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African swine fever virus S273R protein antagonizes type I interferon production by interfering with TBK1 and irf3 interaction

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Virologica Sinica 2023年第6期38卷 911-921页

作者： Hui Li Xiaojie Zheng You Li Yingqi Zhu Yangyang Xu Zilong Yu Wen-Hai Feng State Key Laboratory of Agrobiotechnology College of Biological SciencesChina Agricultural UniversityBeijing100193China Frontiers Science Center for Molecular Design Breeding College of Biological SciencesChina Agricultural UniversityBeijing100193China Ministry of Agriculture Key Laboratory of Soil Microbiology College of Biological SciencesChina Agricultural UniversityBeijing100193China Department of Microbiology and Immunology College of Biological SciencesChina Agricultural UniversityBeijing 100193China

African swine fever(ASF)is originally reported in East Africa as an acute hemorrhagic *** swine fever virus(ASFV)is a giant and complex DNA virus with icosahedral structure and encodes a variety of virulence factors to resist host innate immune response.S273R protein(pS273R),as a SUMO-1 specific cysteine protease,can affect viral packaging by cutting polymeric *** this study,we found that pS273R was an important antagonistic viral factor that suppressed cGAS-STING-mediated type I interferon(IFN-I)production.A detailed analysis showed that pS273R inhibited IFN-I production by interacting with interferon regulatory factor 3(irf3).Subsequently,we showed that pS273R disrupted the association between TBK1 and irf3,leading to the repressed irf3 phosphorylation and *** and point mutation analysis verified that pS273R impaired IFN-I production independent of its cysteine protease *** findings will help us further understand ASFV pathogenesis.

关键词： African swine fever virus(ASFV) cGAS-STING S273R irf3 TBK1 Type I interferon(IFN-I)

SENP2 negatively regulates cellular antiviral response by deSUMOylating irf3 and conditioning it for ubiquitination and degradation

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分子细胞生物学报:英文版 2011年第5期3卷 283-292页

作者： Yong Ran Tian-Tian Liu Qian Zhou Shu Li Ai-Ping Mao Ying Li Li-Juan Liu Jin-Ke Cheng Hong-Bing Shu College of Life Sciences Wuhan UniversityWuhan 430072China Department of Biochemistry and Molecular Cell Biology School of MedicineShanghai Jiao Tong UniversityShanghai 200025China

Transcription factor irf3-mediated type I interferon induction is essential for antiviral innate *** identified the deSUMOylating enzyme Sentrin/SUMO-specific protease(SENP)2 as a negative regulator of virus-triggered IFN-b *** of SENP2 caused irf3 deSUMOylation,K48-linked ubiquitination,and degradation,whereas depletion of SENP2 had opposite *** the SUMOylation and K48-linked ubiquitination of irf3 occurred at lysines 70 and 87,and these processes are *** level of virus-triggered IFN-b was markedly up-regulated and viral replication was reduced in SENP2-deficient cells comparing with wild-type *** findings suggest that SENP2 regulates antiviral innate immunity by deSUMOylating irf3 and conditioning it for ubiquitination and degradation,and provide an example of cross-talk between the ubiquitin and SUMO pathways in innate immunity.

关键词： SENP2 irf3 deSUMOylation ubiquitination innate immunity

IFITM3 inhibits virus-triggered induction of type I interferon by mediating autophagosome-dependent degradation of irf3

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Cellular & Molecular Immunology 2018年第9期15卷 858-867页

作者： Li-Qun Jiang Tian Xia Yun-Hong Hu Ming-Shun Sun Shuang Yan Cao-Qi Lei Hong-Bing Shu Ji-Hua Guo Yu Liu State Key Laboratory of Virology Hubei Key Laboratory of Cell HomeostasisDepartment of Cell BiologyCollege of Life SciencesWuhan UniversityWuhan 430072China Hubei-MOST KLOS&KLOBME School&Hospital of StomatologyWuhan UniversityWuhan 430072China

Interferon-induced transmembrane protein 3 (IFITM3) is a restriction factor that can be induced by viral infectionand interferons (IFNs). It inhibits the entry and replication of many viruses, which are independent of receptorusage but dependent on processes that occur in endosomes. In this study, we demonstrate that IFITM3 playsimportant roles in regulating the RNA-virus-triggered production of IFN-β in a negative-feedback *** of IFITM3 inhibited Sendai virus-triggered induction of IFN-β, whereas knockdown of IFITM3 hadthe opposite effect. We also showed that IFITM3 was constitutively associated with irf3 and regulated thehomeostasis of irf3 by mediating the autophagic degradation of irf3. These findings suggest a novel inhibitoryfunction of IFITM3 on the RNA-virus-triggered production of type I IFNs and cellular antiviral responses.

