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USP3 deubiquitinates and stabilizes the adapter protein ASC to regulate inflammasome activation

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Cellular & Molecular Immunology 2022年第10期19卷 1141-1152页

作者： Wanxin Zhuang Lei Zhang Yi Zheng Bingyu Liu Chunhong Ma Wei Zhao Suxia Liu Feng Liu Chengjiang Gao key laboratory of infection and immunity of shandong province&key laboratory for Experimental Teratology of Ministry of Education Shandong UniversityJinanShandong250012PR China Department of Immunology School of Biomedical SciencesShandong UniversityJinanShandong250012PR China

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 *** activation of inflammasomes is subjected to tight regulation to maintain immune homeostasis,yet the underlying mechanism remains ***,we identify USP3 as a direct deubiquitinating enzyme(DUB)for ASC,the central adapter mediating the assembly and activation of most ***3 removes the K48-linked ubiquitination on ASC and strengthens its stability by blocking proteasomal ***,USP3 promotes inflammasome activation,and this function was confirmed in mouse models of aluminum(Alum)-induced peritonitis,*** infection and flagellin-induced pneumonia in *** 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.

关键词： ASC inflammasome K48-linked ubiquitination proteasomal degradation USP3

Regulation of cellular senescence by innate immunity

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Biophysics Reports 2023年第6期9卷 338-351页

作者： Jinxiu Hou Yi Zheng Chengjiang Gao key laboratory of infection and immunity Shandong Province & Key Laboratory for Experimental TeratologyMinistry of Education Shandong University Department of Immunology the School of Basic Medical Sciences Shandong University

During the COVID-19 pandemic, the interplay between the processes of immunity and senescence is drawing more and more intensive attention. SARS-Co V-2 infection induces senescence in lung cells,failure to clear infected cells and increased presence of inflammatory factors could lead to a cytokine storm and acute respiratory disease syndrome(ARDS), which together with aging and age-associated disease lead to 70% of COVID-19-related deaths. Studies on how senescence initiates upon viral infection and how to restrict excessive accumulation of senescent cells to avoid harmful inflammation are crucially important. Senescence can induce innate immune signaling, and innate immunity can engage cell senescence. Here, we mainly review the innate immune pathways, such as c GAS-STING, TLRs, NF-κB, and NLRP3 inflammasome, participating in the senescence process. In these pathways, IFN-I and inflammatory factors play key roles. At the end of the review, we propose the strategies by which we can improve the immune function and reduce inflammation based on these findings.

关键词： IFN-I NF-κB cGAS-STING TLRs NLRP3 inflammasome Cell senescence

Gut microbiota-derived metabolites as key mucosal barrier modulators in obesity

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World Journal of Gastroenterology 2021年第33期27卷 5555-5565页

作者： Yan-Xia Wei Kui-Yang Zheng Yu-Gang Wang laboratory of infection and immunity Jiangsu Key Laboratory of Immunity and MetabolismDepartment of Pathogenic Biology and ImmunologyXuzhou Medical UniversityXuzhou 221004Jiangsu ProvinceChina

A significant breakthrough in the field of obesity research was the demonstration that an obese phenotype could be manipulated by modulating the gut *** important next step is to elucidate a human-relevant"map"of microbiota-host interactions that regulate the metabolic health of the *** improved understanding of this crosstalk is a prerequisite for optimizing therapeutic strategies to combat *** mucosal barrier dysfunction is an important contributor to metabolic diseases and has also been found to be involved in a variety of other chronic inflammatory conditions,including cancer,neurodegeneration,and *** mechanistic basis for intestinal barrier dysfunction accompanying metabolic disorders remains poorly *** the molecular and cellular modulators of intestinal barrier function will help devise improved strategies to counteract the detrimental systemic consequences of gut barrier *** in the composition and function of the gut microbiota,i.e.,dysbiosis,are thought to drive obesity-related pathogenesis and may be one of the most important drivers of mucosal barrier *** effects of the microbiota on the host are mediated by microbiota-derived *** this review,we focus on several relatively well-studied microbial metabolites that can influence intestinal mucosal homeostasis and discuss how they might affect metabolic *** design and use of microbes and their metabolites that are locally active in the gut without systemic side effects are promising novel and safe therapeutic modalities for metabolic diseases.

