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| 1 | Porcine FcεRI Mediates Porcine Reproductive and Respiratory Syndrome Virus Multiplication and Regulates the Inflammatory Reaction显示文摘Porcine reproductive and respiratory syndrome virus(PRRSV) shows characteristic antibody-dependent enhancement(ADE) of infection and causes porcine systemic inflammation, which is similar to a type I allergic reaction; however, the role of porcine FceεRI in ADE is still unclear. In this study, the expression of different Fc receptors(Fc Rs) on macrophages was investigated in a PRRSV 3D4/21 cell infection model in the presence or absence of PRRSV antibody. The transcription level of Fcc II and FceεRI was significantly up-regulated under PRRSV-antibody complex infection. Internalization and proliferation of PRRSV were promoted by the ADE mechanism when FceεRI was expressed in permissive 3D4/21 cells and the non-permissive cell line HEK 293T. Transcriptome sequencing data showed that the expression levels of AKT,ERK and other signal molecules in the anti-inflammatory pathway were significantly increased, especially in the cells infected with the PRRSV-antibody immune complex. Inflammatory regulatory molecules such as PLA2G6, LOX, TRPM8 and TRPM4 were significantly up-regulated following PRRSV infection but significantly down-regulated in the cells infected with the PRRSV-antibody immune complex. Our results demonstrated that FceεRI could be involved in PRRSV ADE, the antigen presenting process and regulation of the inflammatory response during PRRSV infection, which provides new insights into PRRSV infection mediated by FceεRI and the PRRSV-antibody immune complex. | Peidian Shi Lilin Zhang Jiashun Wang Dong Lu Yi Li Jie Ren Menglu Shen Lei Zhang Jinhai Huang | 2018 | Virologica Sinica2018，33，3： | 3 |
| 2 | Arabidopsis immune-associated nucleotide-binding genes repress heat tolerance at the reproductive stage by inhibiting the unfolded protein response and promoting cell death显示文摘Plants are vulnerable to heat stress,especially during reproductive development.The heat shock response(HSR)in the cytosol and nucleus,as well as the unfolded protein response(UPR)in the endoplasmic reticulum(ER),are two mechanisms that enable plants to survive heat stress.Excessive heat or ER stresses lead to cell death when the UPR cannot repair stress damage,but the means by which cell survival or death is determined remains unclear.In this study,we used a genome-wide association study(GWAS)to identify that a cluster of five Immune-associated nucleotide-binding protein(IAN)genes(IAN2 to IAN6)is responsible for variation in heat tolerance at the reproductive stage in Arabidopsis thaliana.These IAN genes have both unique and overlapping functions in the negative regulation of heat tolerance,and their loss of function singly or in combination confers increased heat tolerance,measured by a lower number of barren siliques and a higher seedling survival rate under heat.The loss of rice IAN1 gene function also leads to enhanced heat tolerance,suggesting a conserved function of plant IANs.Transcriptome analysis revealed enhanced expression of HSR and UPR genes,as well as reduced cell death,under heat and ER stress in the mutant of IAN6,a major effect member in Arabidopsis.Furthermore,the IAN proteins were found to promote cell death induced by heat stress,ER stress,and cell death-inducing molecules.Thus,the Arabidopsis IAN genes repress heat tolerance,probably through the HSR and UPR and by enhancing the cell death pathway.The IAN2 to IAN6 proteins are partially localized to the ER,suggesting a direct role in the UPR and UPR-mediated cell death.In addition,a natural IAN6 variant from more heat-tolerant Arabidopsis accessions confers greater heat tolerance and induces less cell death compared with the natural variant from less heat-tolerant accessions.The heat-tolerant IAN6 variant is associated with a higher maximum temperature of the warmest month at its collection sites compared with the heat-sensitive variant.Taken together,these results reveal an important role of Arabidopsis IAN2 to IAN6 genes in the regulation of the HSR,UPR,and cell death,and suggest that their natural variations have adaptive functions in heat tolerance. | Shan Lu Tianquan Zhu Zhixue Wang Lilin Luo Shuai Wang Minghui Lu Yongmei Cui Baohong Zou Jian Hua | 2021 | Molecular Plant2021，14，2： | 2 |
