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Gut dysbiosis promotes islet-autoimmunity by increasing T-cell attraction in islets via CXCL10 chemokine.

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第一作者： Sakari,Pöysti

第一单位： Institute of Biomedicine, University of Turku, Turku, Finland.

作者： Sakari,Pöysti ^[1] ; Satu,Silojärvi ^[1] ; Thomas C,Brodnicki ^[2] ; Tara,Catterall ^[2] ; Xin,Liu ^[2] ; Leanne,Mackin ^[2] ; Andrew D,Luster ^[3] ; Thomas W H,Kay ^[2] ; Urs,Christen ^[4] ; Helen E,Thomas ^[2] ; Arno,Hänninen ^[5]

作者单位： Institute of Biomedicine, University of Turku, Turku, Finland. ^[1] St. Vincent's Institute of Medical Research, Melbourne, VIC, Australia. ^[2] Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. ^[3] Klinikum der Goethe Universität Frankfurt, Frankfurt Am Main, Germany. ^[4] Institute of Biomedicine, University of Turku, Turku, Finland; Turku University Hospital Laboratory Division, Turku, Finland. Electronic address: arno.hanninen@utu.fi. ^[5]

关键词 Beta-cell autoimmunity CXCL10 CXCR3 Chemokines IGRP-Reactive T-cells IP-10 Insulitis Low-grade endotoxemia Ruminococcus gnavus Type 1 diabetes Type-I-Interferon-signaling