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| 1 | Blockade of Tim-3 Pathway Ameliorates Interferon-γ Production from Hepatic CD8^+ T Cells in a Mouse Model of Hepatitis B Virus Infection显示文摘T cell immunoglobulin-and mucin-domain-containing molecule-3(Tim-3) has been reported to participate in the pathogenesis of inflammatory diseases. However,whether Tim-3 is involved in hepatitis B virus(HBV) infection remains unknown. Here,we studied the expression and function of Tim-3 in a hydrodynamics-based mouse model of HBV infection. A significant increase of Tim-3 expression on hepatic T lymphocytes,especially on CD8+ T cells,was demonstrated in HBV model mice from day 7 to day 18. After Tim-3 knockdown by specific shRNAs,significantly increased IFN-γ production from hepatic CD8+ T cells in HBV model mice was observed. Very interestingly,we found Tim-3 expression on CD8+ T cells was higher in HBV model mice with higher serum anti-HBs production. Moreover,Tim-3 knockdown influenced anti-HBs production in vivo. Collectively,our data suggested that Tim-3 might act as a potent regulator of antiviral T-cell responses in HBV infection. | Ying Ju Nan Hou Xiaoning Zhang Di Zhao Ying Liu Jinjin Wang Fang Luan Wei Shi Faliang Zhu Wensheng Sun Lining Zhang Chengjiang Gao Lifen Gao Xiaohong Liang Chunhong Ma | 2009 | Cellular & Molecular Immunology2009，6，1： | 19 |
| 2 | Biphasic insulin aspart 30 improved glycemic control in Chinese patients with type 2 diabetes poorly controlled on oral glucose-lowering drugs: a subgroup analysis of the A1chieve study显示文摘 | Chen Liming Xing Xiaoyan Lei Minxiang Liu Jie Shi Yongquan Li Pengqiu Qin Guijun Li Chengjiang Li Yukun Wang Qing Gao Tianshu Hu Ling Wang Yangwei Yang Wenying | 2014 | Chinese Medical Journal2014，，2： | 19 |
| 3 | Current Development Situations of Ziziphus Jujuba Industry in South Xinjiang and Recommendations显示文摘Through surveying current development situations and existing problems of planting and processing of Ziziphus jujuba in south Xinjiang,this paper discussed planting,processing mode of Ziziphus Jujuba in south Xinjiang and development direction of enterprises in Ziziphus Jujuba production. It is expected to ensure and increase quality and sales volume of Ziziphus Jujuba and promote sound and sustainable development of Ziziphus Jujuba industrial chain in south Xinjiang. | Xinwen JIN Xuedong YAO Chengjiang LIU Hai LIN Zheng LOU Zhenjiang GAO | 2015 | Asian Agricultural Research2015，7，4： | 4 |
| 4 | Severe acute respiratory syndrome coronavirus 2(SARSCoV-2)membrane(M)protein inhibits type I and III interferon production by targeting RIG-I/MDA-5 signaling显示文摘Coronavirus disease 2019(COVID-19),caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),has quickly spread worldwide and has affected more than 10 million individuals.A typical feature of COVID-19 is the suppression of type I and III interferon(IFN)-mediated antiviral immunity.However,the molecular mechanism by which SARS-CoV-2 evades antiviral immunity remains elusive.Here,we reported that the SARS-CoV-2 membrane(M)protein inhibits the production of type I and III IFNs induced by the cytosolic dsRNA-sensing pathway mediated by RIG-I/MDA-5–MAVS signaling.In addition,the SARS-CoV-2 M protein suppresses type I and III IFN induction stimulated by SeV infection or poly(I:C)transfection.Mechanistically,the SARS-CoV-2 M protein interacts with RIG-I,MAVS,and TBK1,thus preventing the formation of the multiprotein complex containing RIG-I,MAVS,TRAF3,and TBK1 and subsequently impeding the phosphorylation,nuclear translocation,and activation of IRF3.Consequently,ectopic expression of the SARS-CoV-2 M protein facilitates the replication of vesicular stomatitis virus.Taken together,these results indicate that the SARS-CoV-2 M protein antagonizes type I and III IFN production by targeting RIG-I/MDA-5 signaling,which subsequently attenuates antiviral immunity and enhances viral replication.This study provides insight into the interpretation of SARS-CoV-2-induced antiviral immune suppression and illuminates the pathogenic mechanism of COVID-19. | Yi Zheng Meng-Wei Zhuang Lulu Han Jing Zhang Mei-Ling Nan Peng Zhan Dongwei Kang Xinyong Liu Chengjiang Gao Pei-Hui Wang | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 3 |
