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The ubiquitin ligase Pelil inhibits ICOS and thereby Tfh-mediated immunity

Cellular & Molecular Immunology 2021年第4期18卷 969-978页

作者： Xinfang Huang Shumeng Hao Junli Liu Yuanyuan Huang Manman Liu Chunyuan Xiao Yan Wang Siyu Pei Tao Yu Jing Xu Haikun Wang Dongfang Dai Xiao Su Yichuan Xiao Department of Rheumatology Shanghai East Hospital Tongji UnrversitySchool of MedicineShanghai Giina CAS Key Laboratory of Tissue Microenvironment and Tumor Shanghai Institute of Nutrition and HealthChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghaiChina CAS Key Laboratory of Molecular Virology&Immunology Unit of Respiratory Infection and ImmunityInstitut Pasteur of ShanghaiChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghaiChina Department of Radiation Oncology The Affiliated Cancer Hospital of Nanjing M4edical University(Jiangsu Cancer Hospital)and Jiangsu Institute of Cancer ResearchNanjingJiangsuChina

T follicular helper(Tfh)cells are crucial for regulating autoimmune inflammation and protective immunity against viral infection.However,the molecular mechanism controlling Tfh cell differentiation is poorly understood.Here,through two mixed bone marrow chimeric experiments,we identified Peli1,a T cell-enriched E3 ubiquitin ligase,as an intrinsic regulator that inhibits Tfh cell differentiation.Peli1 deficiency significantly promoted c-Rel-mediated inducible T-cell costimulator(ICOS)expression,and PELI1 mRNA expression was negatively associated with ICOS expression on human CD4^(+)T cells.Mechanistically,increased ICOS expression on Peli1-KO CD4^(+)T cells enhanced the activation of PI3K-AKT signaling and thus suppressed the expression of Klf2,a transcription factor that inhibits Tfh differentiation.Therefore,reconstitution of Klf2 abolished the differences in Tfh differentiation and germinal center reaction between WT and Peli1-KO cells.As a consequence,Peli1-deficient CD4^(+)T cells promoted lupus-like autoimmunity but protected against H1N1 influenza virus infection in mouse models.Collectively,our findings established Peli1 as a critical negative regulator of Tfh differentiation and indicated that targeting Peli1 may have beneficial therapeutic effects in Tfhrelated autoimmunity or infectious diseases.

关键词： T follicular helper cells Peli1 ICOS

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Orthogonal quantification of soluble inducible T-cell costimulator(ICOS)in healthy and diseased human serum

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Journal of Pharmaceutical Analysis 2022年第2期12卷 317-323页

作者： Kevin McKinski Dean McNulty Francesca Zappacosta Mary Birchler Matt Szapacs Christopher Evans Bioanalysis Immunogenicity&BiomarkersGlaxoSmithKlineCollegevillePA19426USA

Inducible T-cell costimulator(ICOS),a homodimeric protein expressed on the surface of activated T-cells,is being investigated as a potential therapeutic target to treat various cancers.Recent studies have reported aberrant increases in the soluble form of ICOS(sICOS)in human serum in disease-state patients,primarily using commercial ELISA kits.However,results from our in-house immunoassay did not show these aberrant increases,leading us to speculate that commercial sICOS ELISAs may be prone to interference.We directly tested that hypothesis and found that one widely used commercial kit yields falsepositives and is prone to human anti-mouse antibody interference.We then analyzed a panel of healthy,cancer,chronic hepatitis C virus,systemic lupus erythematosus,and diffuse cutaneous systemic sclerosis human serum using our in-house immunoassay and reported the measured sICOS concentrations in these populations.Since even well characterized immunoassay methods are prone to non-specific interference,we also developed a novel sICOS LC-MS/MS method to confirm the results.Using these orthogonal approaches,we show that sICOS is a low abundance soluble protein that cannot be measured above approximately 20 pg/mL in human serum.

