Monoclonal ribosomal P autoantibody inhibits the expression and release of IL-12, TNF-α and iNOS in activated RAW macrophage cell line

Kuang Hui Sun*, Shye Jye Tang, Chau Yaun Chen, Tai Ping Lee, Chi Kuang Feng, Chia Li Yu, Guang Huan Sun

*此作品的通信作者

研究成果: Article同行評審

18 引文 斯高帕斯(Scopus)

摘要

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.

原文English
頁(從 - 到)135-143
頁數9
期刊Journal of Autoimmunity
24
發行號2
DOIs
出版狀態Published - 3月 2005

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