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Roles and Molecular Mechanisms of Biomarkers in Hepatocellular Carcinoma with Microvascular Invasion: A Review

Journal of Clinical and Translational Hepatology 2023年第5期11卷 1170-1183页

作者： Xudong Zhao Yudan Wang Haoming Xia Shuqiang Liu Ziyue Huang Risheng He Liang Yu Nanfeng Meng Hang Wang Junqi You Jinglin Li Judy Wai Ping Yam Yi Xu Yunfu Cui department of Hepatopancreatobiliary Surgery Second Affiliated Hospital of Harbin Medical UniversityHarbinHeilongjiangChina department of Pathology School of Clinical MedicineLi Ka Shing Faculty of MedicineThe University of Hong KongHong KongChina key laboratory of Basic Pharmacology of Ministry of education Zunyi Medical UniversityZunyiGuizhouChina key laboratory of Functional and Clinical Translational Medicine Fujian Province UniversityXiamen Medical CollegeXiamenFujianChina Jiangsu Province Engineering Research Center of tumor Targeted nano Diagnostic and Therapeutic Materials Yancheng Teachers UniversityYanchengJiangsuChina key laboratory of Biomarkers and In Vitro Diagnosis Translation of Zhejiang province HangzhouZhejiangChina key laboratory of Gastrointestinal Cancer(Fujian Medical University) Ministry of EducationSchool of Basic Medical SciencesFujian Medical UniversityFuzhouFujianChina State key laboratory of Chemical Oncogenomics Key Laboratory of Chemical GenomicsPeking University Shenzhen Graduate SchoolShenzhenGuangdongChina key laboratory of Intelligent Pharmacy and Individualized Therapy of Huzhou Department of PharmacyChangxing People’s HospitalChangxingZhejiangChina

Hepatocellular carcinoma(HCC)being a leading cause of cancer-related death,has high associated mortality and recurrence *** has been of great necessity and urgency to find effective HCC diagnosis and treatment *** have shown that microvascular invasion(MVI)is an independent risk factor for poor prognosis after *** abnormal expression of biomacromolecules such as circ-RNAs,lncRNAs,STIP1,and PD-L1 in HCC patients is strongly correlated with *** of several markers mentioned in this review affects the proliferation,invasion,metastasis,EMT,and anti-apoptotic processes of HCC cells through multiple complex ***,these biomarkers may have an important clinical role and serve as promising interventional targets for *** this review,we provide a comprehensive overview on the functions and regulatory mechanisms of MVI-related biomarkers in HCC.

关键词： Hepatocellular carcinoma Microvascular invasion Biomarkers Progress Molecular mechanism

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A comprehensive profile of TCF1^(+)progenitor and TCF1−terminally exhausted PD-1^(+)CD8^(+)T cells in head and neck squamous cell carcinoma:implications for prognosis and immunotherapy

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International Journal of Oral Science 2022年第1期14卷 91-99页

作者： Dikan Wang Juan Fang Shuqiong Wen Qunxing Li Jinming Wang Lisa Yang Wenxiao Dai Huanzi Lu Junyi Guo Zhongyan Shan Wenqiang Xie Xiangqi Liu Liling Wen Jie Shen Anxun Wang Qianming Chen Zhi Wang Hospital of Stomatology Guanghua School of StomatologyGuangdong Provincial Key Laboratory of StomatologySun Yat-Sen UniversityGuangzhouChina Hospital of Stomatology Key Laboratory of Oral Biomedical Research of Zhejiang ProvinceSchool of StomatologyZhejiang University School of MedicineHangzhouChina department of Oral and Maxillofacial Surgery First Affiliated HospitalSun Yat-Sen UniversityGuangzhouChina