关键词： ICOS Immunoassay LC-MS/MS Biomarker HAMA

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Expression and prognosis of inducible T-cell co-stimulator and its ligand in Chinese stage I–III lung adenocarcinoma patients

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Animal Models and Experimental Medicine 2023年第5期6卷 464-473页

作者： Xiao-Kai Zhan Xi-Kun Liu Sen Zhang Hong Chen Division of Oncology and Hematology Beijing Chao-Yang HospitalCapital Medical UniversityBeijingP.R.China State Key Laboratory of Bioactive Substances and Functions of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingP.R.China Pathology Department Beijing Chao-Yang HospitalCapital Medical UniversityBeijingP.R.China

Background:Immunotherapy has become the fastest-adopting treatment paradigm for lung cancer with improved survival.By binding with its ligand(inducible T-cell costimulator and its ligand[ICOSL]),an inducible T-cell co-stimulator(ICOS)could contribute to reversing immunosuppression and improving immune response and thus be a potential target for cancer immunotherapy.Methods:We selected 54 formalin-fixed,paraffin-embedded tumor tissues from cases with stage I–III lung adenocarcinoma cancer.Immunohistochemical expression of ICOS and ICOSL was evaluated.The correlation with clinical parameters in Chinese patients was also compared with TCGA results.Results:The positive rates of ICOS and ICOSL were 68%and 81.5%,respectively,in lung tumor tissues.Of these,9 cases had a low expression of ICOS,and 22 cases had a high expression of ICOS;ICOSL expression was low in 20 cases and high in 24 cases.According to the International Association for the Study of Lung Cancer(8th edition),phase I lesions were detected in 21 cases,phase II lesions in 15 cases,and phase III lesions in 18 cases.The median survival time of all patients was 44.5 months,and the median disease-free survival was 32 months.Univariate analysis showed that the factors significantly associated with overall survival were tumor size,regional lymph node involvement,stage,and expression level of ICOS/ICOSL.Survival analysis using log-rank test indicated that the lower ICOS+cell infiltration may predict poor prognosis,whereas lower ICOSL protein expression may be associated with better prognosis,but ICOSL data need further validation in larger samples due to inconsistency in TCGA mRNA prediction.Conclusion:ICOS/ICOSL might be associated with prognosis of lung cancer,and ICOS and its ligand may be potential therapeutic targets in non-small cell lung cancer.

关键词： Chinese patients ICOS ICOSL lung adenocarcinoma prognostic factor

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双表现遗传调控药物治疗TET2基因阳性滤泡辅助T细胞表型结内外周T细胞淋巴瘤1例报告并文献复习

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中华血液学杂志 2023年第7期44卷 590-593页

作者：郎筠渊吕瑞宋燕燕邹德慧安刚中国医学科学院血液病医院(中国医学科学院血液学研究所) 实验血液学国家重点实验室国家血液系统疾病临床医学研究中心细胞生态海河实验室天津300020 晋城市人民医院血液科晋城048000

WHO造血与淋巴组织肿瘤新分类中定义了一类来源于滤泡辅助T细胞的特殊亚型,包括结内外周T细胞淋巴瘤伴滤泡辅助T细胞表型(nPTCL-TFH),血管免疫母细胞淋巴瘤(AITL)和滤泡T细胞淋巴瘤(F-TCL)。除表达CD4以外,nPTCL-TFH需至少表达两种以上... 详细信息

WHO造血与淋巴组织肿瘤新分类中定义了一类来源于滤泡辅助T细胞的特殊亚型,包括结内外周T细胞淋巴瘤伴滤泡辅助T细胞表型(nPTCL-TFH),血管免疫母细胞淋巴瘤(AITL)和滤泡T细胞淋巴瘤(F-TCL)。除表达CD4以外,nPTCL-TFH需至少表达两种以上滤泡辅助T细胞(follicular helper-T cell,TFH)标志物(PD1、CD10、BCL6、CXCL13、ICOS、MAF、SAP及CD200),组织学应具备成熟T细胞淋巴瘤的一般异型性特征,但需与AITL和F-TCL相鉴别[1]。nPTCL-TFH与AITL有共同的细胞起源[2],因为它们的突变模式和基因表达谱非常相似,如TET2、DNMT3A、RHOA基因突变,提示nPTCL-TFH可能与AITL相关或是AITL的一种变异型[1]。我们报道1例TET2基因突变且伴TFH表型的结内外周T细胞淋巴瘤接受西达本胺和阿扎胞苷联合细胞毒药物化疗的病例,并进行文献复习,以阐明nPTCL-TFH的病理学、遗传学机制及组蛋白去乙酰化酶抑制剂(HDACi)联合DNA甲基转移酶抑制剂(DNMTi)双表观遗传治疗在nPTCL-TFH中的作用。

