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Oncolytic Activity of Wild-type Newcastle Disease Virus HK84 Against Hepatocellular Carcinoma Associated with Activation of type i interferon Signaling

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Journal of Clinical and Translational Hepatology 2022年第2期10卷 284-296页

作者： Liming Chen Yongdong Niu Jiating Sun Hong Lin Guoxi Liang Min Xiao Dongmei Shi Jia Wang Huachen Zhu Yi Guan Department of Oncology First Affiliated Hospital of Shantou University Medical CollegeShantouGuangdongChina in-ternational Joint Laboratory for Virology and Emerging infectious Diseases(Ministry of Education) Guangdong-Hong Kong Joint Laboratory for Emerging Infectious DiseasesJoint Institute of Virology of STU/HKUShantouGuangdongChina Department of Pharmacology Shantou University Medical CollegeShantouGuangdongChina

Background and Aims:Hepatocellular carcinoma(HCC)is listed as one of the most common causes of cancer-related *** therapy has become a promising treatment because of novel immunotherapies and gene editing technology,but biosafety concerns remain the biggest limitation for clinical *** studied the the antitumor activity and biosafety of the wild-type Newcastle disease virus HK84 strain(NDV/HK84)and 10 other NDV ***-ods:Cell proliferation and apoptosis were determined by cell counting Kit-8 and fluorescein isothiocyanate Annexin V apoptosis *** formation,wound healing,and a xenograft mouse model were used to evaluate in vivo and in vitro oncolytic *** safety of NDV/HK84 was tested in nude mice by an in vivo luciferase imaging *** replication kinetics of NDV/HK84 in normal tis-sues and tumors were evaluated by infectious-dose assays in *** sequencing analysis was performed to explore NDV/HK84 activity and was validated by quantitative real-time ***:The cell counting Kit-8 assays of vi-ability found that the oncolytic activity of the NDV strains differed with the multiplicity of infection(MOi).At an MOi of 20,the oncolytic activity of all NDV strains except the DK/JX/21358/08 strain was>80%.The oncolytic activities of the NDV/HK84 and DK/JX/8224/04 strains were>80%at both MOi=20 and MOi=*** NDV/HK84 had>80%oncolytic activities at both MOi=20 and MOi=*** chose NDV/HK84 as the candidate virus to test the oncolytic effect of NDV in HCC in the in vitro and in vivo ***/HK84 killed human SK-HEP-1 HCC cells without affecting healthy ***:intratumor infection with NDV/HK84 strains compared with vehicle controls or positive controls indicated that NDV/HK84 strain specifically inhib-ited HCC without affecting healthy ***-throughput RNA sequencing showed that the oncolytic activity of NDV/HK84 was dependent on the activation of type i interferon signaling.

关键词： Newcastle disease virus Oncolytic effectiveness type i interferon Hepatocellular carcinoma Biosafety

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type i interferon： the mediator of bacterial infection-induced necroptosis

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Cellular & Molecular immunology 2013年第1期10卷 4-6页

作者： Qinglin Du Jianping Xie Ha-Jeong Kim Xiaojing Ma institute of Modern Biopharmaceuticals School of Life Science Southwest University Chongqing China Oepartment of Microbiololgy and immunology WeillCornell Medical Collese New York NY USA Sheng Yushou Center of Cell Biology and immunology School of Life Sciences and Biotechnology Shanghai Jiao Tong University Shanghai China |

COMMENTARY innate immune responses are essential for the host to fight against invading microbes. innate immune receptors or pattern recog- nition receptors recognize conserved microbial molecules and trigger innate immune res- ponses. Pattern recognition receptors such as Toll-like receptors primarily signal through the adaptor MyD88 to activate NF-~B, while other Toll-like receptors signal v/a TRiF to activate iRF-3 resulting in the expression of type i interferons （iFNs）.a type i iFNs play a crucial role in antiviral immune responses but are also important for the host response against bac- terial infection.2 Paradoxically.

