کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8715889 | 1587874 | 2018 | 32 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Unopposed IL-36 Activity Promotes Clonal CD4+ T-Cell Responses with IL-17A Production in Generalized Pustular Psoriasis
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کلمات کلیدی
LPSPBMCGPPTh17phorbol 12-myristate 13-acetateCFSEDIRAPMA - LDC هاPeripheral blood mononuclear cell - سلول تک هسته ای خون محیطیlipopolysaccharide - لیپوپلی ساکاریدpsoriasis vulgaris - پسوریازیس ولگاریسGeneralized pustular psoriasis - پسوریازیس پوسچر به طور کلیcarboxyfluorescein diacetate succinimidyl ester - کربوکسیفلوورسسین دی سکته سوکسینیمیدیل استر
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Unopposed IL-36 Activity Promotes Clonal CD4+ T-Cell Responses with IL-17A Production in Generalized Pustular Psoriasis Unopposed IL-36 Activity Promotes Clonal CD4+ T-Cell Responses with IL-17A Production in Generalized Pustular Psoriasis](/preview/png/8715889.png)
چکیده انگلیسی
Generalized pustular psoriasis (GPP) is the most severe psoriasis variant. Mutations in the IL-36 antagonist IL36RN, in CARD14 or AP1S3 provide genetic evidence for autoinflammatory etiology but cannot explain its pathogenesis completely. Here we demonstrate that unopposed IL-36 signaling promotes antigen-driven and likely pathogenic T-helper type 17 (Th17) responses in GPP. We observed that CD4+ T cells in blood and skin lesions of GPP patients were characterized by intense hyperproliferation, production of the GPP key mediator, IL-17A, and highly restricted TCR repertoires with identical T-cell clones in blood and skin lesions, indicating antigen-driven T-cell expansions. The clonally expanded CD4+ T cells were major producers of IL-17A. IL-36 signaling substantially enhanced TCR-mediated proliferation of CD4+ T cells. Moreover, GPP patients showed preferences for HLA-DRB1â14, HLA-DQB1â05, and HLA-DQB1â03. We conclude that in GPP unopposed IL-36 signaling and certain HLA-class II alleles may cooperate in promoting antigen-driven Th17 responses, which in the obvious absence of exogenous triggers may reflect autoimmune reactions. This study reveals a pathogenic pathway where innate immune dysregulation promotes T-cellâmediated inflammation in GPP.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 138, Issue 6, June 2018, Pages 1338-1347
Journal: Journal of Investigative Dermatology - Volume 138, Issue 6, June 2018, Pages 1338-1347
نویسندگان
Akiko Arakawa, Sigrid Vollmer, Petra Besgen, Adrian Galinski, Burkhard Summer, Yoshio Kawakami, Andreas Wollenberg, Klaus Dornmair, Michael Spannagl, Thomas Ruzicka, Peter Thomas, Jörg C. Prinz,