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Kim, Woon-Ki,Sul, Ok-Ju,Kwak, Jung-Sook,Hur, Hye-Young,Latour, Anne M.,Koller, Beverly H.,Kwon, Byoung-S.,Jeong, Choon-Soo Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.12
Tumor necrosis factor receptor-related 2 (TR2, HVEM or TNFRSF-14) plays an important role in immune responses, however, the mechanisms regulating its expression are unclear. To understand the control of TR2 gene expression, we studied the upstream region of the gene. Gel supershift assays revealed inducible binding of nuclear factor of activated T cells (NFAT) to a putative NFAT site within the TR2 promoter. Furthermore, cotransfection of a dominant negative NFAT construct, or siRNA for NFAT, resulted in increased expression of a TR2 reporter gene. Our findings demonstrate that NFAT negatively regulates TR2 expression in activated T cells.
김운기,Ok-Ju Sul,곽정숙,Hye-Young Hur,Anne M. Latour,Beverly H. Koller,권병세,Choon-Soo Jeong 생화학분자생물학회 2010 Experimental and molecular medicine Vol.42 No.12
Tumor necrosis factor receptor-related 2 (TR2, HVEM or TNFRSF-14) plays an important role in immune responses,however, the mechanisms regulating its expression are unclear. To understand the control of TR2gene expression, we studied the upstream region of the gene. Gel supershift assays revealed inducible binding of nuclear factor of activated T cells (NFAT)to a putative NFAT site within the TR2 promoter. Furthermore, cotransfection of a dominant negative NFAT construct, or siRNA for NFAT, resulted in increased expression of a TR2 reporter gene. Our findings demonstrate that NFAT negatively regulates TR2expression in activated T cells.
김운기,Jin-Soo Park,Ok-Ju Sul,Jae-Hee Seo,최범규,Hee-Young Park,Anne M. Latour,Beverly H. Koller,권병세,Choon-Soo Jeong 한국분자세포생물학회 2011 Molecules and cells Vol.31 No.2
Previous work has suggested that the LIGHT-TR2 costimulatory pathway plays a role in the acute and chronic stages of dextran sulfate sodium (DSS)-induced colitis [Steinberg et al. (2008); Wang et al. (2005)]. To clarify the role of TNFR-related 2 (TR2) signaling in the maintenance of intestinal homeostasis, we generated a TR2 knock-out (KO) mouse. Using DSS to induce colitis, we compared the colitic symptoms and pathological changes in wild type (WT) and TR2 KO mice, and the production of cytokines by the diseased colons. We also studied the role of TR2 in suppressing innate and adaptive immunity in the DSS model. TR2 deficient mice were characterized by reduced symptoms of intestinal inflammation compared with wildtype mice, and reduced production of cytokines. We therefore generated a monoclonal antibody against mouse TR2 which was specific to TR2 and capable of blocking TR2 signals. With this antibody, we demonstrated that antagonizing TR2 during the development of DSS-induced colitis reduced the symptoms of inflammation. Our findings suggest that TR2 is an important mediator in colitis, and may serve as a therapeutic target in inflammatory bowel disease.