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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.

Overexpression of SOCS3 in T Lymphocytes Leads to Impaired Interleukin-17 Production and Severe Aortic Aneurysm Formation in Mice—Brief Report