a cell permeable peptide inhibitor of nfat inhibits macrophage cytokine expression and ameliorates experimental colitis细胞渗透nfat的肽抑制剂抑制巨噬细胞细胞因子的表达和改善实验性结肠炎.pdfVIP

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a cell permeable peptide inhibitor of nfat inhibits macrophage cytokine expression and ameliorates experimental colitis细胞渗透nfat的肽抑制剂抑制巨噬细胞细胞因子的表达和改善实验性结肠炎.pdf

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a cell permeable peptide inhibitor of nfat inhibits macrophage cytokine expression and ameliorates experimental colitis细胞渗透nfat的肽抑制剂抑制巨噬细胞细胞因子的表达和改善实验性结肠炎

A Cell Permeable Peptide Inhibitor of NFAT Inhibits Macrophage Cytokine Expression and Ameliorates Experimental Colitis 1. 1. 2. 1 1 Houda Z. Elloumi , Nitsan Maharshak , Kavitha N. Rao , Taku Kobayashi , Hyungjin S. Ryu , ¨ 1 1 1 1 Marcus Muhlbauer , Fengling Li , Christian Jobin , Scott E. Plevy * 1 Center for Gastrointestinal Biology and Diseases, Departments of Medicine and Department of Microbiology and Immunology, University of North Carolina School of Medicine, Chapel Hill, North Carolina, United States of America, 2 Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America Abstract Nuclear factor of activated T cells (NFAT) plays a critical role in the development and function of immune and non-immune cells. Although NFAT is a central transcriptional regulator of T cell cytokines, its role in macrophage specific gene expression is less defined. Previous work from our group demonstrated that NFAT regulates Il12b gene expression in macrophages. Here, we further investigate NFAT function in murine macrophages and determined the effects of a cell permeable NFAT inhibitor peptide 11R-VIVIT on experimental colitis in mice. Treatment of bone marrow derived macrophages (BMDMs) with tacrolimus or 11R-VIVIT significantly inhibited LPS and LPS plus IFN-c induced IL-12 p40 mRNA and protein expression. IL-12 p70 and IL-23 secretion were also decreased. NFAT nuclear translocation and binding to the IL-12 p40 promoter was reduced by NFAT inhibition. Experiments in BMDMs from IL-10 deficient (Il102/ 2) mice demonstrate that inhibition of IL-12