| 5 | Comprehensive and high-resolution emission inventory of atmospheric pollutants for the northernmost cities agglomeration of Harbin-Changchun,China:Implications for local atmospheric environment management显示文摘Using a bottom-up estimation method,a comprehensive,high-resolution emission inventory of gaseous and particulate atmospheric pollutants for multiple anthropogenic sectors with typical local sources has been developed for the Harbin-Changchun city agglomeration(HCA).The annual emissions for CO,NO_(x),SO_(2),NH_(3),VOC S,PM_(2.5),PM 10,BC and OC during 2017 in the HCA were estimated to be 5.82 Tg,0.70 Tg,0.34 Tg,0.75 Tg,0.81 Tg,0.67 Tg,1.59 Tg,0.12 Tg and 0.26 Tg,respectively.For PM 10 and SO_(2),the emissions from industry processes were the dominant contributors representing 54.7%and 49.5%,respectively,of the total emissions,while 95.3%and 44.5%of the total NH_(3)and NO x emissions,respectively,were from or associated with agricultural activities and transportation.Spatiotemporal distributions showed that most emissions(except NH_(3))occurred in November to March and were concentrated in the central cities of Changchun and Harbin and the surrounding cities.Open burning of straw made an important contribution to PM_(2.5)in the central regions of the northeastern plain during autumn and spring,while domestic coal combustion for heating purposes was significant with respect to SO_(2)and PM_(2.5)emissions during autumn and winter.Furthermore,based on Principal Component Analysis and Multivariable Linear Regression model,air temperature,relative humidity,electricity and energy consumption,and the urban and rural population were optimized to be representative indicators for rapidly assessing the magnitude of regional atmospheric pollutants in the HCA.Such indicators and equations were demonstrated to be useful for local atmospheric environment management. | Mengduo Zhang Weiwei Chen Xiangjin Shen Hongmei Zhao Chengkang Gao Xuelei Zhang Wei Liu Chengjiang Yang Yang Qin Shichun Zhang Jing Fu Daniel Tong Aijun Xiu | 2021 | Journal of Environmental Sciences2021，33，6： | 3 |
| 6 | Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes显示文摘HBV is considered as a“stealth”virus that does not invoke interferon(IFN)responses;however,the mechanisms by which HBV bypasses innate immune recognition are poorly understood.In this study,we identified adenosine deaminases acting on RNA 1(ADAR1),which is a key factor in HBV evasion from IFN responses in hepatocytes.Mechanically,ADAR1 interacted with HBV RNAs and deaminated adenosine(A)to generate inosine(I),which disrupted host immune recognition and thus promoted HBV replication.Loss of ADAR1 or its deficient deaminase activity promoted IFN responses and inhibited HBV replication in hepatocytes,and blocking the IFN signaling pathways released the inhibition of HBV replication caused by ADAR1 deficiency.Notably,the HBV X protein(HBx)transcriptionally promoted ADAR1 expression to increase the threshold required to trigger intrinsic immune activation,which in turn enhanced HBV escape from immune recognition,leading to persistent infection.Supplementation with 8-azaadenosine,an ADAR1 inhibitor,efficiently enhanced liver immune activation to promote HBV clearance in vivo and in vitro.Taken together,our results delineate a molecular mechanism by which HBx promotes ADAR1-derived HBV immune escape and suggest a targeted therapeutic intervention for HBV infection. | Liyuan Wang Yang Sun Xiaojia Song Zehua Wang Yankun Zhang Ying Zhao Xueqi Peng Xiaodong Zhang Chunyang Li Chengjiang Gao Nailin Li Lifen Gao Xiaohong Liang Zhuanchang Wu Chunhong Ma | 2021 | Cellular & Molecular Immunology2021，18，8： | 2 |