关键词：外周T细胞淋巴瘤组蛋白去乙酰化酶抑制剂基因突变基因表达谱 ICOS 细胞起源药物治疗变异型

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Ubiquitin-specific peptidase 18 regulates the differentiation and function of Treg cells

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Genes & Diseases 2021年第3期8卷 344-352页

作者： Lu Yang Yukai Jing Danqing Kang Panpan Jiang Na Li Xinrong Zhou Yan Chen Lisa S.Westerberg Chaohong Liu Department of Pathogen Biology Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei Province430030PR China Department of Immunology School of MedicineYangtze UniversityJingzhouHubei Province434023PR China Department of Endocrinology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei Province430030PR China The Second Department of Pediatrics Affiliated Hospital of Zunyi Medical UniversityZunyiGuiZhou Province563000PR China Department of Microbiology Tumor and Cell Biology Karolinska InstitutetStockholm17177Sweden

Ubiquitin-specific peptidase 18(USP18)plays an important role in the development of CD11b^(+)dendritic cells(DCs)and Th17 cells,however,its role in the differentiation of other T cell subsets,especially in regulatory T(Treg)cells,is unknown.In our study,we used Usp18 K0 mice to study the loss of USP18 on the impact of Treg cell differentiation and function.We found that USP18 deficiency upregulates the differentiation of Treg cells,which may lead to disrupted homeostasis of peripheral T cells,and downregulates INF-y,IL-2,IL-17A producing CD4^(+)T cells and INF-γproducing CD8^(+)T cells.Mechanistically,we also found that the upre-gulation of Tregs is due to elevated expression of CD25 in Usp18 KO mice.Finally,we found that the suppressive function of Usp18 KO Tregs is downregulated.Altogether,our study was the first to identify the role of USP18 in Tregs differentiation and its suppressive function,which may provide a new reference for the treatment of Treg function in many autoimmune diseases,and USP18 can be used as a new therapeutic target for precise medical treatment.

关键词： CD25 Foxp3 ICOS Regulator T cell USP18

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Transmembrane domain-mediated Lck association underlies bystander and costimulatory ICOS signaling

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Cellular & Molecular Immunology 2020年第2期17卷 143-152页

作者： Zurong Wan Xingxing Shao Xingyu Ji Lihui Dong Jiacheng Wei Zhuqing Xiong Wanli Liu Hai Qi Tsinghua-Peking Center for Life Sciences Tsinghua University100084 BeijingChina Laboratory of Dynamic Immunobiology Institute for Immunology100084 BeijingChina Department of Basic Medical Sciences School of Medicine100084 BeijingChina School of Life Sciences 100084 BeijingChina Beijing Key Lab for Immunological Research on Chronic Diseases 100084 BeijingChina MOE Key Laboratory of Protein Sciences Tsinghua University100084 BeijingChina

The B7-family inducible costimulator(ICOS)activates phosphoinositide-3 kinase(PI3K)and augments calcium mobilization triggered by the T-cell receptor(TCR).We surprisingly found that the entire cytoplasmic domain of ICOS is dispensable for its costimulation of calcium mobilization.This costimulatory function relies on the unique transmembrane domain(TMD)of ICOS,which promotes association with the tyrosine kinase Lck.TMD-enabled Lck association is also required for p85 recruitment to ICOS and subsequent PI3K activation,and Lck underlies both the bystander and costimulatory signaling activity of ICOS.TMD-replaced ICOS,even with an intact cytoplasmic domain,fails to support T FH development or GC formation in vivo.When transplanted onto a chimeric antigen receptor(CAR),the ICOS TMD enhances interactions between T cells and antigen-presenting target cells.Therefore,by revealing an unexpected function of the ICOS TMD,our study offers a new perspective for the understanding and potential application of costimulation biology.