关键词： type i interferon bacterial infection-induced necroptosis

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PTEN-L promotes type i interferon responses and antiviral immunity

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Cellular & Molecular immunology 2018年第1期15卷 48-57页

作者： Yuanyuan Cao Hongyun Wang Liu Yang Zhen Zhang Chenlin Li Xu Yuan Lang Bu Lang Chen Yu Chen Chun-Mei Li Deyin Guo Modern Virology Research Center College of Life SciencesWuhan UniversityWuhan430072China School of Basic Medical Sciences Wuhan UniversityWuhan430072China Laboratory for Medical Virology School of MedicineSun Yat-sen UniversityGuangzhou510080China

Phosphatase and tensin homolog deleted on chromosome ten(PTEN)is a well-known tumor suppressor that acts as a dual-specificity phosphatase and is frequently mutated in human *** previous work has demonstrated that PTEN also plays a vital role in type i interferon responses and antiviral innate ***,a translational variant of PTEN with a long N-terminal extension(PTEN-L)has been discovered that is secreted into the extracellular environment and enters recipient cells,where it exerts a phosphatase function antagonistic to Pi3K/Akt signaling and *** this study,we demonstrate that PTEN-L promotes type i interferon responses and antiviral innate immunity during viral infection in a phosphatase activity-dependent *** with canonical PTEN,PTEN-L also exerts its antiviral function when it is applied exogenously in protein *** finding was confirmed in cell cultures and mouse infection ***,PTEN-L enhances the responses of both type i interferon and proinflammatory cytokines,thus suggesting that PTEN-L might possess additional functions compared with those of ***,the antiviral function of PTEN-L may open an avenue for the use of PTEN-L in antiviral therapy,particularly in patients with PTEN-deficient tumors.

关键词： antiviral responses innate immunity PTEN PTEN-L type i interferon

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SUMOylation of RiG-i positively regulates the type i interferon signaling

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Protein & Cell 2010年第3期1卷 275-283页

作者： Zhiqiang Mi Jihuan Fu Yanbao Xiong Hong Tang Center for Molecular immunology Institute of MicrobiologyChinese Academy of SciencesBeijing 100101China Key Laboratory of infection and immunity of Chinese Academy of Sciences Institute of BiophysicsBeijing 100101China

Retinoic acid-inducible gene-i(RiG-i)functions as an intracellular pattern recognition receptor(PRR)that recognizes the 5'-triphosphate moiety of single-stranded RNA viruses to initiate the innate immune *** studies have shown that Lys63-linked ubiquitylation is required for RiG-i activation and the downstream anti-viral type i interferon(iFN-i)*** we reported that,RiG-i was also modified by small ubiquitin-like modifier-1(SUMO-1).Functional analysis showed that RiG-i SUMOylation enhanced iFN-i production through increased ubiquitylation and the interaction with its downstream adaptor molecule *** results therefore suggested that SUMOylation might serve as an additional regulatory tier for RiG-i activation and iFN-i signaling.

关键词： RiG-i SUMOylation type i interferon innate immunity

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Mechanism of inhibiting type i interferon induction by hepatitis B virus X protein

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Protein & Cell 2010年第12期1卷 1106-1117页

作者： Junyi Jiang Hong Tang Key laboratory of infection and immunity of Chinese Academy of Sciences Institute of BiophysicsBeijing 100101China Graduate School of Chinese Academy of Sciences Beijing 100049China

Hepatitis B virus(HBV)is regarded as a stealth virus,invading and replicating efficiently in human liver undetected by host innate antiviral ***,we show that type i interferon(iFN)induction but not its downstream signaling is blocked by HBV replication in HepG2.2.15 *** effect may be partially due to HBV X protein(HBx),which impairs iFNβpromoter activation by both Sendai virus(SeV)and components implicated in signaling by viral *** a deubiquitinating enzyme(DUB),HBx cleaves Lys63-linked polyubiquitin chains from many proteins except TANK-binding kinase 1(TBK1).it binds and deconjugates retinoic acid-inducible gene i(RiG i)and TNF receptor-associated factor 3(TRAF3),causing their dissociation from the downstream adaptor CARDiF or TBK1 *** addition to RiG i and TRAF3,HBx also interacts with CARDiF,TRiF,NEMO,TBK1,inhibitor of kappa light polypeptide gene enhancer in B-cells,kinase epsilon(iKKi)and interferon regulatory factor 3(iRF3).Our data indicate that multiple points of signaling pathways can be targeted by HBx to negatively regulate production of type i iFN.