| 3 | Fabrication of catalytically active Au/Pt/Pd trimetallic nanoparticles by rapid injection of NaBH4显示文摘 | Haijun Zhang Lilin Lu Yingnan Cao Shuang Du Zhong Cheng Shaowei Zhang | 2014 | Materials Research Bulletin2014，49，1： | 1 |
| 4 | American fall webworm in China:A new case of global biological invasions显示文摘Season of mists and mellow fruitfulness-a wonderful autumn scene was described by the poet John Keats.Unfortunately,in multiple locations in China,this picturesque scenery has been nibbled away by an invasive insect,fall webworm,Hyphantria cunea(Lepidoptera:Arctiidae).By the end of September in 2021,outbreaks were detected in 607 counties in 14 provinces,resulting in cumulative damage of 10,427,300 acres and increasing the amount of infested area by 6.15%than last year(Data from Biological Disaster Prevention and Control Center,China). | Jing Ning Pengfei Lu Jianting Fan Lili Ren Lilin Zhao | 2022 | The Innovation2022，3，1： | 0 |
| 5 | DAPK1(death associated protein kinase 1)mediates mTORC1 activation and antiviral activities in CD8^(+)T cells显示文摘Mechanistic target of rapamycin complex 1(mTORCt)regulates CD8^(+)T-cell differentiation and function.Despite the links between PI3K-AKT and mTORCI activation in CD8^(+)T cells,the molecular mechanism underlying mTORCI activation remains undear.Here,we show that both the kinase activity and the death domain of DAPK1 are required for maximal mTOR activation and CD8^(+)T-cell function.We found that TCR-induced activation of calcineurin activates DAPK1,which subsequently interacts with TSC2 via its death domain and phosphorylates TSC2 to mediate mTORCI activation.Furthermore,both the kinase domain and death domain of DAPK1 are required for CD8^(+)T-cell antiviral responses in an LCMV infection model.Together,our data reveal a novel mechanism of mTORCI activation that mediates optimal CD8^(+)T-cell function and antiviral activity. | Zhengping Wei Pingfei Li Ran He Huicheng Liu Na Liu Yu Xia Guoyu Bi Qiuyang Du Minghui Xia Lei Pei Jing Wang Guihua Wang Zhao-Hui Tang Xiang Cheng Huabin Li Zhuoya Li Lilin Ye Arian Laurence Youming Lu Xiang-Ping Yang | 2021 | Cellular & Molecular Immunology2021，18，1： | 0 |
| 6 | Effects of Modifiers on the Anti-wetting and Anti-icing Property of Aluminum Surface显示文摘The effects of modifiers on the anti-wetting and anti-icing property of the prepared rough aluminum surface were investigated.The rough aluminum substrates were obtained through electrochemical oxidization with 15 wt% sulfuric acid solution as the electrolyte at the constant current of 4 mA for 3 h.And then they were modified with octadecanoic acid (C18),polyethylene (PE),polystyrene (PS),polyethylene glycol (PEG) and hexamethylenetetramine (HMTA),respectively,whose surface free energies were 27.6,31.0,33.0,61.6 and 70.0 mN/m,respectively.The contact angles (CA) were 154.6°,128.4°,127.6°,5.0° and 0.0°,respectively,and the ice adhesion pressures were 15.9,36.3,55.9,155.3 and 216.1 kPa,respectively.The ice adhesion strengths decrease along with the increasing anti-wetting property of aluminum surfaces and the decreasing of the surface energy of modifiers.These provide some new insights when designing the aluminum surface with anti-icing properties in some special applications. | 阮敏 XU Junjie FAN Shilin CHEN Ying WU Hang CHANG Zhongwei CHEN Yue ZHAO Dongnan LU Lilin | 2021 | Journal of Wuhan University of Technology(Materials Science)2021，36，1： | 0 |
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