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HSP70L1-mediated intracellular priming of dendritic cell vaccination induces more potent CTL response against cancer

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Cellular & molecular immunology 2018年第2期15卷 135-145页

作者： Shuxun Liu Lin Yi Ma Ling Jinxia Jiang Lijun Song Juan Liu Xuetao Cao national key laboratory of Medical immunology Institute of ImmunologySecond Military Medical UniversityShanghai200433China department of immunology National Key Laboratory of Medical Molecular BiologyChinese Academy of Medical SciencesBeijing100730China

Heat-shock protein(HSP)-based immunotherapy is established on its adjuvant effects when applied via an extracellular approach to pulse and activate dendritic cells(DCs).Our previous studies indicate that DCs pulsed with recombinant fusion proteins of antigenic fragment and HSP70-like protein 1(HSP70L1)are potent in stimulating antigen-specific Th1 responses.We herein evaluated the cytotoxic T cell(CTL)response by an intracellular approach of priming DCs with transfection of recombinant adenovirus-expressing the fusion gene of the 576–699 fragment of carcinoembryonic antigen(CEA)and HSP70L1.As compared with DCs pulsed with extracellular fusion protein,the DCs transfected with recombinant adenovirus expressing the fusion gene displayed equivalent mature phenotypes but less inflammatory appearance.However,the transfected DCs were superior to the pulsed DCs in inducing CEA-specific CTLs.Consistently,immunization of HLA-A2.1/H-2Kb transgene mice with the transfected DCs could induce more quantities of HLA-A2.1-restricted CEA-specific CTLs,protecting nude mice more significantly from human CEA-expressing colon tumor challenge when adoptively transferred.Mechanistic investigation indicated that intracellular expression of the fusion protein empowered the transfected DCs by activation of STAT1 possibly via inducing IFN-βand ERK pathways.Therefore,the more potent ability to induce anti-CEA CTL responses enables the DCs,which transfected with recombinant adenovirus expressing the fusion gene of antigenic CEA fragment and Th1 adjuvant,as an alternative promising approach for the immunotherapy of CEA-positive tumors.

关键词： CTL dendritic cell HSP70L1 immunotherapy

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Inflammation-induced CD69^+ Kupffer cell feedback inhibits T cell proliferation via membrane-bound TGF-β1

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Science China(Life Sciences) 2016年第12期59卷 1259-1269页

作者： Xiang Zhang Zhengping Jiang Yan Gu Yanfang Liu Xuetao Cao Yanmei Han national key laboratory of Medical immunology & Institute of immunology Second Military Medical University national key laboratory of Medical molecular biology & department of immunology Institute of Basic Medical SciencesChinese Academy of Medical Sciences

Kupffer cells,tissue-resident macrophage lineage cell,are enriched in vertebrate liver.The mouse F4/80^+ Kupffer cells have been subclassified into two subpopulations according to their phenotype and function:CD68^+ subpopulation with potent reactive oxygen species(ROS) production and phagocytic capacities,and CD11b^+ subpopulation with a potent capacity to produce T helper 1 cytokines.In addition,CD11b^+ Kupffer cells/macrophages may be migrated from the bone marrow or spleen,especially in inflammatory conditions of the liver.For analyzing diverse Kupffer cell subsets,we infected mice with Listeria monocytogenes and analyzed the phenotype variations of hepatic Kupffer cells.During L.monocytogenes infection,hepatic CD69^+ Kupffer cells were significantly induced and expanded,and CD69^+ Kupffer cells expressed higher level of CD11 b,and particularly high level of membrane-bound TGF-β1(mTGF-β1) but lower level of F4/80.We also found that clodronate liposome administration did not eliminate hepatic CD69^+ Kupffer cell subset.We consider the hepatic CD69^+ Kupffer cell population corresponds to CD11b^+Kupffer cells,the bone marrow-derived population.Hepatic CD69^+ Kupffer cells suppressed Ag-nonspecific and OVA-specific CD4 T cell proliferation through mTGF-β1 both in vitro and in vivo,meanwhile,they did not interfere with activation of CD4 T cells.Thus,we have identified a new subset of inflammation-induced CD69^+ Kupffer cells which can feedback inhibit CD4 T cell response via cell surface TGF-β1 at the late stage of immune response against infection.CD69^+ Kupffer cells may contribute to protect host from pathological injure by preventing overactivation of immune response.