| 7 | OTUD5 promotes innate antiviral and antitumor immunity through deubiquitinating and stabilizing STING显示文摘Stimulator of interferon genes(STING)is an adaptor protein that is critical for effective innate antiviral and antitumor immunity.The activity of STING is heavily regulated by protein ubiquitination,which is fine-tuned by both E3 ubiquitin ligases and deubiquitinases.Here,we report that the deubiquitinase OTUD5 interacts with STING,cleaves its K48-linked polyubiquitin chains,and promotes its stability.Consistently,knockout of OTUD5 resulted in faster turnover of STING and subsequently impaired type I IFN signaling following cytosolic DNA stimulation.More importantly,Lyz2-Cre Otud5^(fl/Y) mice and CD11-Cre Otud5^(fl/Y) mice showed more susceptibility to herpes simplex virus type 1(HSV-1)infection and faster development of melanomas than their corresponding control littermates,indicating that OTUD5 is indispensable for STING-mediated antiviral and antitumor immunity.Our data suggest that OTUD5 is a novel checkpoint in the cGAS-STING cytosolic DNA sensing pathway. | Yunyun Guo Fei Jiang Lingli Kong Haifeng Wu Honghai Zhang Xiaorong Chen Jian Zhao Baoshan Cai Yanqi Li Chunhong Ma Fan Yi Lei Zhang Bingyu Liu Yi Zheng Lingqiang Zhang Chengjiang Gao | 2021 | Cellular & Molecular Immunology2021，18，8： | 2 |
| 8 | SARS-CoV-2 NSP5 and N protein counteract the RIG-I signaling pathway by suppressing the formation of stress granules显示文摘As a highly pathogenic human coronavirus,SARS-CoV-2 has to counteract an intricate network of antiviral host responses to establish infection and spread.The nucleic acid-induced stress response is an essential component of antiviral defense and is closely related to antiviral innate immunity.However,whether SARS-CoV-2 regulates the stress response pathway to achieve immune evasion remains elusive.In this study,SARS-CoV-2 NSP5 and N protein were found to attenuate antiviral stress granule(avSG)formation.Moreover,NSP5 and N suppressed IFN expression induced by infection of Sendai virus or transfection of a synthetic mimic of dsRNA,poly(I:C),inhibiting TBK1 and IRF3 phosphorylation,and restraining the nuclear translocalization of IRF3.Furthermore,HEK293T cells with ectopic expression of NSP5 or N protein were less resistant to vesicular stomatitis virus infection.Mechanistically,NSP5 suppressed avSG formation and disrupted RIG-I–MAVS complex to attenuate the RIG-I–mediated antiviral immunity.In contrast to the multiple targets of NSP5,the N protein specifically targeted cofactors upstream of RIG-I.The N protein interacted with G3BP1 to prevent avSG formation and to keep the cofactors G3BP1 and PACT from activating RIG-I.Additionally,the N protein also affected the recognition of dsRNA by RIG-I.This study revealed the intimate correlation between SARS-CoV-2,the stress response,and innate antiviral immunity,shedding light on the pathogenic mechanism of COVID-19. | Yi Zheng Jian Deng Lulu Han Meng-Wei Zhuang Yanwen Xu Jing Zhang Mei-Ling Nan Yang Xiao Peng Zhan Xinyong Liu Chengjiang Gao Pei-Hui Wang | 2022 | Signal Transduction and Targeted Therapy2022，7，2： | 1 |
| 9 | USP3 deubiquitinates and stabilizes the adapter protein ASC to regulate inflammasome activation显示文摘Inflammasomes are essential components of the innate immune system and its defense against infections,whereas the dysregulation of inflammasome activation has a detrimental effect on human health.The activation of inflammasomes is subjected to tight regulation to maintain immune homeostasis,yet the underlying mechanism remains elusive.Here,we identify USP3 as a direct deubiquitinating enzyme(DUB)for ASC,the central adapter mediating the assembly and activation of most inflammasomes.USP3 removes the K48-linked ubiquitination on ASC and strengthens its stability by blocking proteasomal degradation.Additionally,USP3 promotes inflammasome activation,and this function was confirmed in mouse models of aluminum(Alum)-induced peritonitis,F.novicida infection and flagellin-induced pneumonia in vivo.Our work unveils that USP3 functions as a key regulator of ASC ubiquitination and maintains the physiological role of ASC in mediating inflammasome activation,and we propose a new mechanism by which the ubiquitination of ASC regulates inflammasome activation. | Wanxin Zhuang Lei Zhang Yi Zheng Bingyu Liu Chunhong Ma Wei Zhao Suxia Liu Feng Liu Chengjiang Gao | 2022 | Cellular & Molecular Immunology2022，19，10： | 1 |