关键词： Obesity Metabolic diseases Microbiota Mucosal homeostasis Gut Microbial metabolites

The hepatic macrophage pool in NASH

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Cellular & Molecular Immunology 2021年第8期18卷 2059-2060页

作者： Tixiao Wang Chunhong Ma key laboratory for Experimental Teratology of Ministry of Education Key Laboratory of Infection and Immunity of Shandong Provinceand Department of ImmunologySchool of Basic Medical SciencesCheeloo Medical College of Shandong UniversityJinanShandongChina Advanced Medical Research Institute Shandong UniversityJinanShandongChina

Nonalcoholic fatty liver disease(NAFLD)and its inflammatory subtype nonalcoholic steatohepatitis(NASH)are currently the most common chronic liver diseases worldwide and emerging risk factors for hepatocellular carcinoma.1 Numerous studies have demonstrated the critical involvement of hepatic macrophages,including resident Kupffer cells(KCs)and recruited monocyte-derived macrophages(MoMFs).

关键词： liver NAFLD NASH

Role of Tim-3 in hepatitis B virus infection:An overview

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World Journal of Gastroenterology 2016年第7期22卷 2294-2303页

作者： yuan liu li-fen gao xiao-hong liang chun-hong ma Department of Immunology Key Laboratory for ExperimentalTeratology of Ministry of EducationShandong Provincial Key Laboratory of Infection and ImmunologyShandong University School of MedicineJinan 250012Shandong provinceChina

Hepatitis B virus(HBV) infection has received increasing public attention. h BV is the prototypical member of hepadnaviruses, which naturally infect only humans and great apes and induce the acute and persistent chronic infection of hepatocytes. A large body of evidence has demonstrated that dysfunction of the host anti-viral immune response is responsible for persistent HBV replication, unresolved inflammation and disease progression. Many regulatory factors are involved in immune dysfunction. Among these, T cell immunoglobulin domain and mucin domain-3(Tim-3), one of the immune checkpoint proteins, has attracted increasing attention due to its critical role in regulating both adaptive and innate immune cells. In chronic HBV infection, Tim-3 expression is elevated in many types of immune cells, such as T helper cells, cytotoxic T lymphocytes, dendritic cells, macrophages and natural killer cells. Tim-3 over-expression is often accompanied by impaired function of the abovementioned immunocytes, and Tim-3 inhibition can at least partially rescue impaired immune function and thus promote viral clearance. A better understanding of the regulatory role of Tim-3 in host immunity during HBV infection will shed new light on the mechanisms of h BV-related liver disease and suggest new therapeutic methods for intervention.

关键词： Tim-3 Hepatitis B virus inflammation immunity liver disease

Role of programmed cell death 4 in diseases: a double-edged sword

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Cellular & Molecular Immunology 2017年第11期14卷 884-886页

作者： Yang Jiang Yufeng Jia Lining Zhang Hematology Department The Second Hospital of Shandong UniversityJinanChina Department of Immunology and key laboratory of infection and immunity of shandong province Shandong University School of Basic Medical Sciences44 Wenhua Xi RoadJinan 250012China

The molecule of programmed cell death 4(PDCD4)is named based on its upregulation during *** is now known that PDCD4 is highly conserved during evolution and widely expressed in the immune cells and non-immune cells of humans and other ***4,as an inhibitor of gene transcription and translation,is very important in maintaining the normal function of cells.1,2 PDCD4 protein contains an N-terminal domain and two MA-3 domains in the central and C-terminal *** MA-3 domains can competitively bind to the translation initiation factor eIF4A with eIF4G to inhibit eIF4A activity and to impact the translation of specific mRNAs containing structured 5′-untranslated regions(5′UTRs).

