期刊
JOURNAL OF AUTOIMMUNITY
卷 24, 期 2, 页码 135-143出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jaut.2005.01.002
关键词
anti-P autoantibody; interleukin-12; macrophage; systemic lupus erythematosus; tumor necrosis factor alpha; interleukin-10
类别
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 (9136) 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 9136 for 6 or 24 h, the levels of mRNA and protein expression of IL-12, TNF-alpha, and NOS 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 1h. The productions of IL-10 in LPS-activated RAW 264.7 and human macrophages were potentiated by 9136 up to 65% and 51%, respectively. Since anti-P Abs inhibit productions of IL-12 and TNF-alpha and enhance IL-10 production in macrophages, these autoantibodies may augment Th2 responses and amplify lupus manifestations by causing immunological polarity and lymphocyte dysfunction. (c) 2005 Elsevier Ltd. All rights reserved.
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