کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8738297 | 1591527 | 2018 | 35 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Deficiency of IL-1 receptor antagonist suppresses IL-10-producing B cells in autoimmune arthritis in an IL-17/Th17-dependent manner
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Rheumatoid arthritis (RA) is a systemic autoimmune disease with CD4+ T cell infiltration and hyperplasia of synovial tissues leading to progressive destruction of articular cartilage. In addition to the central role of T cells in the pathogenesis of RA, recent reports have suggested that B cells also contribute to RA. To explore the effects of interleukin (IL)-17 on B cell development and response in excess IL-1 signaling, we generated IL-17 and IL-1 receptor antagonist (IL-1Ra) double-deficient mice via backcrossing IL-17 knockout (KO) and ILâ1RaKO mice. We studied the effect of IL-17 deficiency on antibody-producing B cells and regulatory B cells in IL-1RaKO mice. Excess IL-1 signal increased the frequency of B220+ IgG+ cells and plasma cells. It also promoted the production of immunoglobulins in vitro. Moreover, IL-17 deficiency significantly enhanced the frequency of regulatory IL-10-producing regulatory B cells in IL-1RaKO mice. IL-17 deficiency ameliorated disease symptoms of inflammatory arthritis in IL-1RaKO mice by suppressing the frequency of plasma cells and antibody production while enhancing the frequency of IL-10-producing B cells. These findings suggest that IL-17 can trigger an inflammatory immune reaction by activating antibody-producing B cells while suppressing immune regulatory B cells in RA.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunology Letters - Volume 199, July 2018, Pages 44-52
Journal: Immunology Letters - Volume 199, July 2018, Pages 44-52
نویسندگان
Jin-Sil Park, Na-Rae Kim, Mi-Ae Lim, Sung-Min Kim, Sun-Hee Hwang, Kyung-Ah Jung, JeongWon Choi, Sung-Hwan Park, Mi-La Cho,