关键词： PDCD4 death diseases

First small-molecule PROTACs for G protein-coupled receptors:inducing α1A-adrenergic receptor degradation

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Acta Pharmaceutica Sinica B 2020年第9期10卷 1669-1679页

作者： Zhenzhen Li Yuxing Lin Hui Song Xiaojun Qin Zhongxia Yu Zheng Zhang Gaopan Dong Xiang Li Xiaodong Shi Lupei Du Wei Zhao Minyong Li Department of Medicinal Chemistry Key Laboratory of Chemical Biology(MOE)School of PharmacyShandong UniversityJinan 250012China Department of Immunology Key Laboratory of Infection and Immunity of Shandong ProvinceSchool of Basic Medical ScienceShandong UniversityJinan 250012China Department of Chemistry University of South FloridaTampaFL 33620USA State key laboratory of Microbial Technology Shandong UniversityJinan 250100China

Proteolysis targeting chimeras(PROTACs)are dual-functional hybrid molecules that can selectively recruit an E3 ubiquitin ligase to a target protein to direct the protein into the ubiquitinproteasome system(UPS),thereby selectively reducing the target protein level by the ubiquitinproteasome ***,small-molecule PROTACs are gaining popularity as tools to desrade pathogenic ***,we present the first small-molecule PROTACs that can induce the alA-adrenergic receptor(α1 A-AR)degradation,which is also the first small-molecule PROTACs for G proteincoupled receptors(GPCRs)to our *** degradation inducers were developed through conjugation of knownα1-adrenergic receptors(α1-ARs)inhibitor prazosin and cereblon(CRBN)ligand pomalidomide through the different *** representative compound 9 c is proved to inhibit the proliferation of PC-3 cells and result in tumor growth regression,which highlighted the potential of our study as a new therapeutic strategy for prostate cancer.

关键词： Small-molecule PROTACs α1A-Adrenergic receptor Ubiquitylation Degradation Prostate cancer

Monocyte-derived KCs(MoKCs)contribute to the KC pool in NASH

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Cellular & Molecular Immunology 2021年第3期18卷 518-519页

作者： Yingchun Wang Lifen Gao key laboratory for Experimental Teratology of Ministry of Education Shandong Key Laboratory of Infection and Immunityand Department of ImmunologySchool of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong 250012P.R.China

Nonalcoholic fatty liver disease(NAFLD)is now recognized as the most common liver disease worldwide and has increasingly become a serious hazard to human *** consists of a spectrum of disease states ranging from simple steatosis to more severe disease termed nonalcoholic steatohepatitis(NASH),fibrosis,cirrhosis,and even hepatocellular carcinoma.

关键词： NAFLD liver NASH

Targeting Haemaphysalis longicornis serpin to prevent tick feeding and pathogen transmission

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Insect Science 2024年第3期31卷 694-706页

作者： Tingting Feng Hao Tong Qianqian Zhang Zhihao Ming Zhenyu Song Xia Zhou Jianfeng Dai Institute of Biology and Medical Sciences Jiangsu Key Laboratory of Infection and ImmunitySoochow UniversitySuzhouJiangsu ProvinceChina School of Biology and Basic Medical Science Suzhou Medical College of Soochow UniversitySuzhouJiangsu ProvinceChina

Serine proteinase inhibitors(serpins),identified from the hard tick Haemaphysalis longicornis of China,play significant roles in various animal physiological *** this study,we showed that *** serpins(Hlserpin-a and Hlserpin-b)were induced during blood-feeding in nymph ticks and exhibited anticoagulation activity in *** Hlserpins through RNA interference(RNAi)significantly impaired tick *** of mice with recombinant Hlserpins or passive transfer of Hlserpin antiserum significantly curtails the efficacy of tick ***,the transmission of the Langat virus(LGTV)from ticks to mice witnessed a substantial decrease when Hlserpins were *** findings suggest that inhibiting Hlserpins can hamper tick engorgement and pathogen transmission,indicating the potential of Hlserpins as a vaccine to countertick-borne diseases.

关键词： feeding LGTV serpin TBEV tick