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Acta Pharmaceutica Sinica B 2023年第12期13卷 4733-4747页

作者： Mingjin Wang Weida Wang Shen You Zhenyan Hou Ming Ji Nina Xue Tingting Du Xiaoguang Chen Jing Jin Department of Pharmacology State Key Laboratory of Bioactive Substances and Functions of Natural MedicinesInstitute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100050China

Glioblastoma(GBM)is a highly aggressive and lethal brain tumor with an immunosuppressive tumor microenvironment(TME).In this environment,myeloid cells,such as myeloid-derived suppressor cells(MDSCs),play a pivotal role in suppressing antitumor *** is closely related to the function of myeloid ***,our study reports that acetyl-CoA acetyltransferase 1(ACAT1),the key enzyme of fatty acid oxidation(FAO)and ketogenesis,is significantly downregulated in the MDSCs infiltrated in GBM *** investigate the effects of ACAT1 on myeloid cells,we generated mice with myeloid-specific(LyzM-cre)depletion of *** results show that these mice exhibited a remarkable accumulation of MDSCs and increased tumor progression both ectopically and *** mechanism behind this effect is elevated secretion of C-X-C motif ligand 1(CXCLI)of macrophages(Mo).Overall,our findings demonstrate that ACAT1 could serve as a promising drug target for GBM by regulating the function of MDSCs in the TME.

关键词： Glioblastoma myeloid cells myeloid-derived suppressor cells Acetyl-CoA acetyltransferase 1 CXCL1 Tumor microenvironment Lipid metabolism Macrophages

Pik3c3 deficiency in myeloid cells imparts partial resistance to experimental autoimmune encephalomyelitis associated with reduced IL-1βproduction

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Cellular & Molecular Immunology 2021年第8期18卷 2024-2039页

作者： Guan Yang Wenqiang Song Jielin Xu JLuke Postoak Feixiong Cheng Jennifer Martinez Jianhua Zhang Lan Wu Luc Van Kaer Department of Pathology Microbiology and ImmunologyVanderbilt University School of MedicineNashvilleTN37232USA Genomic Medicine Institute Lerner Research InstituteCleveland ClinicClevelandOH44195USA Department of Molecular Medicine Cleveland Clinic Lerner College of MedicineCase Western Reserve UniversityClevelandOH44195USA Case Comprehensive Cancer Center Case Western Reserve University School of MedicineClevelandOH44106USA Immunity Inflammationand Disease LaboratoryNational Institute of Environmental Health SciencesResearch Triangle ParkDurhamNC27709USA Department of Pathology University of Alabama at BirminghamBirminghamAL35294USA Birmingham Veterans Affairs Medical Center BirminghamAL35233USA

The PIK3C3/VPS34 subunit of the class III phosphatidylinositol 3-kinase(PtdIns3K)complex plays a role in both canonical and noncanonical autophagy,key processes that control immune-cell responsiveness to a variety of *** previous studies found that PIK3C3 is a critical regulator that controls the development,homeostasis,and function of dendritic and T *** this study,we investigated the role of PIK3C3 in myeloid cell biology using myeloid cell-specific Pik3c3-deficient *** found that Pik3c3-deficient macrophages express increased surface levels of major histocompatibility complex(MHC)class I and class II *** addition,myeloid cell-specific Pik3c3 ablation in mice caused a partial impairment in the homeostatic maintenance of macrophages expressing the apoptotic cell uptake receptor ***3c3 deficiency caused phenotypic changes in myeloid cells that were dependent on the early machinery(initiation/nucleation)of the classical autophagy ***,myeloid cell-specific Pik3c3-deficient animals showed significantly reduced severity of experimental autoimmune encephalomyelitis(EAE),a primarily CD4^(^(+))T-cell-mediated mouse model of multiple sclerosis(MS).This disease protection was associated with reduced accumulation of myelin-specific CD4^(^(+))T cells in the central nervous system and decreased myeloid cell IL-1β***,administration of SAR405,a selective PIK3C3 inhibitor,delayed disease ***,our studies establish PIK3C3 as an important regulator of macrophage functions and myeloid cell-mediated regulation of *** findings also have important implications for the development of small-molecule inhibitors of PIK3C3 as therapeutic modulators of MS and other autoimmune diseases.