关键词： Kupffer 房间有免疫力的规定 CD69 TGF-1 Listeria monocytogenes

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Highlights of the advances in basic immunology in 2011

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Cellular & molecular immunology 2012年第3期9卷 197-207页

作者： Juan Liu Shuxun Liu Xuetao Cao national key laboratory of Medical immunology and Institute of immunology Second Military Medical UniversityShanghaiChina national key laboratory of Medical molecular biology and department of immunology Chinese Academy of Medical SciencesBeijingChina

In this review, we summarize the major fundamental advances in immunological research reported in 2011. The highlights focus on the improved understanding of key questions in basic immunology, including the initiation and activation of innate responses as well as mechanisms for the development and function of various T-cell subsets. The research includes the identification of novel cytosolic RNA and DNA sensors as well as the identification of the novel regulators of the Toll-like receptor （TLR） and retinoic acid-inducible gene I （RIG-I）-Iike receptor （RLR） signaling pathway. Moreover, remarkable advances have been made in the developmental and functional properties of innate lymphoid cells （I LCs）. Helper T cells and regulatory T （Treg） cells play indispensable roles in orchestrating adaptive immunity. There have been exciting discoveries regarding the regulatory mechanisms of the development of distinct T-cell subsets, particularly Th17 cells and Treg cells. The emerging roles of microRNAs （miRNAs） in T cell immunity are discussed, as is the recent identification of a novel T-cell subset referred to as follicular regulatory T （TFR） cells.

关键词： ILC innate immunity Th17 cells TFR cells TLR

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Advances in innate immune signaling:new activators and regulators

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national Science Review 2016年第2期3卷 160-162页

作者： Juan Liu Xuetao Cao national key laboratory of Medical immunology & Institute of immunology Second Military Medical University national key laboratory of Medical molecular biology & department of immunology Institute of Basic Medical SciencesChinese Academy of Medical Sciences

The innate immune system can detect the invading microbe components via three major pattern recognition receptorsToll-like receptors,RIG-I-like receptors and NOD-like receptors as well as a variety of cytoplasmic DNA or RNA sensors.These innate receptors induce a series of intracellular downstream signaling pathways,leading to the efficient innate immune responses to eliminate pathogens(Fig.1).Meanwhile,

关键词： Advances in innate immune signaling IKK DNA TLR

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Long noncoding RNAs in innate immunity

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Cellular & molecular immunology 2016年第2期13卷 138-147页

作者： Yuan Zhang Xuetao Cao national key laboratory of Medical molecular biology & department of immunology Institute of Basic Medical Sciences Chinese Academy of MedicalSciences Beijing 100005 China

Long noncoding RNAs （IncRNAs） have been shown to play important roles in immune cell development and immune responses through different mechanisms, such as dosage compensation, imprinting, enhancer function, and transcriptional regulation. Although the functions of most IncRNAs are unclear, some IncRNAs have been found to control transcriptional or post-transcriptional regulation of the innate and adaptive immune responses via new methods of protein-protein interactions or pairing with DNA and RNA. Interestingly, increasing evidence has elucidated the importance of IncRNAs in the interaction between hosts and pathogens. In this review, an overview of the IncRNAs modes of action, as well as the important and diversified roles of IncRNAs in immunity, are provided, and an emerging paradigm of IncRNAs in regulating innate immune responses is highlighted.

关键词： host-pathogen interaction innate immunity long noncoding RNA

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cGAS-STING pathway in senescence-related inflammation

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national Science Review 2018年第3期5卷 308-310页

作者： Kun Chen Juan Liu Xuetao Cao national key laboratory of Medical molecular biology Department of Immunology & Center for Immunotherapy Institute of Basic Medical Sciences Peking Union Medical College Chinese Academy of Medical Sciences national key laboratory of Medical immunology & Institute of immunology Second Military Medical University

Cellular senescence marked with persistent cell cycle arrest plays critical roles in orchestrating tissue remodeling and immune surveillance in response to multiple developmental and physiological stimuli.However,chronic or persistent cellular senescence can promote aberrant inflammatory responses,therefore is linked with variable pathogeneses such as fibrosis,cancer,autoimmune diseases,

关键词： GAS cGAS-STING pathway in senescence-related inflammation

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Fine-tuning MAVS- and STING-mediated antiviral innate immunity

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national Science Review 2015年第3期2卷 262-264页

作者： Xingguang Liu Xuetao Cao national key laboratory of Medical immunology& Institute of immunology Second Military Medical University national key laboratory of Medical molecular biology & department of immunology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences

The pathogen-associated molecules or nucleic acids derived from the invading pathogens can initiate the production of type I interferons(IFNs)and IFN-inducible genes,resulting in the establishment of an efective antimicrobial environment.In case of viral infection,nucleic acids from viruses are detected by patern recognition receptors mainly including several endosomal members of

