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F-box protein FBXL19-mediated ubiquitination and degradation of the receptor for IL-33 limits pulmonary inflammation.

Abstract：

:The ST2L receptor for interleukin 33 (IL-33) mediates pulmonary inflammation and immune system-related disorders, such as asthma and rheumatoid arthritis. At present, very little is known about the molecular regulation of ST2L expression. Here we found that FBXL19, an 'orphan' member of the Skp1-Cullin-F-box family of E3 ubiquitin ligases, selectively bound to ST2L to mediate its polyubiquitination and elimination in the proteasome. Degradation of ST2L involved phosphorylation of ST2L at Ser442 catalyzed by the kinase GSK3β. Overexpression of FBXL19 abrogated the proapoptotic and inflammatory effects of IL-33 and lessened the severity of lung injury in mouse models of pneumonia. Our results suggest that modulation of the IL-33-ST2L axis by ubiquitin ligases might serve as a unique strategy for lessening pulmonary inflammation.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Zhao J,Wei J,Mialki RK,Mallampalli DF,Chen BB,Coon T,Zou C,Mallampalli RK,Zhao Y

doi

10.1038/ni.2341

subject

Has Abstract

pub_date

2012-06-03 00:00:00

pages

651-8

issue

7

eissn

1529-2908

issn

1529-2916

pii

ni.2341

journal_volume

13

pub_type

杂志文章

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