-13Ra2 exerts its regulatory effect on the binding of IL-4 to IL-4Ra via interaction of the extracellular domains of the two receptors, or via the interaction of the cytoplasmic domains of IL-4Ra and IL-13a2.…”

Section: Introductionmentioning

confidence: 99%

The association of the cytoplasmic domains of interleukin 4 receptor alpha and interleukin 13 receptor alpha 2 regulates interleukin 4 signaling

et al. 2013

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“…Apart from IL-13Rα1, IL-13 has another cognate receptor, IL-13Rα2, which binds IL-13 with a markedly high affinity, although it lacks any significant cytoplasmic domain and, therefore, does not mediate signal transduction (11,12). It was reported that IL-13Rα2 may regulate IL-13 and IL-4 signal transduction through internalization of IL-13 (13) and that the extracellular domain of IL-13Rα2 may serve as a decoy receptor for IL-13 (14,15).…”

Section: Introductionmentioning

confidence: 99%

Interleukin-13 and its receptors in colorectal cancer (Review)

Zhou

Shen

et al. 2013

Biomedical Reports

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Abstract. Interleukin (IL)-13 is an immunoregulatory cytokine secreted by numerous immune cells. Its functions are similar to those of IL-4 and they share a common receptor. This cytokine has been included in recent studies on human tumors and malignant diseases, evoking a scientific interest to investigate the role of IL-13 and its receptors as novel biomarkers and targets for therapy. Colorectal cancer is one of the most common human malignancies, its prognosis is not promising and the efficacy of molecular-targeted therapy has not been established. This review summarizes the currently available data on the role of IL-13 and its receptors in colorectal cancer, including the signaling pathways involved in mediating the effects of IL-13, the role of IL-13 and/or its receptors in the prediction of cancer and several drugs targeting IL-13 or its receptors that are currently under evaluation.

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IL-13 receptor α 2: A regulator of IL-13 and IL-4 signal transduction in primary human fibroblasts

Cited by 86 publications

References 37 publications

IL-33 Induces IL-13–Dependent Cutaneous Fibrosis

IL-33 Induces IL-13–Dependent Cutaneous Fibrosis

The association of the cytoplasmic domains of interleukin 4 receptor alpha and interleukin 13 receptor alpha 2 regulates interleukin 4 signaling

Interleukin-13 and its receptors in colorectal cancer (Review)

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