The heterogeneity of exhausted T cells(Tex)is a critical determinant of immune checkpoint blockade therapy ***,few studies have explored exhausted T cell subpopulations in human *** the present study,we examined samples from two cohorts of 175 patients with head and neck squamous cell cancer(HNSCC)by multiplex immunohistochemistry(mIHC)to investigate two subsets of Tex,CD8+PD1+TCF1+progenitor exhausted T cells(TCF1+Texprog)and CD8+PD1+TCF1−terminally exhausted T cells(TCF1−Texterm).Moreover,fresh tumor samples from 34 patients with HNSCC were examined by flow cytometry and immunohistochemistry to further investigate their properties and cytotoxic capabilities and their correlation with regulatory T cells(Tregs)in the tumor immune microenvironment(TIME).mIHC and flow cytometry analysis showed that TCF1−Texterm represented a greater proportion of CD8+PD1+Tex than TCF1+Texprog in most ***1+Texprog produced abundant TNFα,while TCF1−Texterm expressed higher levels of CD103,TIM-3,CTLA-4,and ***1−Texterm exhibited a polyfunctional TNFα+GZMB+IFNγ+phenotype;and were associated with better overall survival and recurrence-free *** results also indicated that larger proportions of TCF1−Texterm were accompanied by an increase in the proportion of ***,it was concluded that TCF1−Texterm was the major CD8+PD1+Tex subset in the HNSCC TIME and that these cells favor patient survival.A high proportion of TCF1−Texterm was associated with greater Treg abundance.

关键词： PD1 progenitor squamous

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用于血清、活细胞及小鼠荷瘤中β-葡萄糖醛酸苷酶检测成像的高灵敏点亮型近红外荧光探针

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Science China Materials 2022年第3期65卷 836-844页

作者：周鑫王德平高志远何明玥侯佳宜张辉张国强丁丹冯光雪 College of Medical Imaging and Key Laboratory of Cellular PhysiologyMinistry of EducationShanxi Medical UniversityTaiyuan 030001China key laboratory of Bioactive Materials Ministry of education College of Life Sciencesand State Key Laboratory of Medicinal Chemical BiologyNankai UniversityTianjin 300071China department of Clinical laboratory Shanxi Provincial Academy of Traditional Chinese MedicineTaiyuan 030001China AIE Institute State Key Laboratory of Luminescent Materials and DevicesGuangdong Provincial Key Laboratory of Luminescence from Molecular AggregatesSchool of Materials Science and EngineeringSouth China University of TechnologyGuangzhou 510640China

β-葡萄糖醛酸苷酶(GUS)在肿瘤的发生、转移和进展中具有关键作用,因而成为一种很有应用前景的癌症生物标志物.在本研究中,我们设计出一种酶激活的近红外荧光探针(DCM-βGlcA),可在体内和体外快速、准确地检测GUS的活性.该探针是由葡萄... 详细信息

β-葡萄糖醛酸苷酶(GUS)在肿瘤的发生、转移和进展中具有关键作用,因而成为一种很有应用前景的癌症生物标志物.在本研究中,我们设计出一种酶激活的近红外荧光探针(DCM-βGlcA),可在体内和体外快速、准确地检测GUS的活性.该探针是由葡萄糖醛酸残基与荧光基团吡喃腈(DCM)衍生物构成.在GUS作用下,该探针在680 nm处具有明显的近红外荧光增强,而且它的斯托克位移达到了150 nm.此外,该探针对于GUS有很高的灵敏度,检测限低至0.19 U L^(-1).我们利用该探针分析了人血清样本中的GUS含量,其结果与ELISA检测结果一致.该探针还可用于示踪活细胞中的GUS,而且能够对荷瘤小鼠体内和肝癌组织中的GUS进行检测成像.因此,该探针可作为检测GUS的理想工具.

关键词：近红外荧光探针葡萄糖醛酸探针分析酶激活血清样本肝癌组织荧光基团活细胞

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Cancer metabolism and tumor microenvironment:fostering each other?

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Science China(Life Sciences) 2022年第2期65卷 236-279页

