郑世军
1) 畜禽传染病免疫防制; 2) 固有免疫杀灭和清除病原微生物的作用和分子机制;3) 新型高效动物疫苗的研制。
个性化签名
- 姓名:郑世军
- 目前身份:
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学术头衔:
博士生导师, 国家杰出青年科学基金获得者
- 职称:-
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学科领域:
海洋化学
- 研究兴趣:1) 畜禽传染病免疫防制; 2) 固有免疫杀灭和清除病原微生物的作用和分子机制;3) 新型高效动物疫苗的研制。
郑世军,博士,教授,博士生导师,国家杰出青年基金获得者。1987年毕业于中国农业大学动物医学院获学士学位(5年制),随后师从著名动物传染病学家甘孟侯教授攻读硕士学位,1990年获该校传染病与预防兽医学硕士学位并留校从事教学与研究工作,先后参加鸡白痢净化措施的研究,国家85攻关课题“集约化养猪场疫病综合防治的研究”等科研项目。1996年8月获美国麻省大学奖学金,前往该校攻读免疫学博士学位, 并于2000年底获免疫学博士学位(Ph.D.), 随后在美国宾夕法尼亚大学医学院做博士后,从事抗感染免疫及自身免疫病发病机制的研究工作。2005年7月接受中国农业大学特聘教授之职,全职回到母校动物医学院工作,任预防兽医学教授,博士生导师,兼任农业生物技术国家重点实验室研究员。主要代表性学术成果以第一或共同第一作者或通讯作者发表于Nature Immunology,Journal of Clinical Investigation,Journal of Immunology,Diabetes,PLoS ONE等。目前主持科技部973课题、863课题、自然科学基金面上项目以及国家杰出青年基金。发表文章30余篇,主编和参编专著与教材9部。现任中国畜牧兽医学会家畜传染病学分会常务理事、中国畜牧兽医学会禽病学分会理事兼副秘书长、科技部项目预算评估专家组成员、中国兽医杂志编委、中国禽病杂志编委等职。
目前的研究领域 : 1) 畜禽传染病免疫防制; 2) 固有免疫杀灭和清除病原微生物的作用和分子机制;3) 新型高效动物疫苗的研制。讲授课程:1)分子免疫学;2)人兽共患病;3)专业英语
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7
【期刊论文】Critical Roles of Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand in Type 1 Diabetes
郑世军, Salah-Eddine Lamhamedi-Cherradi, Shijun Zheng, Roland M. Tisch, and Youhai H. Chen
DIABETES, VOL. 52, SEPTEMBER 2003,-0001,():
-1年11月30日
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis of tumor cells but not most normal cells. Its roles in normal nontransformed tissues are not clear. To explore the potential roles of TRAIL in type 1 diabetes, we examined the consequences of TRAIL blockade or TRAIL deficiency in two animal models of autoimmune diabetes. In the first model, NOD mice received an injection of a soluble TRAIL receptor to block TRAIL function. This significantly accelerated the diabetes and increased the degree of autoimmune inflammation in both pancreatic islets and salivary glands. The GAD65-specific immune responses were also significantly enhanced in animals that received the soluble TRAIL receptor. In the second model, we treated normal and TRAIL-deficient C57BL/6 mice with multiple low-dose streptozotocin to induce diabetes. We found that both the incidence and the degree of islet inflammation were significantly enhanced in TRAIL-deficient animals. On the basis of these observations, we conclude that TRAIL deficiency accelerates autoimmune diabetes and enhances autoimmune responses.
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郑世军, Shixi Chen, Yu Wang, Fuyong Chen, Hanchun Yang, Menghou Gan, Shijun J. Zheng
January 2007, Issue 1, e147,-0001,():
-1年11月30日
Staphylococcus sciuri are important human pathogens responsible for endocarditis, peritonitis, septic shock, urinary tract infection, pelvic inflammatory disease and wound infections. However, little information is known regarding the pathogenicity of S. sciuri to animals. From the pericardial fluid of a diseased piglet with exudative epidermitis (EE), we isolated a strain of Staphylococcus in pure culture. Surprisingly, this isolate was a member of S. sciuri rather than S. hyicus as identified by its biochemical traits and also by analysis of 23S ribosomal DNA using Internal Transcribed Spacer PCR. In addition, inoculation of newborn piglets with 161010 CFU of the isolate by oral feeding or intra-muscular injection successfully reproduced EE in piglets, which suggested that the oral intake of the pathogen by the animals is one of the major routes of exposure. These unexpected findings prioritized S. sciuri as important zoonotic agents, which may have ramifications for human medicine.