关键词： autophagy IFITM3 IFNs irf3

ZDHHC11 modulates innate immune response to DNA virus by mediating MITA–irf3 association

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Cellular & Molecular Immunology 2018年第10期15卷 907-916页

作者： Ying Liu Qian Zhou Li Zhong Heng Lin Ming-Ming Hu Yan Zhou Hong-Bing Shu Shu Li College of Life Sciences Medical Research InstituteWuhan UniversityWuhanHubei 430072China

MITA is a central adaptor in innate immune responses to DNA *** mechanisms responsible for recruitment of downstream kinase TBK1 and the transcription factor irf3 to MITA remains *** we identified ZDHHC11,a member of DHHC palmitoyl transferase family,as a positive regulator of DNA virus-triggered *** of ZDHHC11 activated the IFN-βpromoter,while ZDHHC11-deficiency specifically impaired DNA virus HSV-1-induced transcription of downstream antiviral ***11^(−/−)mice exhibited lower serum cytokine levels and higher lethality after HSV-1 ***,ZDHHC11 facilitated the optimal recruitment of irf3 to *** findings support an important role for ZDHHC11 in mediating MITA-dependent innate immune responses against DNA viruses.

关键词： ZDHHC11 MITA irf3 innate immune response

Host HDAC4 regulates the antiviral response by inhibiting the phosphorylation of irf3

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Journal of Molecular Cell Biology 2019年第2期11卷 158-169页

作者： Qi Yang Jielin Tang Rongjuan Pei XiaoXiao Gao Jing Guo Chonghui Xu Yun Wang QianWang Chunchen Wu Yuan Zhou Xue Hu He Zhao Yanyi Wang Xinwen Chen Jizheng Chen State Key Laboratory of Virology Wuhan Institute of Virology Chinese Academy of Sciences Wuhan 430071 China University of Chinese Academy of Sciences Beijing 100049 China Key Laboratory of Human Functional Genomics of Jiangsu Province School of Basic Medical Science Nanjing Medical University Nanjing 210093 China

Class II HDACs, such as HDAC4, are critical regulators of the immune response in various immune cells;however, its role in innate immunity remains largely ***, we report that the overexpression of HDAC4 suppresses the production of type I interferons triggered by pattern-recognition receptors (PRRs). HDAC4 repressed the translocation of transcription factor irf3 to the nucleus, thereby decreasing irf3-mediated IFN-β expression. In particular, we also determined that HDAC4 can be phosphorylated and simultaneously block the phosphorylation of irf3 at Ser386 and Ser396 by TBK1 and IKKε, respectively, by interacting with the kinase domain of TBK1 and IKKε. Furthermore, IFN-β may stimulate the expression of HDAC4. Our findings suggest that HDAC4 acts as a regulator of PRR signaling and is a novel mechanism of negative feedback regulation for preventing an overreactive innate immune response.

关键词： HDAC4 antiviral response irf3 TBK1 IKKε

The methyltransferase PRMT6 attenuates antiviral innate immunity by blocking TBK1–irf3 signaling

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Cellular & Molecular Immunology 2019年第10期16卷 800-809页

作者： Hua Zhang Chaofeng Han Tianliang Li Nan Li Xuetao Cao National Key Laboratory of Medical Immunology&Institute of Immunology Second Military Medical UniversityShanghai 200433China Department of Immunology&Center for Immunotherapy Institute of Basic Medical SciencesPeking Union Medical CollegeChinese Academy of Medical SciencesBeijing 100005China

Protein arginine methyltransferases(PRMTs)play diverse biological roles and are specifically involved in immune cell development and ***,their role in antiviral innate immunity has not been *** infection triggers the TBK1–irf3 signaling pathway to stimulate the production of type-I interferon,which mediates antiviral *** performed a functional screen of the nine mammalian PRMTs for regulators of IFN-βexpression and found that PRMT6 inhibits the antiviral innate immune *** infection also upregulated PRMT6 protein *** generated PRMT6-deficient mice and found that they exhibited enhanced antiviral innate ***6 deficiency promoted the TBK1–irf3 interaction and subsequently enhanced irf3 activation and type-I interferon ***,viral infection enhanced the binding of PRMT6 to irf3 and inhibited the interaction between irf3 and TBK1;this mechanism was independent of PRMT6 methyltransferase ***,PRMT6 inhibits antiviral innate immunity by sequestering irf3,thereby blocking TBK1-irf3 *** work demonstrates a methyltransferase-independent role for *** also identifies a negative regulator of the antiviral immune response,which may protect the host from the damaging effects of an overactive immune system and/or be exploited by viruses to escape immune detection.