作者： Yiyuan Yuan Huimin Li Wang Pu Leilei Chen Dong Guo Hongfei Jiang Bo He Siyuan Qin Kui Wang Na Li Jingwei Feng Jing Wen Shipeng Cheng Yaguang Zhang Weiwei Yang Dan Ye Zhimin Lu Canhua Huang Jun Mei Hua-Feng Zhang Ping Gao Peng Jiang Shicheng Su Bing Sun Shi-Min Zhao Obstetrics&Gynecology Hospital of Fudan University State Key Laboratory of Genetic EngineeringFudan UniversityShanghai 200438China State key laboratory of Cell Biology Center for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China Molecular and Cell Biology Lab Institutes of Biomedical Sciences and School of Life SciencesFudan UniversityShanghai 200032China Zhejiang provincial key laboratory of Pancreatic Disease The First Affiliated Hospitaland Institute of Translational MedicineZhejiang University School of MedicineHangzhou 310029China West China School of Basic Medical Sciences&Forensic Medicine Sichuan Universityand State Key Laboratory of Biotherapy and Cancer CenterWest China Hospitaland Collaborative Innovation Center for BiotherapyChengdu 610041China department of Biochemistry and Molecular Cell Biology Shanghai Key Laboratory of Tumor Microenvironment and InflammationShanghai Jiao Tong University School of MedicineShanghai 200025China guangdong provincial key laboratory of Malignant tumor Epigenetics and Gene Regulation Medical Research CenterSun Yat-Sen Memorial HospitalSun Yat-Sen UniversityGuangzhou 510120China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China CAS Centre for Excellence in Cell and Molecular Biology the CAS Key Laboratory of Innate Immunity and Chronic DiseaseSchool of Basic Medical SciencesDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230027China School of Medicine Institutes for Life SciencesSouth China University of TechnologyGuangzhou 510006China Tsinghua University School of Life Sciences and Tsinghua-Peking Center for Life SciencesBeijing 100084China

The changes associated with malignancy are not only in cancer cells but also in environment in which cancer cells *** reprogramming supports tumor cells’high demand of biogenesis for their rapid proliferation,and helps tumor cells to survive under certain genetic or environmental *** evidence suggests that metabolic alteration is ultimately and tightly associated with genetic changes,in particular the dysregulation of key oncogenic and tumor suppressive signaling *** cells activate HIF signaling even in the presence of oxygen and in the absence of growth factor *** cancer metabolic phenotype,described firstly by German physiologist Otto Warburg,ensures enhanced glycolytic metabolism for the biosynthesis of *** conception of metabolite signaling,i.e.,metabolites are regulators of cell signaling,provides novel insights into how reactive oxygen species(ROS)and other metabolites deregulation may regulate redox homeostasis,epigenetics,and proliferation of cancer ***,the unveiling of noncanonical functions of metabolic enzymes,such as the moonlighting functions of phosphoglycerate kinase 1(PGK1),reassures the importance of metabolism in cancer *** metabolic,microRNAs,and ncRNAs alterations in cancer cells can be sorted and delivered either to intercellular matrix or to cancer adjacent cells to shape cancer microenvironment via media such as *** them,cancer microenvironmental cells are immune cells which exert profound effects on cancer *** of all these processes is a prerequisite for the development of a more effective strategy to contain cancers.

关键词： cancer metabolism cancer microenvironment epigenetics cancer immunology

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Elevated nuclear PIGL disrupts the cMyc/BRD4 axis and improves PD-1 blockade therapy by dampening tumor immune evasion

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Cellular & Molecular Immunology 2023年第8期20卷 867-880页

作者： Hua Yu Tiezhu Shi Linli Yao Dongwei Xu Yufeng Ding Qiang Xia Wei Liu Xiongjun Wang Precise Genome Engineering Centre School of Life SciencesGuangzhou UniversityGuangzhou510006China State key laboratory of Systems Medicine for Cancer Shanghai Cancer InstituteRen Ji HospitalShanghai Jiaotong University School of MedicineShanghai200240China department of Liver Surgery Renji HospitalShanghai Jiaotong University School of MedicineShanghai200127China guangdong provincial key laboratory of Liver Disease Research The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong510630China

To improve the efficacy of lenvatinib in combination with programmed death-1(PD-1)blockade therapy for hepatocellular carcinoma(HCC),we screened the suppressive metabolic enzymes that sensitize HCC to lenvatinib and PD-1 blockade,thus impeding HCC *** analysis of the CRISPR‒Cas9 screen,phosphatidylinositol-glycan biosynthesis class L(PIGL)ranked first in the positive selection *** depletion had no effect on tumor cell growth in vitro but reprogrammed the tumor microenvironment(TME)in vivo to support tumor cell ***,nuclear PIGL disrupted the interaction between cMyc/BRD4 on the distant promoter of target genes and thus decreased the expression of CCL2 and CCL20,which are involved in shaping the immunosuppressive TME by recruiting macrophages and regulatory T *** phosphorylation at Y81 by FGFR2 abolished the interaction of PIGL with importinα/β1,thus retaining PIGL in the cytosol and facilitating tumor evasion by releasing CCL2 and ***,elevated nuclear PIGL predicts a better prognosis for HCC patients and presents a positive correlation with CD8+T-cell enrichment in ***,our findings highlight that the nuclear PIGL intensity or the change in PIGL-Y81 phosphorylation should be used as a biomarker to guide lenvatinib with PD-1 blockade therapy.

