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Overexpression of SOCS3 in T Lymphocytes Leads to Impaired Interleukin-17 Production and Severe Aortic Aneurysm Formation in Mice—Brief Report
Author(s) -
Mélissa Romain,
Soraya Taleb,
Marion Dalloz,
Padmapriya Ponnuswamy,
Bruno Esposito,
Nicolas Pérez,
Yu Wang,
Akihiko Yoshimura,
Alain Tedgui,
Ziad Mallat
Publication year - 2013
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.112.300516
Subject(s) - socs3 , cytokine , aneurysm , stat3 , abdominal aortic aneurysm , medicine , biology , stat protein , signal transduction , immunology , cancer research , microbiology and biotechnology , surgery
Mutations of signal transducer and activator of transcription 3 (STAT3) are responsible for autosomal dominant hyperimmunoglobulin E syndrome. Recently, we reported frequent vascular abnormalities, including aneurysms in these patients, and demonstrated that STAT3 inhibition promoted aneurysm in mice. The purpose of this study was to investigate the role of cell-specific STAT3 signaling in the susceptibility to aneurysm.

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