通讯机构：
[Xiao, Jianhua] U;Univ South China, Inst Pathogen Biol, Hengyang 421001, Hunan, Peoples R China.
摘要：
This article has been retracted: please see Elsevier Policy on Article Withdrawal.This article has been retracted at the request of the authors for the following reason: The results in Figure 4B are invalid because the conditions between the experimental group and the control group were not similar. The samples in the experimental group contained BSA whereas the samples in the control group did not. The authors found that BSA interferes with their experimental model and this makes the results invalid.
作者机构：
[Aiping Zang; Chuanping Yuan; Dapeng Ma; Min Du; Chun Zhou; Li He; Xulin Huang; Huanjin Shi; Qiang Deng; Jianhua Xiao; Ke Lan; Xiaoxia Li; Zhong Huang; Hui Xiao] Institut Pasteur of Shanghai,Chinese Academy of Sciences;[Aiping Zang; Chuanping Yuan; Dapeng Ma; Min Du; Chun Zhou; Li He; Xulin Huang; Huanjin Shi; Qiang Deng; Jianhua Xiao; Ke Lan; Xiaoxia Li; Zhong Huang; Hui Xiao] Institute of Pathogenic Biology,University of South China;[Aiping Zang; Chuanping Yuan; Dapeng Ma; Min Du; Chun Zhou; Li He; Xulin Huang; Huanjin Shi; Qiang Deng; Jianhua Xiao; Ke Lan; Xiaoxia Li; Zhong Huang; Hui Xiao] Department of Immunology,Lerner Research Institute,Cleveland Clinic Foundation,Cleveland,OH 44195,USA
会议名称：
第五届武汉现代病毒学国际研讨会
会议时间：
2013-11-15
会议地点：
中国湖北武汉
摘要：
<正>Development of better adjuvant is urgently needed for vaccines whose efficacy depends on potent Th1 response.While TLR ligands represent the most promising adjuvants for Thl response,induction of o
作者机构：
[Liang, Yu; Yin, Wei-Guo; Xiao, Jian-Hua; Li, Ying-Ju] Univ South China, Inst Pathogen Biol, Hengyang 421001, Hunan, Peoples R China.;[Li, Ying-Ju] Univ South China, Dept Infect Dis, Affiliated Hosp 1, Hengyang 421001, Hunan, Peoples R China.;[Zhu, Ping] Guangdong Acad Med Sci, Guangdong Gen Hosp, Guangdong Cardiovasc Inst, Guangzhou 510080, Guangdong, Peoples R China.
通讯机构：
[Xiao, Jian-Hua] U;Univ South China, Inst Pathogen Biol, Hengyang 421001, Hunan, Peoples R China.
关键词：
Hepatitis;B;virus;TOLL-LIKE;receptors;Lowdensity;LIPOPROTEIN;receptor;3-hydroxy-3-methylglutharyl-coenzyme;A;REDUCTASE;Toll-like receptors;Low-density lipoprotein receptor;3-hydroxy-3-methylglutharyl-coenzyme A reductase
摘要：
AIM: To investigate whether hepatitis B virus (HBV) exacerbates hepatic cholesterol accumulation, and explore the underlying mechanisms. METHODS: HepG2 cells were infected with adenovirus (Ad) containing 1.3-fold overlength HBV genome. Real-time polymerase chain reaction and Western blotting were used to measure mRNA and protein expression of target genes. Cholesterol accumulation was measured by fluorescence microscopy. Cell toxicity due to Ad-HBV treatment was determined by the mitochondrial tetrazolium assay. The protein levels of toll-like receptors (TLRs) were determined by Western blotting. RESULTS: Ad-HBV increased hepatic cholesterol accumulation and enhanced the mRNA and protein levels of low-density lipoprotein receptor (LDLR) and 3-hydroxy-3-methylglutharyl-coenzyme A reductase (HMGCoAr) mRNA and protein expression in HepG2 cells. In addition, these inductive effects were partly offset by suppressing TLR2 expression levels by small interfering RNA in HepG2 cells. CONCLUSION: Ad-HBV increases LDLR and HMGCoAr expression, resulting in exacerbated cholesterol accumulation in HepG2 cells, which was mediated via the TLR2 pathway.
摘要：
目的:研究乙型肝炎病毒(hepatitis B virus,HBV)重组腺病毒对HepG2细胞的IL-17R和接头蛋白Actl表达的影响,以及HBV对IL-17诱导NF-kB活化的影响.方法:采用实时荧光定量PCR(real-time PCR)检测HepG2细胞的IL-17、IL-17R和Actl的mRNA表达;蛋白免疫印迹法(Westem blot)检测IL-17R和Actl的蛋白表达；免疫荧光检测NF-kB核移位；ELISA检测上清的IL-17含量.结果:各组HepG2细胞培养上清液中均未检测到1L-17且亦未检测HepG2细胞有IL-17的mRNA表达；HBV重组腺病毒组的IL-17RmRNA和蛋白的表达明显低于相应浓度对照组(0.68±0.02 vs 0.89±0.03,0.33±0.06 vs0.81±0.01,0.12±0.01 vs 0.86±0.05,P＜0.05;蛋白:0.84±0.12 vs l.01±0.13,0.56±0.09vs l.01±0.08,0,24±0.08 vs 0.98±0.05),且呈剂量和时间依赖性.但HBV重组腺病毒组与对照组比较,对HepG2细胞接头蛋白Actl的mRNA和蛋白表达水平无明显影响；同时HBV重组腺病毒能抑制IL-17R诱导HepG2细胞的NF-kB活化,但HBV重组腺病毒与对照组比较,对接头蛋白Acti在mRNA和蛋白表达水平上影响无明显变化；同时HBV重组腺病毒能抑制IL- 17 R诱-导HepG2细胞的NF-kB活化,结论:HBV重组腺病毒可降低HepG2细胞的IL- 17R mRNA和蛋白的表达,抑制IL-17R诱导HepG2细胞的NF-kB活化,对HepG2细胞的IL-17R信号通路发挥抑制作用.