| 10 | Roles of TIPE2 in hepatitis B virus-induced hepatic inflammation in humans and mice显示文摘 | Wenjin Xi Yejia Hu Yugang Liu Jiao Zhang Lei Wang Yunwei Lou Zhonghua Qu Jian Cui Guizhong Zhang Xiaohong Liang Chunhong Ma Chengjiang Gao Youhai Chen Suxia Liu | 2011 | Molecular Immunology2011，，9： | 1 |
| 11 | PI4P STimulatING innate immune activation:beyond the Golgi显示文摘The cGAS–STING pathway is pivotal for sensing cytosolic DNA[2].cGAS,a cytoplasmic DNA sensor,can be stimulated by DNA,and it consumes ATP and GTP to synthesize a second messenger,2'3'-cGAMP,which binds to STING,resulting in STING conformational change,oligomerization,and activation;ultimately,this process leads to the production of cytokines such as type I interferon to mediate antiviral and antitumor immune responses(Fig.1).Phosphoinositides,derived from phosphatidylinositol(PI),are phospholipids in membranes and are also crucial signaling molecules[3].The D-3,D-4,or D-5 positions in the inositol head group can be phosphorylated;therefore,a total of seven different PIP molecules exist in eukaryotes.Phosphatidylinositol 4-phosphate(PI4P)is distributed in various membrane components,with the highest amount in the trans-Golgi network(TGN)[4].The PI4P level in cells is regulated by its PI4K synthetases(PI4KA,PI4KB,PI4K2A,and PI4K2B)and the lipid phosphatase SAC1.In addition to being a precursor for PIP2 and PIP3,PI4P is a crucial signaling molecule involved in vesicular transport,lipid transport,and organelle morphology maintenance. | Yi Zheng Xuejing Zhang Chengjiang Gao | 2023 | Cellular & Molecular Immunology2023，20，12： | 0 |
| 12 | MAVS-loaded unanchored Lys63-linked polyubiquitin chains activate the RIG-I-MAVS signaling cascade显示文摘The adaptor molecule MAVS forms prion-like aggregates to govern the RIG-I-like receptor(RLR)signaling cascade.Lys63(K63)-linked polyubiquitination is critical for MAVS aggregation,yet the underlying mechanism and the corresponding E3 ligases and deubiquitinating enzymes(DUBs)remain elusive.Here,we found that the K63-linked polyubiquitin chains loaded on MAVS can be directly recognized by RIG-I to initiate RIG-I-mediated MAVS aggregation with the prerequisite of the CARDRIG-I-CARDMAVS interaction.Interestingly,many K63-linked polyubiquitin chains attach to MAVS via an unanchored linkage.We identified Ube2N as a major ubiquitin-conjugating enzyme for MAVS and revealed that Ube2N cooperates with the E3 ligase Riplet and TRIM31 to promote the unanchored K63-linked polyubiquitination of MAVS.In addition,we identified USP10 as a direct DUB that removes unanchored K63-linked polyubiquitin chains from MAVS.Consistently,USP10 attenuates RIG-I-mediated MAVS aggregation and the production of type I interferon.Mice with a deficiency in USP10 show more potent resistance to RNA virus infection.Our work proposes a previously unknown mechanism for the activation of the RLR signaling cascade triggered by MAVS-attached unanchored K63-linked polyubiquitin chains and establishes the DUB USP10 and the E2:E3 pair Ube2N-Riplet/TRIM31 as a specific regulatory system for the unanchored K63-linked ubiquitination and aggregation of MAVS upon viral infection. | Feng Liu Wanxin Zhuang Bin Song Yuan Yang Junqi Liu Yi Zheng Bingyu Liu Jie Zheng Wei Zhao Chengjiang Gao | 2023 | Cellular & Molecular Immunology2023，20，10： | 0 |