关键词： ICOS stimulation stimulator

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ICOS与4-1BB共刺激域增强CAR-T细胞在肺癌中的抗肿瘤活性

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中国免疫学杂志 2022年第22期38卷 2753-2757页

作者：张志东魏海龙林振海陈吉柏彭文儋州市人民医院胸心肿瘤外科儋州571700

目的:探究整合ICOS共刺激结构域的三代CAR-T细胞是否可对肺癌产生显著抗肿瘤活性。方法:采用慢病毒感染法构建二代CAR-T细胞(MSLN-BBz CAR-T)及三代CAR-T细胞(MSLN-ICOSBBz CAR-T),流式细胞术检测CAR-T细胞阳性率、效靶细胞共孵育后T细... 详细信息

目的:探究整合ICOS共刺激结构域的三代CAR-T细胞是否可对肺癌产生显著抗肿瘤活性。方法:采用慢病毒感染法构建二代CAR-T细胞(MSLN-BBz CAR-T)及三代CAR-T细胞(MSLN-ICOSBBz CAR-T),流式细胞术检测CAR-T细胞阳性率、效靶细胞共孵育后T细胞CD69表达以及肿瘤浸润T细胞抗肿瘤表型;荧光显微镜观察效靶细胞共孵育后T细胞增殖情况;活体成像检测肺癌细胞在小鼠体内的生长情况;HE染色检测CAR-T细胞对主要脏器的毒性。结果:流式细胞术结果显示,成功采用慢病毒构建MSLN-BBz CAR-T及MSLN-ICOSBBz CAR-T,阳性率约为40%;效靶细胞共孵育后,MSLN-ICOSBBz CAR-T较MSLN-BBz CAR-T CD69表达显著升高(PICOSBBz CAR-T靶细胞杀伤能力更强(PICOSBBz CAR-T比MSLN-BBz CAR-T拥有更强的体内抑瘤能力(PICOSBBz CAR-T IFN-γ表达更高(PICOSBBz CAR-T均未对主要脏器造成明显损伤。结论:ICOS协同4-BB共刺激结构域可显著提高CAR-T细胞对肺癌的抗肿瘤活性,为MSLN-ICOSBBz CAR-T对肺癌治疗的进一步探索提供了依据。

关键词：肺癌嵌合抗原受体T细胞 ICOS 免疫治疗

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METTL3介导的m6A甲基化通过抑制CD8+ T细胞功能调控抗肿瘤免疫反应的机制研究

METTL3介导的m6A甲基化通过抑制CD8+ T细胞功能调控抗肿瘤免疫反...

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作者：阳青杉郑州大学

学位级别：硕士

背景和目的N6-甲基腺苷(N6-methyladenosine,m6A)甲基化是真核细胞中最常见的一种RNA表观遗传修饰,参与多种哺乳动物的RNA转录后调控。m6A的关键酶包含3种独立组分的复合物:甲基转移酶(writers),去甲基酶(erasers),m6A阅读蛋白(reader p... 详细信息