关键词： hepatitis B virus(HBV) HBV X protein(HBx) deubiquitination type i interferon

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Relevance of placental type i interferon beta regulation for pregnancy success

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Cellular & Molecular immunology 2018年第12期15卷 1010-1026页

作者： Ja-Young Kwon Paulomi Aldo Yuan You Jiahui Ding Karen Racicot Xiaoyan Dong John Murphy Guy Glukshtad Michelle Silasi Jian Peng Li Wen Vikki MAbrahams Roberto Romero Gil Mor Division of Reproductive Sciences Department of ObstetricsGynecology and Reproductive SciencesYale School of MedicineNew HavenCTUSA Department of Obstetrics and Gynecology Institute of Women’s Life Medical ScienceYonsei University College of MedicineSeoulKorea Department of Obstetrics Gynecology&Reproductive BiologyCollege of Human MedicineMichigan State University400 Monroe Avenue NEGrand RapidsMI 49503USA Department of Pulmonary Shanghai Children’s HospitalShanghai Jiaotong University School of MedicineShanghaiChina Division of Endocrinology Department of Internal MedicineYale School of MedicineNew HavenCTUSA Perinatal Research Branch NICHD/NIHDetroitMIUSA

Pregnancy is a unique immunologic and microbial condition that requires an adequate level of awareness to provide a fast and protective response against pathogens as well as to maintain a state of tolerance to paternal *** of inflammatory pathways in the placenta triggered by pathogens is one of the main factors responsible for pregnancy *** i iFNs are key molecules modulating immune responses at the level of the placenta and are crucial for protection of the pregnancy via their antiviral and immune modulatory *** this study,we elucidate the mechanisms controlling the basal expression of iFNβand its negative *** in vitro and in vivo animal models,we found that TLR signaling maintains basal iFNβlevels through the TLR4-MyD88-independent TBK/iRF3 signaling *** describe the role of the TAM receptor Axl in the regulation of iFNβfunction in human and mouse trophoblast *** absence of TAM receptors in vivo is associated with fetal demise due to dysregulation of iFNβexpression and its pro-apoptotic downstream ***,our data describe a feedback signaling pathway controlling the expression and function of iFNβin the trophoblast that is essential for an effective response during viral and microbial infections.

关键词： trophoblast immune regulation cytokine TAM receptors type i interferon interferon beta iSGs

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A functional type i interferon pathway drives resistance to cornea herpes simplex virus type 1 infection by recruitment of leukocytes

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The Journal of Biomedical Research 2011年第2期25卷 111-119页

作者： Christopher D. Conrady Heather Jones Min Zheng Daniel J.J. Carr Departments of Microbiology Immunology The University of Oklahoma Health Science Center Oklahoma City OK 73104 USA Departments of Ophthalmology The University of Oklahoma Health Science Center Oklahoma City OK 73104 USA

type i interferons are critical antiviral cytokines produced following herpes simplex virus type-1 （HSV-1） infection that act to inhibit viral spread. in the present study, we identify HSV-infected and adjacent uninfected corneal epithelial cells as the source of interferon-a. We also report mice deficient in the A1 chain of the type i iFN receptor （CDl18-/） are extremely sensitive to ocular infection with low doses （100 PFU） of HSV-1 as seen by significantly elevated viral titers in the cornea Compared to wild type （WT） controls. The enhanced susceptibil- ity correlated with a loss of CD4＋ and CD8＋ T cell recruitment and aberrant chemokine production in the cornea despite mounting an adaptive immune response in the draining mandibular lymph node of CDll8/ mice. Taken together, these results highlight the importance of iFN production in both the innate immune response as well as eliciting chemokine production required to facilitate adaptive immune cell trafficking.

