IL-13Rα2 uses TMEM219 in chitinase 3-like-1-induced signalling and effector responses

Chang-Min Lee, Chuan Hua He, Adel M. Nour, Yang Zhou, Bing Ma, Jin Wook Park, Kyung Hee Kim, Charles Dela Cruz, Lokesh Sharma, Mahmoud L. Nasr, Yorgo Modis, Chun Geun Lee and Jack A. Elias ()
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Chang-Min Lee: Brown University
Chuan Hua He: Brown University
Adel M. Nour: Brown University
Yang Zhou: Brown University
Bing Ma: Brown University
Jin Wook Park: Brown University
Kyung Hee Kim: Emory University School of Medicine
Charles Dela Cruz: Section of Pulmonary and Critical Care and Sleep Medicine, Yale University School of Medicine
Lokesh Sharma: Section of Pulmonary and Critical Care and Sleep Medicine, Yale University School of Medicine
Mahmoud L. Nasr: Harvard Medical School
Yorgo Modis: Harvard Medical School
Chun Geun Lee: Brown University
Jack A. Elias: Brown University

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Recent studies demonstrated that chitinase 3-like-1 (Chi3l1) binds to and signals via IL-13Rα2. However, the mechanism that IL-13Rα2 uses to mediate the effects of Chi3l1 has not been defined. Here, we demonstrate that the membrane protein, TMEM219, is a binding partner of IL-13Rα2 using yeast two-hybrid, co-immunoprecipitation, co-localization and bimolecular fluorescence complementation assays. Furthermore, fluorescence anisotropy nanodisc assays revealed a direct physical interaction between TMEM219 and IL-13Rα2-Chi3l1 complexes. Null mutations or siRNA silencing of TMEM219 or IL-13Rα2 similarly decreased Chi3l1-stimulated epithelial cell HB-EGF production and macrophage MAPK/Erk and PKB/Akt activation. Null mutations of TMEM219 or IL-13Rα2 also phenocopied one another as regards the ability of Chi3l1 to inhibit oxidant-induced apoptosis and lung injury, promote melanoma metastasis and stimulate TGF-β1. TMEM219 also contributed to the decoy function of IL-13Rα2. These studies demonstrate that TMEM219 plays a critical role in Chi3l1-induced IL-13Rα2 mediated signalling and tissue responses.

Date: 2016
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DOI: 10.1038/ncomms12752

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