背景和目的N6-甲基腺苷(N6-methyladenosine,m6A)甲基化是真核细胞中最常见的一种RNA表观遗传修饰,参与多种哺乳动物的RNA转录后调控。m6A的关键酶包含3种独立组分的复合物:甲基转移酶(writers),去甲基酶(erasers),m6A阅读蛋白(reader proteins)。m6A修饰可以通过对靶RNA进行甲基化修饰来调控生物学功能,即通过甲基转移酶和去甲基化酶改变RNA的甲基化状态,以及阅读蛋白结合到具有m6A修饰位点的RNA上,调控RNA的稳定性与核转运等生物学进程,进而改变靶基因的表达水平。目前,大量研究已经证实m6A修饰广泛参与肿瘤的发生发展。随着研究的深入,m6A修饰在肿瘤免疫中发挥的重要作用已被揭示。例如,甲基转移酶METTL3是m6A修饰中主要的调控酶之一,发挥催化活性并将m6A添加到RNA上。最新研究发现,METTL3对肿瘤的发生发展、树突状细胞及CD4+T细胞的分化具有重要调控作用。然而,METTL3如何调控CD8+T细胞的分化及功能尚不清楚。CD8+T细胞在肿瘤免疫治疗中发挥抗肿瘤效应,它能够通过T细胞表面受体,特异性识别肿瘤细胞表面表达的主要组织相容性复合物(MHC-抗原肽分子)进而杀伤靶细胞。CD8+T细胞受到抗原刺激后,绝大部分形成效应细胞并在杀伤后发生凋亡,仅一小部分细胞能够形成在体内长期存在的记忆性亚群,当再次受抗原刺激后记忆性T细胞能够快速分化并发挥杀伤作用。然而,研究表明肿瘤患者体内CD8+T细胞功能记忆亚群比例降低或处于耗竭状态,使其不能持续发挥杀伤作用。因此,促进T细胞记忆亚群的分化,维持其在体内的抗肿瘤效应是肿瘤免疫治疗中亟待解决的关键科学问题。在本研究中,我们通过构建条件性敲除METTL3小鼠,探究METTL3对CD8+T细胞分化与抗肿瘤效应的影响,从表观修饰角度阐明调控CD8+T细胞分化及功能的机制,能够为改善肿瘤免疫治疗提供新的策略。方法(1)利用CRISPR/Cas9技术构建Mettl3fl/fl小鼠,与Lck-Cre小鼠杂交获得Mettl3fl/fl LckCe小鼠,即条件性敲除小鼠;(2)采用流式细胞术分析Mettl3fl/flLckCre小鼠与Mettl3fl/fl小鼠脾脏中CD8+T细胞与分化相关的标志物(CD44和CD62L)、表面激活和抑制分子的标志物(CD69和PD-1)以及细胞功能相关的分子(TNF-α、IFN-γ、GranzymeB、IL-2和Perforin)的表达差异;(3)构建小鼠肺癌模型,分析Mettl3fl/fl LckCre小鼠与Mettl3fl/fl小鼠肿瘤生长情况,以及脾脏中CD8+T细胞中分化相关的分子标志物(CD44和CD62L)、表面激活和抑制分子的标志物(CD69和PD-1)以及脾脏和肿瘤组织中细胞功能相关的分子标志物(TNF-α、IFN-γ、Granzyme B、IL-2和Perforin)的表达差异;(4)采用流式细胞术分析肺腺癌患者外周血METTL3高表达和低表达CD8+T 细胞功能分子(TNF-α、IFN-γ、Granzyme B、IL-2、Perforin)分泌的差异;(5)采用测序技术对Mettl3fl/flLckCre小鼠与Mettl3fl/fl小鼠脾脏中CD8+T细胞进行miRNA测序,分析差异基因以及差异基因富集的通路;(6)通过靶基因预测网站,预测miRNA可能作用的靶基因,并采用qPCR、流式细胞术等方法验证其表达;(7)采用双荧光素酶报告实验验证miRNA与靶基因相互作用关系;(8)使用 miRNA 对照(NC),类似体(mimics),抑制剂(inhibitor)转染CD8+T细胞,并用流式细胞术检测靶基因的表达和功能分子(TNF-α、IFN-y、Granzyme B、IL-2、Perforin)的表达差异。结果(1)与Mettl3fl/fl小鼠相比,条件性敲除Mettl3fl/fl LckCre小鼠中CD8+T细胞记忆亚群比例、表面激活型标志表达及杀伤功能相关细胞因子的分泌增加,而抑制型标志表达减少;(2)与Mettl3fl/fl小鼠相比,条件性敲除Mettl3fl/fl LckCre小鼠肿瘤体积增长缓慢,肿瘤内CD8+T细胞功能增强。(3)肺癌患者外周血中CD8+T细胞中METTL3低表达促进杀伤功能相关因子的表达;(4)ICOS是mmu-miR-1195的靶基因,METTL3敲除后通过下调mmu-miR-1195,增加ICOS的表达,从而促进T细胞功能。结论CD8+T细胞敲除METTL3可以促进记忆分化、提高其增殖能力和杀伤功能;同时,METTL3通过mmu-miR-1195,降低ICOS的表达从而抑制CD8+T细胞的抗肿瘤效应,为免疫治疗提供了理论依据。