关键词： PIK3C3 Autophagy myeloid cells Experimental autoimmune encephalomyelitis IL-1β

Degradation-resistant implanted biomaterials establish an immunosuppressive microenvironment that induces T cell exhaustion by recruiting myeloid cells

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Fundamental Research 2022年第4期2卷 648-658页

作者： Qin Fan Huaxing Dai Jinyu Bai Jialu Xu Qingle Ma Ziying Fei Xiaozhong Zhou Kam W.Leong Chao Wang Institute of Functional Nano&Soft Materials Jjangsu Key Laboratory for Carbon-based Functional Materials and evices Soochow UniversitySuzhou 215123China Department of Orthopedics The Second Affliated Hospital of Soochow UniversitySuzhou 215004China Department f Biomedical Enginering Columbia UniversityNew YorkNY 10027USA

Implanted biomaterials have transformed healthcare and the treatment of injury and disease,but their infuence on the local immune landscape remains *** we discovered that degradation-resistant titanium-based implants establish an immunosuppressive microenvironment by recruiting myeloid cells,including monocytes,macrophages,neutrophils,and myeloid-lineage dendritic *** normal tissues,the tissues nearby implants exhibit an chronic inflamed and immunosuppressive status characterised by myeloid-rich,T cell-exhaustion gene signature by single-cell RNA *** C treatment provides an effective strategy to rescue the immunosuppressive microenvironment,which can be used as a regular supplement to reduce the risk of malignant cell survival around the implants.

关键词： TiO_(2)nanoparicles Immune microenvironment myeloid cells mplants Immunosuppressive

Role of myeloid cells in the tumor microenvironment

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Journal of Cancer Metastasis and Treatment 2022年第1期8卷 317-333页

作者： Arpita Balakrishnan Mohini Vig Shweta Dubey Amity Institute of Virology and Immunology Amity University Uttar Pradesh(AUUP)Noida 201303India

The dynamic interplay between tumor cells and immune cells in the microenvironment plays a crucial role in determining disease severity and therapeutic outcome in *** cells are the most abundantly available cell population in the tumor *** cells have been shown to exist in diverse phenotypes and play both antitumoral and protumoral roles in *** the biology of myeloid cells can lay the foundation for the development of therapeutic strategies aimed at enhancing the antitumoral role of myeloid *** article presents an overview of the role of myeloid cells in tumor development and various mechanisms by which myeloid cells aid tumor *** drugs against cancer that utilize myeloid cells and the role of myeloid cells in drug resistance are also discussed.

关键词： myeloid cells tumor cancer tumor microenvironment tumor-associated macrophages dendritic cells tumor-associated neutrophils myeloid-derived suppressor cells

Conditional Knockout of Src Homology 2 Domain-containing Protein Tyrosine Phosphatase-2 in myeloid cells Attenuates Renal Fibrosis after Unilateral Ureter Obstruction

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Chinese Medical Journal 2015年第9期128卷 1196-1201页

作者： Jing-Fei Teng Kai Wang Yao Li Fa-Jun Qu Qing Yuan Xin-Gang Cui Quan-Xing Wang Dan-Feng Xu Department of Urology Shanghai Changzheng Hospital Second Military Medical University Shanghai 200003 China Department of Urology General Hospital of Beijing Military Command Beijing 100700 China Department of Urology 309 Hospital of Chinese People's Liberation Army Beijing 100091 China National Key Laboratory of Medical Immunology and Institute of Immunology Second Military Medical University Shanghai 200433 China

Background：Src homology 2 domain-containing protein tyrosine phosphatase-2 （SHP-2） is a kind of intracellular protein tyrosine *** have revealed its roles in various disease,however,whether SHP-2 involves in renal fibrosis remains *** aim of this study was to explore the roles of myeloid cells SHP-2 in renal interstitial ***：myeloid cells SHP-2 gene was conditionally knocked-out （CKO） in mice using loxP-Cre system,and renal interstitial fibrosis was induced by unilateral ureter obstruction （UUO）.The total collagen deposition in the renal interstitium was assessed using picrosirius red stain.F4/80 immunostaing was used to evaluate macrophage infiltration in renal tubular *** real-time polymerase chain reaction and enzyme linked immunosorbent assay were used to analyze the production of cytokines in the ***-mediated dUTP nick-end labeling stain was used to assess the apoptotic renal tubular epithelial ***：Src homology 2 domain-containing protein tyrosine phosphatase-2 gene CKO in myeloid cells significantly reduced collagen deposition in the renal interstitium after *** infiltration was evidently decreased in renal tubular interstitium of SHP-2 CKO ***,the production of pro-inflammatory cytokines was significantly suppressed in SHP-2 CKO ***,no significant difference was observed in the number of apoptotic renal tubular epithelial cells between wild-type and SHP-2 CKO ***：Our observations suggested that SHP-2 in myeloid cells plays a pivotal role in the pathogenesis of renal fibrosis,and that silencing of SHP-2 gene in myeloid cells may protect renal from inflammatory damage and prevent renal fibrosis after renal injury.