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【期刊论文】Reduced Apoptosis and Ameliorated Listeriosis in TRAIL-Null Mice1
郑世军, Shi-Jun Zheng, Jiu Jiang, Hao Shen, and Youhai H. Chen
The American Association of Immunologists, Inc.,-0001,():
-1年11月30日
Listeriosis is an infectious disease caused by the bacterium Listeria monocytogenes. Although it is well recognized that apoptosis plays a critical role in the pathogenesis of the disease, the molecular mechanisms of cell death in listeriosis remain to be established. We report in this study that mice deficient in TRAIL were partially resistant to primary listeriosis, and blocking TRAIL with a soluble death receptor 5 markedly ameliorated the disease. The numbers of Listeria in the liver and spleen of TRAIL-/- mice were 10–100 times greater than those in TRAIL-/- mice following primary Listeria infection. This was accompanied by a significant increase in the survival rate of TRAIL-/- mice. Lymphoid and myeloid cell death was significantly inhibited in TRAIL-/- mice, which led to marked enlargement of the spleen. These results establish a critical role for TRAIL in apoptosis during listeriosis.
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【期刊论文】Transcriptional Regulation of Type I Diabetes by NF-_B1
郑世军, Salah-Eddine Lamhamedi-Cherradi, Shijun Zheng, Brendan A. Hilliard, Lingyun Xu, Jing Sun, Saaib Alsheadat, Hsiou-Chi Liou, and Youhai H. Chen
The American Association of Immunologists, Inc.,-0001,():
-1年11月30日
Development of type I diabetes requires coordinated expression of myriad genes responsible for the initiation and progression of the disease. Expression of these genes are regulated by a small number of transcription factors including the Rel/NF-кB family. To determine the roles of the Rel/NF-кB family in type I diabetes, we studied multiple low-dose streptozotocin-induced diabetes in mice deficient in either c-Rel or NF-кB1. We found that mice deficient in each of these NF-кB subunits were resistant to streptozotocin-induced diabetes. However, the mechanisms of the disease resistance may differ in different cases. Deficiency in c-Rel selectively reduced Th1, but not Th2 responses, whereas NF-кB1 deficiency had little effect on T cell responses to anti-CD3 stimulation. Death of dendritic cells was accelerated in the absence of NF-кB1, whereas death of macrophages and granulocytes was affected primarily by c-Rel deficiency. Furthermore, Stat-1 expression was significantly reduced in macrophages deficient in NF-кB1, but not c-Rel. These results indicate that both c-Rel and NF-_B1are essential for the development of type I diabetes and that strategies targeting each of these subunits would be effective in preventing the disease.
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【期刊论文】Critical roles of TRAIL in hepatic cell death and hepatic inflammation
郑世军, Shi-Jun Zheng, Pu Wang, Galit Tsabary, and Youhai H. Chen
J. Clin. Invest. 113: 58-64 (2004),-0001,():
-1年11月30日
The TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis of tumor cells but not most normal cells. Its role in hepatic cell death and hepatic diseases is not clear. In vitro studies suggest that murine hepatocytes are not sensitive to TRAIL-induced apoptosis, indicating that TRAIL may not mediate hepatic cell death. Using two experimental models of hepatitis, we found that hepatic cell death in vivo was dramatically reduced in TRAIL-deficient mice and mice treated with a blocking TRAIL receptor. Although both TRAIL and its death receptor 5 were constitutively expressed in the liver, TRAIL expression by immune cells alone was sufficient to restore the sensitivity of TRAIL-deficient mice to hepatitis. Thus, TRAIL plays a crucial role in hepatic cell death and hepatic inflammation.
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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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