关键词： Nuclear PIGL cMyc PD-1 antibody CCL2/20 tumor immune evasion

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LncRNA DACH1 protects against pulmonary fibrosis by binding to SRSF1 to suppress CTNNB1 accumulation

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Acta Pharmaceutica Sinica B 2022年第9期12卷 3602-3617页

作者： Jian Sun Tongzhu Jin Zhihui Niu Jiayu Guo Yingying Guo Ruoxuan Yang Qianqian Wang Huiying Gao Yuhan Zhang Tianyu Li Wenxin He Zhixin Li Wenchao Ma Wei Su Liangliang Li Xingxing Fan Hongli Shan Haihai Liang department of Pharmacology(State-Province key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150081China Northern Translational Medicine Research and Cooperation Center Heilongjiang Academy of Medical SciencesHarbin Medical UniversityHarbin 150081China department of Thoracic Surgery Shanghai Pulmonary HospitalTongji UniversityShanghai 200433China State key laboratory of Quality Research in Chinese Medicine/Macao Institute for Applied Research in Medicine and Health Macao University of Science and TechnologyMacao(SAR)China Research Unit of Noninfectious Chronic Diseases in Frigid Zone(2019RU070) Chinese Academy of Medical SciencesHarbin 150081China Zhuhai People's Hospital Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and TreatmentZhuhai Hospital Affiliated with Jinan UniversityJinan UniversityZhuhai 519000China

Idiopathic pulmonary fibrosis(IPF)is a progressive disease with unknown etiology and limited therapeutic *** of fibroblasts is a prominent feature of pulmonary *** we report that lncRNA DACH1(dachshund homolog 1)is downregulated in the lungs of IPF patients and in an experimental mouse model of lung ***1 knockout mice develop spontaneous pulmonary fibrosis,whereas overexpression of LncDACH1 attenuated TGF-β1-induced aberrant activation,collagen deposition and differentiation of mouse lung ***,forced expression of LncDACH1 not only prevented bleomycin(BLM)-induced lung fibrosis,but also reversed established lung fibrosis in a BLM ***,LncDACH1 binding to the serine/arginine-rich splicing factor 1(SRSF1)protein decreases its activity and inhibits the accumulation of *** expression of SRSF1 blocked the anti-fibrotic effect of LncDACH1 in lung ***,loss of LncDACH1 promoted proliferation,differentiation,and extracellular matrix(ECM)deposition in mouse lung fibroblasts,whereas such effects were abolished by silencing of *** addition,a conserved fragment of LncDACH1 alleviated hyperproliferation,ECM deposition and differentiation of MRC-5 cells driven by TGF-β***,LncDACH1 inhibits lung fibrosis by interacting with SRSF1 to suppress CTNNB1 accumulation,suggesting that LncDACH1 might be a potential therapeutic target for pulmonary fibrosis.

关键词： Idiopathic pulmonary fibrosis LncRNA DACH1 SRSF1 CTNNB1 Fibroblast Myofibroblast Extracellular matrix Proliferation

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AstragalosideⅣameliorates insulin induced insulin resistance in HepG2 cells through reactive oxygen species mediated c-Jun N-terminal kinase pathway

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Journal of Traditional Chinese Medicine 2023年第1期43卷 60-67页

作者： YE Xiaomei XING Xiaowei YUAN Kangrui WANG Dongming WU Dudu CHEN Zhi YU Zhiqiang School of Pharmacy Guangdong Medical UniversityDongguan 523808China department of Clinical Pharmacy SSL Central Hospital of Dongguan City(the Third People's Hospital of Dongguan City)Dongguan 523326China department of Pharmacy Central People's Hospital of ZhanjiangGuangzhou 510515China School of Pharmaceutical Sciences Guangdong Provincial Key Laboratory of New Drug ScreeningSouthern Medical UniversityZhanjiang 524037China