关键词： Fibrosis Inflammation myeloid cells Obstructive Nephropathy Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase-2

Comprehensive Understanding of Immune cells in The Pathogenesis of Non-alcoholic Fatty Liver Disease

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生物化学与生物物理进展 2024年第9期51卷 2082-2100页

作者： OUYANG Fei-Fan RASHEED Madiha LI Bo DENG Yu-Lin Advanced Research Institute of Multidisciplinary Science Beijing Institute of TechnologyZhuhai 519088China Beijing Key Laboratory for Separation and Analysis in Biomedicine and Pharmaceuticals School of Life ScienceBeijing Institute of TechnologyBeijing 100081China Advanced Research Institute of Multidisciplinary Science Beijing Institute of TechnologyBeijing 100081China

Non-alcoholic fatty liver disease(NAFLD)is the most common chronic liver disease,defined by several phases,ranging from benign fat accumulation to non-alcoholic steatohepatitis(NASH),which can lead to liver cancer and *** NAFLD is a disease of disordered metabolism,it also involves several immune cell-mediated inflammatory processes,either promoting and/or suppressing hepatocyte inflammation through the secretion of pro-inflammatory and/or anti-inflammatory factors to influence the NAFLD ***,the underlying disease mechanism and the role of immune cells in NAFLD are still under investigation,leaving many open-ended *** this review,we presented the recent concepts about the interplay of immune cells in the onset and pathogenesis of *** also highlighted the specific non-immune cells exhibiting immunological properties of therapeutic significance in *** hope that this review will help guide the development of future NAFLD therapeutics.

关键词： non-alcoholic fatty liver disease metabolically associated fatty liver disease(MAFLD) T cells myeloid cells mesenchymal stem cells

Meningeal lymphatic vessel crosstalk with central nervous system immune cells in aging and neurodegenerative diseases

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Neural Regeneration Research 2025年第3期20卷 763-778页

作者： Minghuang Gao Xinyue Wang Shijie Su Weicheng Feng Yaona Lai Kongli Huang Dandan Cao Qi Wang Science and Technology Innovation Center Guangzhou University of Chinese MedicineGuangzhouGuangdong ProvinceChina Institute of Clinical Pharmacology Guangzhou University of Chinese MedicineGuangzhouGuangdong ProvinceChina The Sixth Affiliated Hospital Sun Yat-sen UniversityGuangzhouGuangdong ProvinceChina

Meningeal lymphatic vessels form a relationship between the nervous system and periphery, which is relevant in both health and disease. Meningeal lymphatic vessels not only play a key role in the drainage of brain metabolites but also contribute to antigen delivery and immune cell activation. The advent of novel genomic technologies has enabled rapid progress in the characterization of myeloid and lymphoid cells and their interactions with meningeal lymphatic vessels within the central nervous system. In this review, we provide an overview of the multifaceted roles of meningeal lymphatic vessels within the context of the central nervous system immune network, highlighting recent discoveries on the immunological niche provided by meningeal lymphatic vessels. Furthermore, we delve into the mechanisms of crosstalk between meningeal lymphatic vessels and immune cells in the central nervous system under both homeostatic conditions and neurodegenerative diseases, discussing how these interactions shape the pathological outcomes. Regulation of meningeal lymphatic vessel function and structure can influence lymphatic drainage, cerebrospinal fluid-borne immune modulators, and immune cell populations in aging and neurodegenerative disorders, thereby playing a key role in shaping meningeal and brain parenchyma immunity.