关键词： METTL3 CD8+ T细胞甲基化修饰分化与功能 mmu-miR-1195 ICOS

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Reciprocal costimulatory molecules control the activation of mucosal type 3 innate lymphoid cells during engagement with B cells

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Cellular & Molecular Immunology 2023年第7期20卷 808-819页

作者： Xinping Lv Shan Zhu Jing Wu Jinfeng Shi Qiuyu Wei Tete Li Ning Yang Chunyan Liu Lingli Qi Guoxia Zang Hang Cheng Zhiguang Yang Chengyan Jin Yusheng Wang Jiuwei Cui Hideki Ueno Yong-Jun Liu Jingtao Chen Cancer Center First Hospital of Jilin UniversityChangchunJilin 130021China Laboratory for Tumor Immunology First Hospital of Jilin UniversityChangchunJilin 130061China Department of Otolaryngology Head and Neck Surgery First Hospital of Jilin UniversityChangchunJilin 130021China Department of Translational Medicine Changchun GeneScience Pharmaceuticals Co.Ltd.ChangchunJilin 130012China Department of Gynecology First Hospital of Jilin UniversityChangchunJilin 130021China Department of Pediatric Gastroenterology First Hospital of Jilin UniversityChangchunJilin 130021China Department of Pediatrics First Hospital of Jilin UniversityChangchunJilin 130021China Department of Thoracic Surgery First Hospital of Jilin UniversityChangchunJilin 130021China Department of Thoracic Surgery Second Hospital of Jilin UniversityChangchunJilin 130041China Department of Immunology Graduate School of MedicineKyoto UniversityKyotoJapan ASHBi Institute for the Advanced Study of Human Biology Kyoto UniversityKyotoJapan

Innate lymphoid cells(ILCs)are the counterpart of T helper cells in the innate immune system and share multiple phenotypes with T helper cells.Inducible T-cell costimulator(ICOS)is recognized on T cells and participates in T-cell activation and T and B-cell engagement in lymphoid tissues.However,the role of ICOS in ILC3s and ILC3-involved interactions with the immune microenvironment remains unclear.Here,we found that ICOS expression on human ILC3s was correlated with the activated state of ILC3s.ICOS costimulation enhanced the survival,proliferation,and capacity of ILC3s to produce cytokines(IL-22,IL-17A,IFN-γ,TNF,and GM-CSF).Via synergistic effects of ICOS and CD40 signaling,B cells promoted ILC3 functions,and ILC3-induced T-cellindependent B-cell IgA and IgM secretion primarily required CD40 signaling.Hence,ICOS is essential for the nonredundant role of ILC3s and their interaction with adjacent B cells.

关键词： Innate lymphoid cell B cell Tonsil ICOS Costimulatory molecule

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CD200和ICOS在血管免疫母细胞性T细胞淋巴瘤中表达的意义与预后研究

CD200和ICOS在血管免疫母细胞性T细胞淋巴瘤中表达的意义与预后研...