关键词： PRMT6 TBK1 irf3 IFN antiviral innate immunity

RIG-I-like receptor-induced irf3 mediated pathway of apoptosis （RIPA）： a new antiviral pathway

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Protein & Cell 2017年第3期8卷 165-168页

作者： Saurabh Chattopadhyay Ganes C. Sen Department of Medical Microbiology and Immunology University of Toledo College of Medicine and Life Sciences 3000 Arlington Avenue Mailstop 1021 Toledo OH 43614 USA Cleveland Clinic Department of Immunology 9500 Euclid Avenue NE20 Cleveland OH 44195 USA

The innate immune response is the first line of host defense to eliminate viral infection. Pattern recognition receptors in the cytosol, such as RIG-I-like receptors （RLR） and Nod-like receptors （NLR）, and membrane bound Toll like receptors （TLR） detect viral infection and initiate transcription of a cohort of antiviral genes, including interferon （IFN） and interferon stimulated genes （ISGs）, which ultimately block viral replication. Another mechanism to reduce viral spread is through RIPA, the RLR-induced irf3-mediated pathway of apoptosis, which causes infected cells to undergo pre- mature death. The transcription factor irf3 can mediate cellular antiviral responses by both inducing antiviral genes and triggering apoptosis through the activation of RIPA. The mechanism of irf3 activation in RIPA is dis- tinct from that of transcriptional activation; it requires linear polyubiquitination of specific lysine residues of irf3. Using RIPA-active, but transcriptionally inactive, irf3 mutants, it was shown that RIPA can prevent viral replication and pathogenesis in mice.

关键词： RIPA irf3 innate immunity

草鱼(Ctenopharyngodon idella)长链非编码RNA ISG152-L2激活irf3和ISG152的表达

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南昌大学学报（理科版） 2023年第3期47卷 272-282页

作者：胡霁欢胡美玲史骁周鹏程常凯乐向阳徐小文南昌大学生命科学学院江西南昌330031

长链非编码RNA(lncRNA,非编码RNA≥200 bp)以前被认为是转录中的“噪音”。然而,近年来已经发现了相当多的具有重要功能的lncRNA。LncRNA在疾病、发育、细胞分化和先天免疫反应中起着至关重要的作用。本研究通过使用TopHat2软件和Cuffli... 详细信息

长链非编码RNA(lncRNA,非编码RNA≥200 bp)以前被认为是转录中的“噪音”。然而,近年来已经发现了相当多的具有重要功能的lncRNA。LncRNA在疾病、发育、细胞分化和先天免疫反应中起着至关重要的作用。本研究通过使用TopHat2软件和Cufflinks软件分析草鱼的转录组数据,鉴定了与免疫相关的长链非编码RNA。筛选出一个lncRNA序列,命名为ISG152-L2,它位于草鱼ISG152的上游。使用综合基因组学查看器(IGV)测定ISG152-L2和草鱼ISG152的同步表达。研究了ISG152-L2的共表达,并确定了包括草鱼ISG152在内的相关基因网络,功能富集分析表明,这些基因在免疫相关过程中功能富集。用poly(I:C)刺激时,ISG152-L2在被测组织(脑,眼,肠,鳃,心脏,肝胰腺,脾脏和肾脏)中上调。同时,ISG152-L2和ISG152在CIK细胞受到poly(I:C)刺激后均上调。双荧光素酶基因检测发现,CIK细胞中的ISG152-L2显著增强了ISG152启动子活性,并且这种增强取决于ISG152-L2的特定620~1 190 bp区域。免疫共沉淀试验表明,草鱼ISG152可以在体外irf3相互作用。此外,isg152-l2过表达增加了CIK细胞中irf3的蛋白质水平,而ISG152-L2的干扰则产生了相反的结果。总之,我们筛选了一个免疫相关的lncRNA,即ISG152-L2,它位于ISG152的上游,并通过诱导其启动子的活性,上调irf3的蛋白表达水平来增强ISG152的表达。

关键词：长链非编码RNA ISG152-L2 ISG152 irf3 先天免疫鱼类

irf3激动剂KIN1148对HEK293细胞及阿霉素诱导的肾损伤大鼠细胞凋亡的影响

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IRF3激动剂KIN1148对HEK293细胞及阿霉素诱导的肾损伤大鼠细胞凋...