通讯机构：
[Xiao, Jianhua] U;Univ S China, Inst Pathogen Biol, Hengyang 421001, Hunan, Peoples R China.
关键词：
Schistosoma japonicum;eggshell protein gene;hammerhead ribozyme;in vitro cleavage;anti-reproduction
摘要：
Schistosoma japonicum (S. japonicum) is an extremely harmful pathogen, which infects humans and causes severe public health problems. To date, no effective therapeutic drugs for this pathogen are available. In this study, we designed and constructed three hammerhead ribozymes targeting the eggshell protein gene of S. japonicum (SjESG). The cleavage activities of these three ribozymes were determined using cleavage experiments. The in vitro cleavage results showed that among the three synthesized ribozymes (Rz1, Rz2 and Rz3), Rz1 and Rz3 cleaved their target RNAs effectively. However, Rz2 did not cleave its target RNA detectably. The putative therapeutic roles of these three ribozymes to inhibit the reproduction of S. japonicum in mice were studied in vivo. Compared with the negative controls, Rz1 and Rz3 treatments resulted in increased levels of IFN-γ but decreased levels of IL-4 in mice. Rz2 affected levels of IFN-γ and IL-4 to degrees similar with those caused by the vector controls. In addition, Rz1 and Rz3 reduced the amounts of adult worms and eggs in the livers of mice more extensively than Rz2 and the vector controls. Altogether, these results suggest a correlation between the in vitro cleavage abilities of Rz1 and Rz3 and their roles in reproduction inhibition of S. japonicum.
作者机构：
Institute of Pathogenic Biology, University of South China, Hunan 421001, PR China;Beijing Anzhen Hospital, Beijing 100092, PR China
摘要：
This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the authors for the following reason: The results in Figure 4B are invalid because the conditions between the experimental group and the control group were not similar. The samples in the experimental group contained BSA whereas the samples in the control group did not. The authors found that BSA interferes with their experimental model and this makes the results invalid.
通讯机构：
[Li, Xiaoxia] C;Cleveland Clin Fdn, Lerner Res Inst, Dept Immunol, 9500 Euclid Ave,NE20, Cleveland, OH 44195 USA.
关键词：
Cytokines
摘要：
Interleukin-1 receptor-associated kinase 2 (IRAK2) has been shown to be essential for lipopolysaccharide (LPS)-mediated posttranscriptional control of cytokine and chemokine production. In this study, we investigated the role of IRAK2 kinase activity in LPS-mediated posttranscriptional control by reconstituting IRAK2-deficient macrophages with either wild-type or kinase-inactive IRAK2. Compared with wild-type IRAK2 (IRAK2-WT) macrophages, kinase-inactive IRAK2 (IRAK2-KD) macrophages show reduced cytokine and chemokine mRNA stability and translation in response to LPS. Further, LPS-treated IRAK2-KD macrophages also show reduced activation of MKK3/6, MNK1, and eIF4E and attenuated toll-like receptor 4-induced tristetraprolin modification and stabilization. Taken together, these results suggest that the kinase activity of IRAK2 is required for the optimal activation of mitogen-activated protein kinase signaling, which regulates cytokine and chemokine production at posttranscriptional levels.
作者机构：
[陆学东] Department of Laboratory Medical, Guangdong Medical College, Shenzhen 518033, China;[胡杰; 焦海春; 肖建华] Institute of Pathogen Biology, Nanhua University, Hengyang 421001, China;[何涛君] Department of Laboratory Medical, Guangdong Medical College, Shenzhen 518033, China, Institute of Pathogen Biology, Nanhua University, Hengyang 421001, China
通讯机构：
[He, T.-J.] D;Department of Laboratory Medical, Guangdong Medical College, China
摘要：
CD40L and B lymphocyte-activating factor (BAFF), members of the TNF superfamily, play critical roles in B cell survival and activation, and in the regulation of humoral immunity. We previously reported that the adaptor molecule Act1 functions as a negative regulator of CD40- and BAFF-mediated B cell survival. Here we demonstrated that mice deficient in Act1 developed systemic autoimmune disease with histological and serological features of human Sjogren's syndrome (SS), in association with systemic lupus erythematosus-like nephritis. Analyses of Act1(-/-)CD40(-/-) and Act1(-/-)BAFF(-/-) double-deficient mice revealed that Act1 regulates different stages of the disease development through its impact on both CD40- and BAFF-mediated pathways. We found that Act1 modulates the survival of autoreactive B cells mainly through its negative regulatory role in BAFF-mediated cell survival, while the effect of Act1 on autoantibody production is likely through modulation of CD40-mediated T cell-dependent antibody response. The impact of Act1 on both BAFF and CD40 pathways establishes Act1-deficient mice as a unique model to study distinct steps of autoimmunity and regulation of self tolerance.