OBJECTIVE:To investigate the effects and elucidate the mechanism of Astragaloside IV(AS-IV)for insulin resistance(IR)and type 2 diabet es mellitus(T2DM).METHODS:CCK8 kit was used to detect cell viability,glucose detection kit was used to detect the concentration of glucose in cell supernatant,reactive oxygen species(ROS)detection kit and Western blot were used to explore the mechanism of Astragaloside IV(AS-IV)in improving IR.A diabetic rat model was also established by feeding high sugar and fat diet and streptozotocin(STZ)*** treatment with AS-IV,rosiglitazone(ROZ),or normal saline,the fasting blood glucose(FBG),C peptide(C-P),tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and the glucose tolerance were ***:AS-IV could effectively reduce the content of ROS and increase the glucose uptake in high insulintreated IR-type HepG 2 *** results of molecular mechanisms indicated that AS-IV could improve insulin resistance by reducing JNK phosphorylation and regulating c-Jun N-terminal kinase(JNK)downstream protein ***,AS-IV could significantly reduce the levels of FBG,TNF-α,IL-6 and the glucose tolerance in diabetic rats(P<0.05 or<0.01).The high and medium dose groups of AS-IV could significantly increase the C-P levels in diabetic rats(P<0.05 or<0.01).CONCLUSIONS:Our results indicated that AS-IV improve liver IR through the JNK pathway and ROS,which meant a new molecular target for the treatment of *** AS-IV also helped to prevent and improved the insulin resistance of rats.

关键词： AstragalosideⅣ Insulin resistance Glucose consumption ROS JNK HepG2 cells

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Enhancement of CAR-T cell activity against cholangiocarcinoma by simultaneous knockdown of six inhibitory membrane proteins

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Cancer Communications 2023年第7期43卷 788-807页

作者： Yidan Qiao Jie Chen Xuemei Wang Shumei Yan Jizhou Tan Baijin Xia Yongjian Chen Keming Lin Fan Zou Bingfeng Liu Xin He Yiwen Zhang Xu Zhang Hui Zhang Xiangyuan Wu Lijuan Lu department of Medical Oncology the Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdongP.R.China key laboratory of Tropical Disease Control of Ministry education Guangdong Engineering Research Center for Antimicrobial Agent and ImmunotechnologyInstitute of Human VirologySun Yat-sen UniversityGuangzhouGuangdongP.R.China Guangzhou National laboratory Bio-IslandGuangzhouGuangdongP.R.China

Background:Existing treatments for cholangiocarcinoma have poor ***,chimeric antigen receptor-T(CAR-T)cells are emerging as a potential therapeutic *** tumors possess multiple adverse factors in an immunosuppressive microenvironment that impair CAR-T cell infiltration and *** study aimed to improve the function of CAR-T cells through knock down immune checkpoints and immunosuppressive molecular ***:We evaluated the expression of epidermal growth factor receptor(EGFR)and B7 homolog 3 protein(B7H3)antigens in cholangiocarcinoma tissues using immunohistochemistry and screened specific immune checkpoints in the cholangiocarcinoma microenvironment via flow ***,we engineered CAR-T cells targeting EGFR and B7H3 *** simultaneously knocked down immune checkpoints and immunosuppressive molecular receptors in CAR-T cells by constructing two clusters of small hairpin RNAs and evaluated the engineered CAR-T cells for antitumor activity both in vitro,using tumor cell lines and cholangiocarcinoma organoid models,and in vivo,using humanized mouse ***:We observed high expression of EGFR and B7H3 antigens in cholangiocarcinoma ***-CAR-T and B7H3-CAR-T cells demonstrated specific anti-tumor *** found an abundance of programmed cell death protein 1(PD-1),T cell immunoglobulin and mucin domain-containing protein 3(Tim-3),and T cell immunoglobulin and ITIM domain(Tigit)on infiltrated CD8^(+)T cells in the cholangiocarcinoma *** then decreased the expression of these 3 proteins on the surface of CAR-T cells,named PTG-scFV-CAR-T ***,we knocked-down the expression of transforming growth factor beta receptor(TGFβR),interleukin-10 receptor(IL-10R),and interleukin-6 receptor(IL-6R)of PTG-scFV-CAR-T *** cells,named PTG-T16R-scFVCAR-T cells,potently killed tumor cells in vitro and promoted apoptosis of tumor cells in a cholangiocarcinoma ***

