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【期刊论文】Tumor Suppressor p53 Inhibits Autoimmune Inflammation and Macrophage Function
郑世军, Shi-Jun Zheng, Salah-Eddine Lamhamedi-Cherradi, , Pu Wang, Lingyun Xu, and Youhai H. Chen
DIABETES, VOL. 54, MAY 2005,-0001,():
-1年11月30日
The tumor suppressor p53 regulates apoptosis, cell cycle, and oncogenesis. To explore the roles of p53 in autoimmunity, we studied type 1 diabetes and innate immune responses using C57BL/6 mice deficient in p53. We found that p53-deficient mice were more susceptible to streptozotocin-induced diabetes than control mice, and they produced higher levels of interleukin-1, -6, and -12. The innate immune response of p53-/- macrophages to lipopolysaccharides and γ-interferon was significantly enhanced compared with p53-/- cells. p53-/- macrophages produced more proinflammatory cytokines and higher levels of total and phosphorylated signal transducer and activator of transcription (STAT)-1. These results indicate that p53 inhibits autoimmune diabetes and innate immune responses through downregulating STAT-1 and proinflammatory cytokines.
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【期刊论文】Defective thymocyte apoptosis and accelerated autoimmune diseases in TRAIL–/– mice
郑世军, Salah-Eddine Lamhamedi-Cherradi, Shi-Jun Zheng, Kimberly A. Maguschak, Jacques Peschon, Youhai H. Chen
Nature immunology Volume 4, No. 3, March 2003,-0001,():
-1年11月30日
TRAIL, the tumor necrosis factor-related apoptosis-inducing ligand, selectively induces apoptosis of tumor cells, but not most normal cells. Its role in normal, nontransformed tissues is not clear. We report here that mice deficient in TRAIL have a severe defect in thymocyte apoptosis-thus, thymic deletion induced by T cell receptor ligation is severely impaired. TRAIL-deficient mice are also hypersensitive to collagen-induced arthritis and streptozotocin-induced diabetes and develop heightened autoimmune responses.Thus,TRAIL mediates thymocyte apoptosis and is important in the induction of autoimmune diseases.
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