关键词： central nervous system meningeal lymphatic vessels immunity myeloid cells lymphatic cells neurodegenerative disease

Cellular crosstalk of regulatory T cells in pancreatic ductal adenocarcinoma

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胰腺病学杂志(英文) 2024年第2期07卷 131-140页

作者： Shi Xuqing Liu Hangqi Liang Zhiyong Department of Pathology State Key Laboratory of Complex Severe and Rare Disease Molecular Pathology Research Center Peking Union Medical College Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid tumors and is characterized by dense desmoplasia and immune desert. Regulatory T cells (Tregs) are critical components of the immune tumor microenvironment (TIME) of PDAC. Treg-induced immune evasion presents a significant hurdle in enhancing the efficacy of conventional and emerging therapeutic strategies. Nonetheless, Treg deficiency alone led to inconsistent outcomes. To unveil the underlying potential reasons for these results and to determine the role of Tregs in other therapeutic strategies, in-depth insights into the crosstalk between Tregs and other cells in PDAC are indispensable and currently lacking. Therefore, in this review, we comprehensively delineate the direct and indirect interplay between Tregs and various cellular constituents ranging from cancer cells and immune cells to stromal cells in PDAC in an attempt to uncover potential leads for the development of Treg-associated therapies.

关键词： Cancer-associated fibroblasts Cellular crosstalk myeloid cells Pancreatic ductal adenocarcinoma Regulatory T cells

myeloid STAT3 promotes hepatocarcinogenesis by inactivating natural killer T cells

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Myeloid STAT3 promotes hepatocarcinogenesis by inactivating ...

Kupffer cell restoration after partial hepatectomy is mainly driven by local cell proliferation in IL-6-dependent autocrine and paracrine manners

第十一届全国免疫学学术大会

作者： wang hua Yin Shi Li Jun Gao Bin Department of Oncology The First Affiliated Hospital of Anhui Medical University NIAAA National Institutes of Health Department of Geriatrics Affiliated Provincial Hospital of Anhui Medical University Institute for Liver Diseases Anhui Medical University

Background/objectives:Activation of signal transducer and activator of transcription 3(STAT3)occurs virtually in most liver diseases,but how STAT3 links liver inflammation and cancer remains *** and results:Using cell-specific STAT3 deletions mouse strains,we have investigated the interplay of myeloid and hepatic STAT3 in controlling hepatocarcinogenesis induced by diethylinitrosamine(DEN).We show that

关键词： myeloid cells STAT3 hepatocarcinogenesis natural killer T cells

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Cellular & Molecular Immunology 2021年第9期18卷 2165-2176页

作者： Yeni Ait Ahmed Yaojie Fu Robim M.Rodrigues Yong He Yukun Guan Adrien Guillot Ruixue Ren Dechun Feng Juan Hidalgo Cynthia Ju Fouad Lafdil Bin Gao Laboratory of Liver Diseases National Institute on Alcohol Abuse and AlcoholismNational Institutes of HealthBethesdaMDUSA UniversitéParis-Est-Créteil CréteilFrance Universitat Autònoma de Barcelona BarcelonaSpain Department of Anesthesiology McGovern Medical SchoolUniversity of Texas Health Science Center at HoustonHoustonTXUSA INSERM U955 Institut Mondor de Recherche BiomédicaleCréteilFrance Institut Universitaire de France(IUF) ParisFrance

Kupffer cells(KCs),which are liver-resident macrophages,originate from the fetal yolk sac and represent one of the largest macrophage populations in the ***,the current data on the origin of the cells that restore macrophages during liver injury and regeneration remain ***,we address the question of whether liver macrophage restoration results from circulating monocyte infiltration or local KC proliferation in regenerating livers after partial hepatectomy(PHx)and uncover the underlying *** using several strains of genetically modified mice and performing immunohistochemical analyses,we demonstrated that local KC proliferation mainly contributed to the restoration of liver macrophages after *** KC proliferation was impaired in Il6-knockout(KO)mice and restored after the administration of IL-6 protein,whereas KC proliferation was not affected in Il4-KO or Csf2-KO *** source of IL-6 was identified using hepatocyte-and myeloid-specific Il6-KO mice and the results revealed that both hepatocytes and myeloid cells contribute to IL-6 production after ***,peak KC proliferation was also impaired in myeloid-specific Il6 receptor-KO mice after PHx,suggesting that IL-6 signaling directly promotes KC *** using several inhibitors to block the IL-6 signaling pathway revealed that sirtuin 1(SIRT1)contributed to IL-6-mediated KC proliferation in *** deletion of the Sirt1 gene in myeloid cells,including KCs,impaired KC proliferation after *** conclusion,our data suggest that KC repopulation after PHx is mainly driven by local KC proliferation,which is dependent on IL-6 and SIRT1 activation in KCs.

关键词： IL-6 Sirtuin 1 Liver regeneration Kupffer cells myeloid cells