关键词： herpes simplex virus type 1 type i interferon comea viral infection leukocytes ocular immunology

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Promotion of TLR-mediated production of type i interferon by Clec16a

Promotion of TLR-mediated production of type I interferon by...

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第八届全国免疫学学术大会

作者： Chuan Ouyang Jun Lou Linrong Lu institute of immunology Program in Molecular and Cellular Biology Zhejiang University School of Medicine

Clec16a is a C-type lectin and encodes a protein of unknown *** independent genomewide as-sociation studies(GWAS) have implicated the CLEC16 A gene in several autoimmune diseases, including multiple sclerosis and type 1 ***, how CLEC16 A SNPs confer susceptibility to autoimmune diseases remains *** we report that Clec16 a is considerably expressed in innate immune cells including dendritic cells(DCs), macrophages and microglias and it locates to endosome and *** also found that Clec16 a regulated the activation of type i interferon mediated by LPS or double-stranded RNA in DCs and *** of Clec16 a promoted T RiF-dependent type i interferon signaling pathway and knockdown of Clec16 a inhibited the secretion of type i interferon and the activation of TBK1 and i *** biochemical analysis revealed that Clec16 a interacted with TBK1-iKKi complex and overexpression of Clec16 A enhanced phosphroylation and K63-linked polyubiquitination of TBK1 suggesting a regulatory role of Clec16 A in this signaling *** study identified a previously unrecognized role for Clec16 a in the regulation of type i interferon production and provided molecular insight into the underling mechanisms for the involvement of Clec16 a in autoimmune diseases.

关键词： Clec16a TLR type i interferon TBK1

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Raf kinase inhibitor protein and TANK-binding kinase 1 form a positive feedback loop to promote type i interferon production in innate immune

Raf kinase inhibitor protein and TANK-binding kinase 1 form ...

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第十届全国免疫学学术大会

作者： Meidi Gu Zhiyong Liu Ming Shi Rongrong Lai Wenlong lin Chuan Ouyang Sheng Ye Xiaojian Wang 浙江大学医学院免疫研究所 Life Sciences institute and innovation Center for Cell Signaling Network Zhejiang University

TANK-binding kinase 1(TBK1)activation is a central event in type i interferon production in anti-virus innate ***,the regulatory mechanism underlying TBK1 activation remains *** we report that raf kinase inhibitory protein(RKiP)is essential for TBK1 activation and type i interferon production triggered by virus *** virus infection,RKiP is phosphorylated at serine 109(S109)by *** of RKiP enhances its interaction

关键词： TBK1 RKiP type i interferon antiviral immunity

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inactivation of type i interferon signaling promotes the establishment of immune privileged tumor microenvironment

Inactivation of type I interferon signaling promotes the est...

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第十四届全国免疫学学术大会

作者： Jun Gui Ren Ji Hospital School of Medicine Shanghai Jiao Tong University

Refractoriness of solid tumors to immunotherapies is attributed to the immunosuppressive tumor microenvironment(TME). type i interferons(iFNs) which elicit the signaling through binding to interferon receptors iFNAR1/iFNAR2 are vital to mediate anti-tumor effects by inhibiting tumor cell proliferation, promoting apoptosis and immune surveillance. Here our research demonstrated that TME stress-triggered iFNAR1 degradation mediated by ubiquitination on cytotoxic T lymphocytes(CTLs) is the key for the establishment of immune privileged niche of TME. Downregulation of iFNAR1 in tumor stroma predicted poor prognosis in human colorectal cancer patients. Genetic or pharmacologic stabilization of iFNAR1 improved CTLs survival and increased the efficacy of immunotherapies. Our study revealed that inactivation of type i interferon signaling in TME promotes tumor immune evasion. Reactivation of type i interferon signaling could be beneficial for anti-cancer therapies. Based on this, we further found that chemotherapy stimulated type i interferon signaling which enhances anti-tumor immunity through iFN-mediated crosstalk between tumor cells and CTLs. Our findings may provide valuable insights for optimal combination with chemotherapy and immunotherapy.

关键词： Tumor microenvironment immunosuppression cytotoxic T lymphocytes type i interferon

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