关键词： Fine-tuning MAVS and STING-mediated antiviral innate immunity IFN

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HBXIP blocks myosin-ⅡA assembly by phosphorylating and interacting with NMHC-ⅡA in breast cancer metastasis

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Acta Pharmaceutica Sinica B 2023年第3期13卷 1053-1070页

作者： Lu Zhang Xiaolei Zhou Bowen Liu Xuhe Shi Xianmeng Li Feifei Xu Xueli Fu Xue Wang Kai Ye Tianzhi Jin Huimin Sun Qianqian Li Weiying Zhang Lihong Ye State key laboratory of Medicinal Chemical biology Tianjin Key Laboratory of Protein SciencesDepartment of Biochemistry and Molecular BiologyCollege of Life SciencesNankai UniversityTianjin 300071China College of Food Science&biology Hebei University of Science and TechnologyShijiazhuang 050091China Henan key laboratory of immunology and Targeted Drugs School of Laboratory MedicineXinxiang Medical UniversityXinxiang 453003China

Tumor metastasis depends on the dynamic balance of the actomyosin cytoskeleton.As a key component of actomyosin filaments,non-muscle myosin-ⅡA disassembly contributes to tumor cell spreading and migration.However,its regulatory mechanism in tumor migration and invasion is poorly understood.Here,we found that oncoprotein hepatitis B X-interacting protein(HBXIP) blocked the myosin-ⅡA assemble state promoting breast cancer cell migration.Mechanistically,mass spectrometry analysis,co-immunoprecipitation assay and GST-pull down assay proved that HBXIP directly interacted with the assembly-competent domain(ACD) of non-muscle heavy chain myosin-ⅡA(NMHC-ⅡA).The interaction was enhanced by NMHC-ⅡA S1916 phosphorylation via HBXIP-recruited protein kinase PKCβⅡ.Moreover,HBXIP induced the transcription of PRKCB,encoding PKCβⅡ,by coactivating Sp1,and triggered PKCβⅡ kinase activity.Interestingly,RNA sequencing and mouse metastasis model indicated that the anti-hyperlipidemic drug bezafibrate(BZF) suppressed breast cancer metastasis via inhibiting PKCβⅡ-mediated NMHC-ⅡA phosphorylation in vitro and in vivo.We reveal a novel mechanism by which HBXIP promotes myosin-ⅡA disassembly via interacting and phosphorylating NMHC-ⅡA,and BZF can serve as an effective anti-metastatic drug in breast cancer.

关键词： Breast cancer metastasis Actomyosin cytoskeleton HBXIP Myosin-IIA NMHC-IIA Phosphorylation PKCβII Bezafibrate

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Microbial Dark Matter: from Discovery to Applications

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Genomics, Proteomics & Bioinformatics 2022年第5期20卷 867-881页

作者： Yuguo Zha Hui Chong Pengshuo Yang Kang Ning MOE key laboratory of molecular Biophysics Hubei Key Laboratory of Bioinformatics and Molecular-imagingCenter of Artificial Intelligence BiologyDepartment of Bioinformatics and Systems BiologyCollege of Life Science and TechnologyHuazhong University of Science and TechnologyWuhan 430074China

With the rapid increase of the microbiome samples and sequencing data,more and more knowledge about microbial communities has been gained.However,there is still much more to learn about microbial communities,including billions of novel species and genes,as well as countless spatiotemporal dynamic patterns within the microbial communities,which together form the microbial dark matter.In this work,we summarized the dark matter in microbiome research and reviewed current data mining methods,especially artificial intelligence(AI)methods,for different types of knowledge discovery from microbial dark matter.We also provided case studies on using AI methods for microbiome data mining and knowledge discovery.In summary,we view microbial dark matter not as a problem to be solved but as an opportunity for AI methods to explore,with the goal of advancing our understanding of microbial communities,as well as developing better solutions to global concerns about human health and the environment.

关键词： Microbiome Dark matter Artificial intelligence Knowledge discovery Application

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Mycobacterium tuberculosis favors its survival by utilizing host ubiquitin to impair innate immunity

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national Science Review 2015年第3期2卷 260-261页

作者： Zhubo Chen national key laboratory of Medical molecular biology and department of immunology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences

The host innate immune system can eliminate invading pathogens by activating innate signaling pathways upon recognition of pathogenic components;meanwhile,the pathogens have developed strategies to evade innate response and be able to survive in host cells.Feedback inhibition of the host innate immune system is one of well-known strategies

关键词： Mycobacterium tuberculosis favors its survival by utilizing host ubiquitin to impair innate immunity

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