Constitutively active Stat5b signaling confers tolerogenic functions to dendritic cells of NOD mice and halts diabetes progression

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• 作者：Echarki Zerif^a ; Aida Maalem^a ; Simon Gaudreau^a ; Chantal Guindi^a ; Muhammad Ramzan^a ; Steeve Vé ; roneau^a ; Denis Gris^a ; Jana Stankova^a ; Marek Rola-Pleszczynski^a ; Walid Mourad^b ; Gilles Dupuis^c ; Abdelaziz Amrani^a ; ^{Abdelaziz.Amrani@USherbrooke.ca}
• 关键词：DCs ; Dendritic cells ; Stat5 ; Signal Transducer and Activator of Transcription 5 ; Tregs ; regulatory T cells ; NOD ; nonobese diabetic ; T1D ; type 1 diabetes
• 刊名：Journal of Autoimmunity
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：76
• 期：Complete
• 页码：63-74
• 全文大小：2975 K
• 卷排序：76

文摘

NOD.CD11cStat5b-CA mice were protected from diabetes. Stat5b-CA.DCs induced antigen specific Treg differentiation, enhanced Treg suppressive activity and promoted Th2/Tc2 immune deviation. Stat5b-CA.DC educated CD4+CD25− T cells delay diabetes onset whereas Stat5b-CA.DC educated Tregs blocked ongoing diabetes. A single injection of Stat5b-CA.DCs halted diabetes progression and educated their splenocytes to loose their diabetogenic potential.