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Article

Overexpression of SOCS3 in T lymphocytes leads to impaired interleukin-17 production and severe aortic aneurysm formation in mice--brief report.

Arteriosclerosis, thrombosis, and vascular biology - 1 Mar 2013

Romain Mélissa, Taleb Soraya, Dalloz Marion, Ponnuswamy Padmapriya, Esposito Bruno, Pérez Nicolas, Wang Yu, Yoshimura Akihiko, Tedgui Alain, Mallat Ziad

Abstract excerpt

OBJECTIVE: 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...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 23329138
DOI: 10.1161/ATVBAHA.112.300516

Genes

STAT3
SOCS3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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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.PMID 23329138Read ↗

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