作者：李国铭福建医科大学

学位级别：硕士

目的:课题组前期通过全基因组关联研究和独立样本验证发现干扰素调节因子3(interferon regulatory factor 3,irf3)为新的狼疮易感基因,且基因型-表型相关性分析表明irf3与狼疮性肾炎(lupus nephritis,LN)相关,但其致病机制尚不明确。细... 详细信息

目的:课题组前期通过全基因组关联研究和独立样本验证发现干扰素调节因子3(interferon regulatory factor 3,irf3)为新的狼疮易感基因,且基因型-表型相关性分析表明irf3与狼疮性肾炎(lupus nephritis,LN)相关,但其致病机制尚不明确。细胞凋亡机制在LN的发生发展中起重要作用。本研究通过观察irf3激动剂KIN1148干预对人胚肾上皮细胞293(human embryonic kidney 293,HEK293)及阿霉素诱导的肾损伤SD大鼠肾组织细胞凋亡的影响,揭示irf3是否可通过细胞凋亡机制参与肾损伤。方法:(1)细胞实验(1)细胞分组及药物干预:以HEK293细胞为研究对象。按irf3激动剂KIN1148干预浓度将细胞分为0μΜ、5μΜ、20μΜ、50μΜ四组,按干预时间分为0h、3h、6h、12h四组,干预后采用CCK-8法测定细胞活力;(2)细胞凋亡情况:根据CCK-8结果予0μΜ、5μΜ、20μΜ、50μΜ的浓度梯度KIN1148干预HEK293细胞12h后采用4',6-二脒基-2-苯基吲哚(4',6-diamidino-2-phenylindole,DAPI)染色观察各组细胞核情况;采用Western blot测定各组促凋亡蛋白Cleaved-Caspase 3、Bax及抑凋亡蛋白Bcl-2表达水平。(2)动物实验(1)动物分组及药物干预:将45只生后21天(postnatal day 21,P21)的雌性SD大鼠随机分为三组,其中一组为正常对照组;另外两组拟行阿霉素处理诱导肾损伤。肾损伤组以阿霉素处理前是否予以KIN1148干预分为肾损伤药物干预组及肾损伤非药物干预组。肾损伤药物干预组予KIN1148 1.5mg/kg/d、肾损伤非药物干预组予以等量溶剂、正常对照组予以等量生理盐水,腹腔注射,连续7天。P28时,肾损伤药物干预组及肾损伤非药物干预组予10mg/kg阿霉素单次尾静脉注射诱导肾损伤。P35时获取各组大鼠肾组织。(2)肾组织病理改变:采用苏木精-伊红染色法(hematoxylin-eosin staining,HE)评估;(3)细胞凋亡情况:采用TUNEL(Td T-mediated d UTP nick-end labeling)染色评估细胞凋亡情况,采用免疫组织化学法(immunohistochemistry,IHC)检测各组大鼠肾组织促凋亡蛋白Bax、抑凋亡蛋白Bcl-2蛋白表达情况。结果:(1)细胞实验(1)细胞活力:KIN1148干预后HEK293细胞活力明显下降,且呈时间依赖性与浓度依赖性。未干预时,各组间细胞活力无差异(P值均>0.05);以0、5、20、50μΜ不同浓度KIN1148干预3h,各组细胞活力分别为0μΜ组(99.84±3.36)>5μΜ组(92.66±3.43)>20μΜ组(84.97±1.53)>50μΜ组(74.27±2.80)(P5μΜ组(85.47±1.07)>20μΜ组(77.01±2.7)>50μΜ组(70.65±2.94)(P35±0.59)>5μΜ组(79.23±2.01)>20μΜ组(69.48±1.57)>50μΜ组(56.99±1.99)(P3)Western blot检测蛋白表达:KIN1148干预后促凋亡蛋白蛋白Cleaved-Caspase 3及Bax表达增加,抑凋亡蛋白Bcl-2表达减少。干预时间为12h时,不同浓度KIN1148干预Cleaved-Caspase 3蛋白相对表达量分别为:0μΜ组(0.17±0.02)36±0.02)3)34±0.02)5μΜ组(0.21±0.01)>20μΜ组(0.13±0.01)>50μΜ组(0.07±0.01)(P<0.05)。(2)动物实验(1)HE染色:HE染色结果示KIN1148干预加重阿霉素诱导的肾损伤大鼠病理损伤程度。肾损伤药物干预组及肾损伤非药物干预组较正常对照组均有不同程度的病理受损,肾损伤药物干预组受损最为严重,表现为肾小球萎缩,肾小管上皮细胞空泡及颗粒变性,细胞碎片堵塞管腔;(2)

关键词： irf3 KIN1148 阿霉素细胞凋亡狼疮性肾炎