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作者：李爱平南华大学

学位级别：硕士

目的:通过免疫组织化学检测方法研究CD200和ICOS蛋白在血管免疫母细胞性T细胞淋巴瘤、外周T细胞淋巴瘤,非特指型及经典霍奇金淋巴瘤中的表达情况;比较AITL中CD200、ICOS与CXCL-13、PD-1、CD10、BCL-6等蛋白表达的差异;分析CD200和ICOS... 详细信息

目的:通过免疫组织化学检测方法研究CD200和ICOS蛋白在血管免疫母细胞性T细胞淋巴瘤、外周T细胞淋巴瘤,非特指型及经典霍奇金淋巴瘤中的表达情况;比较AITL中CD200、ICOS与CXCL-13、PD-1、CD10、BCL-6等蛋白表达的差异;分析CD200和ICOS蛋白表达与AITL预后的关系。方法:1、收集郴州地区(郴州市第一人民医院、郴州市第三人民医院、郴州市第四人民医院和湘南附属医院)在2012年6月至2019年12月期间,通过组织学形态及免疫组织化学诊断为AITL的患者40例,并收集其临床资料、随访资料及组织标本。经两名高级职称医生复审,有39例患者确诊为AITL。2、收集郴州市第一人民医院在2016年8月至2019年7月期间诊断为CHL及PTCL-NOS病例各10例,并收集其组织标本。3、通过免疫组织化学检测方法,检测AITL患者中CD200、ICOS、CXCL-13、PD-1、CD10和BCL-6等蛋白表达情况。用同样的方法检测CHL和PTCL-NOS患者中CD200和ICOS蛋白表达情况。4、采用SPSS.23.0统计软件进行统计分析。运用卡方检验分析AITL患者中CD200和ICOS蛋白表达与患者性别、年龄、临床分期、LDH、肝脾肿大、骨髓受累、B症状、PD-1、CD10和BCL-6蛋白表达水平的比较,PICOS、PD-1、CD10、BCL-6等蛋白及患者性别、年龄、临床分期、LDH、肝脾肿大、骨髓受累、B症状等临床参数进行单因素生存分析,并绘制生存曲线;运用Cox比例风险模型进行多因素分析,PICOS的阳性率分别为57.69%(15/26)、41.03%(16/39)、87.18%(34/39)、74.36%(29/39)、71.79%(28/39)、61.54%(24/39);在CHL患者中CD200和ICOS阳性率分别为70%(7/10)和0%(0/10);在PTCL-N0S患者中CD200和ICOS阳性率分别为40%(4/10)和10%(1/10)。2、分析CD200和ICOS蛋白在AITL、CHL、PTCL-NOS患者中表达差异。结果显示:ICOS蛋白在AITL与CHL(P=0.001)/PTCL-NOS(P=0.004)之间的表达差异均有统计学意义;但CD200在AITL与CHL/PTCL-NOS之间的表达差异均无统计学意义(P>0.05)。3、分析AITL患者中CD200和ICOS蛋白表达与临床参数及CD10、PD-1、BCL-6蛋白表达的差异。统计结果显示:CD200在AITL患者的LDH(P=0.012)及IPI评分(P=0.001)之间表达有显著差异,而CD200在AITL患者的性别、年龄、ECOG体能评分、临床分期、结外受累、肝脾肿大、B症状及CD10、PD-1、BCL-6蛋白表达等参数之间的表达无统计学意义(P>0.05);ICOS在AITL患者的LDH(P=0.010)及PD-1(P=0.002)之间表达有显著差异,而ICOS在AITL患者的性别、年龄、ECOG体能评分、临床分期、结外受累、IPI评分、肝脾肿大、B症状及CD10、BCL-6蛋白表达等参数之间的表达无统计学意义(P>0.05)。4、Kaplan-Meier法单因素分析结果显示:CD200蛋白表达(PICOS蛋白表达(P=0.011)、结外受累数≥2个(PICOS蛋白可以作为辅助诊断AITL的免疫组织化学指标。2、ICOS蛋白有助于AITL与CHL/PTCL-NOS的鉴别。3、CD200可以作为判断AITL患者预后和病情恶化的指标,也是判断AITL患者预后及病情进展的独

关键词： CD200 ICOS 血管免疫母细胞性T细胞淋巴瘤滤泡辅助T细胞霍奇金淋巴瘤外周T细胞淋巴瘤,非特指型预后

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