کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9267919 | 1218813 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Monoclonal ribosomal P autoantibody inhibits the expression and release of IL-12, TNF-α and iNOS in activated RAW macrophage cell line
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Monoclonal ribosomal P protein antibody (anti-P mAb) may bind to the cell surface, penetrate into cells, and induce apoptosis of Jurkat T cells. Recently, modulation of cytokines has been considered to be important in the pathogenesis of systemic lupus erythematous (SLE). In this study, effects of anti-P mAbs (9B6) on gene expression of cytokines, apoptosis, and reactive oxygen species in murine macrophage RAW 264.7 were analyzed by RT-PCR and ELISA and those on IL-12 promoter activity was determined in an IL-12p40 promoter-reporter gene transfected cell line RAW (IL-12p40-SEAP). After treating LPS-activated RAW 264.7 with 9B6 for 6 or 24 h, the levels of mRNA and protein expression of IL-12, TNF-α, and iNOS were significantly inhibited by 25%, 16%, and 13%, respectively. The IL-12 promoter activity of RAW (IL-12p40-SEAP) was also inhibited by 13-22%. However, inhibitory effects were not observed in cells pre-treated with IgG1 for 1 h. The productions of IL-10 in LPS-activated RAW 264.7 and human macrophages were potentiated by 9B6 up to 65% and 51%, respectively. Since anti-P Abs inhibit productions of IL-12 and TNF-α and enhance IL-10 production in macrophages, these autoantibodies may augment Th2 responses and amplify lupus manifestations by causing immunological polarity and lymphocyte dysfunction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Autoimmunity - Volume 24, Issue 2, March 2005, Pages 135-143
Journal: Journal of Autoimmunity - Volume 24, Issue 2, March 2005, Pages 135-143
نویسندگان
Kuang-Hui Sun, Shye-Jye Tang, Chau-Yaun Chen, Tai-Ping Lee, Chi-Kuang Feng, Chia-Li Yu, Guang-Huan Sun,