| 13 | The role of macrophages in the formation of hypertrophic scars and keloids显示文摘Numerous studies have shown that macrophages can orchestrate the microenvironment from the early stage of wound healing to the later stages of scar formation.However,few reviews have highlighted the significance of macrophages during the formation of abnormal scars.The purpose of this reviewwas to outline the polarization of macrophages from early to late stage of pathological scar formation,focusing on spatiotemporal diversity of M1 and M2 macrophages.In this review,the role of macrophages in the formation of hypertrophic scars and keloids is summarized in detail.First,an increased number of M2 cells observed before injuries are significantly associated with susceptibility to abnormal scar pathogenesis.Second,decreased expression of M1 at the early stage and delayed expression of M2 at the late stage results in pathological scar formation.Third,M2 cells are highly expressed at both the margin and the superficial region,which is consistent with the invasive property of keloids.Finally,this review helps to characterize strategies for the prediction and prevention of pathological scar formation. | Xiangwen Xu Shuchen Gu Xin Huang Jieyi Ren Yihui Gu Chengjiang Wei Xiang Lian Haizhou Li Yashan Gao Rui Jin Bin Gu Tao Zan Zhichao Wang | 2020 | Burns & Trauma2020，8，1： | 0 |
| 14 | TRIM31 facilitates K27-linked polyubiquitination of SYK to regulate antifungal immunity显示文摘Spleen tyrosine kinase(SYK)is a non-receptor tyrosine kinase,which plays an essential role in both innate and adaptive immunity.However,the key molecular mechanisms that regulate SYK activity are poorly understood.Here we identified the E3 ligase TRIM31 as a crucial regulator of SYK activation.We found that TRIM31 interacted with SYK and catalyzed K27-linked polyubiquitination at Lys375 and Lys517 of SYK.This K27-linked polyubiquitination of SYK promoted its plasma membrane translocation and binding with the C-type lectin receptors(CLRs). | Xueer Wang Honghai Zhang Zhugui Shao Wanxin Zhuang Chao Sui Feng Liu Xiaorong Chen Jinxiu Hou Lingli Kong Hansen Liu Yi Zheng Bingyu Liu Tian Chen Lei Zhang Xinming Jia Chengjiang Gao | 2021 | Signal Transduction and Targeted Therapy2021，6，9： | 0 |
| 15 | Severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) membrane (M) protein inhibits type I and IIIinterferon production by targeting RIG-I/MDA-5 signaling显示文摘Coronavirus disease 2019(COVID-19),caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),has quickly spread worldwide and has affected more than 10 million individuals.A typical feature of COVID-19 is the suppression of type I and III interferon(IFN)-mediated antiviral immunity.However,the molecular mechanism by which SARS-CoV-2 evades antiviral immunity remains elusive.Here,we reported that the SARS-CoV-2 membrane(M)protein inhibits the production of type I and III IFNs induced by the cytosolic dsRNA-sensing pathway mediated by RIG-I/MDA-5–MAVS signaling.In addition,the SARS-CoV-2 M protein suppresses type I and III IFN induction stimulated by SeV infection or poly(I:C)transfection.Mechanistically,the SARS-CoV-2 M protein interacts with RIG-I,MAVS,and TBK1,thus preventing the formation of the multiprotein complex containing RIG-I,MAVS,TRAF3,and TBK1 and subsequently impeding the phosphorylation,nuclear translocation,and activation of IRF3.Consequently,ectopic expression of the SARS-CoV-2 M protein facilitates the replication of vesicular stomatitis virus.Taken together,these results indicate that the SARS-CoV-2 M protein antagonizes type I and III IFN production by targeting RIG-I/MDA-5 signaling,which subsequently attenuates antiviral immunity and enhances viral replication.This study provides insight into the interpretation of SARS-CoV-2-induced antiviral immune suppression and illuminates the pathogenic mechanism of COVID-19. | Yi Zheng Meng-Wei Zhuang Lulu Han Jing Zhang Mei-Ling Nan Peng Zhan Dongwei Kang Xinyong Liu Chengjiang Gao Pei-Hui Wang | 2021 | Signal Transduction and Targeted Therapy2021，6，1： | 0 |
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