Dermatitis Research Today is a free monthly online journal that collates and summarizes the latest research about Dermatitis, including details on contact-, seborrheic-, atopic-, allergic-dermatitis, treatment. | ||||||||
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IFN-gamma regulates the expression of B7-H1 in dermal fibroblast cells.Lee SK, Seo SH, Kim BS, Kim CD, Lee JH, Kang JS, Maeng PJ, Lim JS Institute of Traditional Medicine and Bioscience, Daejeon University, 96-3 Yongun-dong, Daejeon 300-716, Republic of Korea. BACKGROUND: Programmed cell death ligand 1 (B7-H1) was recently cloned in antigen presenting cells (APCs) and represents a third member of the B7 family. Thus, B7-H1 may be a novel target for clinical intervention in human inflammatory disease. OBJECTIVE: The aim of this study is to investigate the signal transduction mechanism and transcriptional regulation of B7-H1 expression in human dermal fibroblasts. METHODS: We performed reverse transcription PCR (RT-PCR) for the detection of mRNA expression, luciferase reporter assays with B7-H1 promoter constructs, and Western blot analysis. RESULTS: From RT-PCR analysis, IFN-gamma can induce the expression of B7-H1 mRNA in dermal fibroblast. This expression is similar to the results of luciferase reporter assay with B7-H1 promoter. Western blot analysis and EMSA revealed that NF-kappaB transcription factors mediate the induction of B7-H1 expression via the transient phosphorylation of ERK1/2 and PI3K when cells are stimulated by IFN-gamma. Also, Specific destruction of the NF-kappaB binding site abolished the induction of the promoter activity by IFN-gamma. CONCLUSION: Our data not only provides the first evidence to demonstrate that dermal fibroblast express the B7-H1 mRNA in the process of skin inflammation, but also suggests the involvement of NF-kappaB and MAPK and PI3K, that may play some important roles in inflammation process in human skin diseases. Published 17 October 2005 in J Dermatol Sci, 40(2): 95-103.
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