- 作者: Mary Bradford ,Arin J. Schroeder, Herbert C. Morse 3rd Stefanie N. Vogel John S. Cowdery
- 作者服務機構: Department of Veterans Affairs Medical Center, Department of Internal Medicine and Interdisciplinary Immunology Program , University of lowa , College of Medicine , lowa City , lowa , and National Institute of Allergy and Infectious Diseases , National Institute of Health and Department of Microbiology and Immunology , Uniformed Services University of Health Sciences , Bethesda , Md., USA
- 中文摘要: --
- 英文摘要: gene nor did CpG DNA induce ICSBP transcription. CpGDNA, which activates macrophages by the TLR9 path-way, is a strong inducer of IL-12 p40, yet does so inde-pendently of IFN- , STAT1 or ICSBP. Thus, CpG DNA-induced IL-12 p40 secretion is mediated by one or moresignaling elements distinct from those induced by eitherLPS or IFN - .The host immune system responds to CpG motifs in bac-terial DNA by rapidly producing proinflammatory cyto-kines. The host response to CpG DNA resembles, inmany ways, the response to bacterial lipopolysaccharide(LPS). While both agents can induce a powerful inflam-matory response, CpG DNA promotes Th1 and sup-presses Th2 immunity. The regulation of macrophage IL-12 p40 secretion in response to stimulation with LPS andinterferon- (IFN- ) is dependent on the action of anuclear transacting factor, interferon consensus se-quence binding protein (ICSBP), a STAT1-dependentgene product. We found that CpG DNA induced IL-12 p40secretion by macrophages from mice with either dis-rupted STAT1 or ICSBP genes. Additionally, CpG DNAdid not induce translocation of transcription factors thatbind to the gamma-activated sequence in the ICSBP
- 中文關鍵字: --
- 英文關鍵字: CpG DNA, Interleukin-12, Interferon-Y, Interferon consensus sequence binding protein