关键词： CAR-T cholangiocarcinoma immunosuppression liver cancer T cell receptor tumor microenvironment

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Targeting hypoxia-induced CBS expression inhibits breast cancer stem cells through the induction of ferroptosis

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Genes & Diseases 2023年第6期10卷 2195-2198页

作者： Guangyao Wei Jia Liu Jie Lan Guangyu Ji Huize Xia Zhiqun Zhao Zhaoxue Yu Rong Sun Chuanzhao Zhang Haiquan Lu The Second Hospital and Advanced Medical Research Institute Cheeloo College of MedicineShandong UniversityJinanShandong 250012China key laboratory for Experimental Teratology of the Ministry of education Cheeloo College of MedicineShandong UniversityJinanShandong 250012China department of Radiation Oncology Cancer Center and State Key Laboratory of BiotherapyWest China HospitalSichuan UniversityChengduSichuan 610041China Shandong Zhongke Institute for Regenerative Medicine JinanShandong 250012China department of General Surgery Guangdong Provincial People's HospitalGuangdong Academy of Medical SciencesGuangzhouGuangdong 510080China Center for Reproductive Medicine Cheeloo College of MedicineShandong UniversityJinanShandong 250012China

Triple-negative breast cancer(TNBC)has a poor prognosis because of its aggressive characteristics and lack of targeted therapies.1 Recently,it has been reported that TNBC is sensitiveto ferroptosis,an iron-dependent type of programmed cell death,making it a potential target for the treatment of TNBC.2 Breast cancer stem cells(BCSCs),a small population of cancer cells that possess the infinite proliferative potential and tumor-initiating properties,play important roles in drug resistance.3 The responses of BCsCs to ferroptosis-inducing agents are controversial and remain elusive.

关键词： breast cancer prognosis

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γδT cells:origin and fate,subsets,diseases and immunotherapy

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Signal Transduction and Targeted Therapy 2023年第12期8卷 5769-5806页

作者： Yi Hu Qinglin Hu Yongsheng Li Ligong Lu Zheng Xiang Zhinan Yin Dieter Kabelitz Yangzhe Wu Microbiology and Immunology department School of MedicineFaculty of Medical ScienceJinan UniversityGuangzhouGuangdong 510632China guangdong provincial key laboratory of Tumour Interventional Diagnosis and Treatment Zhuhai Institute of Translational MedicineZhuhai People’s Hospital Affiliated with Jinan UniversityJinan UniversityZhuhaiGuangdong 519000China department of Medical Oncology Chongqing University Cancer HospitalChongqing 400030China Biomedical Translational Research Institute Jinan UniversityGuangzhouGuangdong 510632China Institute of Immunology Christian-Albrechts-University KielKielGermany

The intricacy of diseases,shaped by intrinsic processes like immune system exhaustion and hyperactivation,highlights the potential of immune renormalization as a promising strategy in disease *** recent years,our primary focus has centered onγδT cell-based immunotherapy,particularly pioneering the use of allogeneic Vδ2+γδT cells for treating late-stage solid tumors and tuberculosis ***,we recognize untapped potential and optimization opportunities to fully harnessγδT cell effector functions in *** review aims to thoroughly examineγδT cell immunology and its role in ***,we elucidate functional differences betweenγδT cells and theirαβT cell *** also provide an overview of major milestones inγδT cell research since their discovery in ***,we delve into the intricate biological processes governing their origin,development,fate decisions,and T cell receptor(TCR)rearrangement within the *** examining the mechanisms underlying the anti-tumor functions of distinctγδT cell subtypes based onγδTCR structure or cytokine release,we emphasize the importance of accurate subtyping in understandingγδT cell *** also explore the microenvironment-dependent functions ofγδT cell subsets,particularly in infectious diseases,autoimmune conditions,hematological malignancies,and solid ***,we propose future strategies for utilizing allogeneicγδT cells in tumor *** this comprehensive review,we aim to provide readers with a holistic understanding of the molecular fundamentals and translational research frontiers ofγδT cells,ultimately contributing to further advancements in harnessing the therapeutic potential ofγδT cells.

关键词： γδT immunotherapy diseases

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