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New insights into the immunopathogenesis of systemic lupus erythematosus： the role of t follicular helper cells

Chinese Medical Journal 2014年第19期127卷 3496-3502页

作者： Ma Huijuan Xia Changqing Wan Suigui Department of Hematology Xuanwu Hospital Capital MedicalUniversity Beijing 100053 China

Objective to review the development of t follicular helper （tFH） cells and their role in systemic lupus erythematosus （SLE） pathogenesis, the effect of dendritic cells （DCs） on tFH cells in SLE, as well as the potential use of tFH cells as a new therapeutic target in clinical practice. Data sources the data used in this review were retrieved mainly from the PubMed database （1989-2013）. the terms used in the literature search were ＂t follicular helper cells,＂＂systemic lupus erythematosus,＂ and ＂dendritic cells.＂ Study selection Relevant publications about the tFH cells development, the interaction between the tFH cells and the DCs, and the clinical applications of tFH cells were identified, retrieved, and reviewed. Results tFH cells, a novel distinct CD4＋ t cell subset, are specialized in providing help to B cells in the formation of germinal centers （GCs） and long-term protective humoral immune responses. the development of tFH cells from naive CD4＋ t cell is a multistep process. As the pivot of immunoregulation, DCs are indispensable for tFH cells generation. In addition to receptor-ligand interactions between tFH cells and DCs, the cytokines secreted by DCs are also necessary for tFH cell generation. tFH cell dysregulation has been implicated in the development of SLE. More evidence from animal models of SLE and SLE patients suggests that tFH cells are necessary for pathogenic autoantibody production. therefore, therapeutically targeting tFH cells can be a promising approach to treat antibody-mediated autoimmune diseases including SLE. Conclusion tFH cells play a critical role in the pathogenesis of SLE, making them attractive therapeutic targets in clinical practice.

关键词： systemic lupus erythematosus t follicular helper cells dendritic cells autoantibodies

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Shared and distinct roles of t peripheral helper and t follicular helper cells in human diseases

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Cellular & Molecular Immunology 2021年第3期18卷 523-527页

作者： Hiroyuki Yoshitomi Hideki Ueno Department of Immunology Graduate School of MedicineKyoto UniversitySakyo-kuf Kyoto 606-8501Japan lnstitute for the Advanced Study of Human Biology Kyoto UniversitySakyo-kuKyoto 606-8501Japan Department of Microbiology Icahn School of Medicine at Mount SinaiNew York 10029 NYUSA Global Health and Emerging Pathogens Institute Icahn School of Medicine at Mount SinaiNew York 10029 NYUSA

the interactions of CD4^(+)t cells and B cells are fundamental for the generation of protective antibody responses,as well as for the development of harmful autoimmune diseases.Recent studies of human tissues and blood samples have established a new subset of CD4^(+)B helper t cells named peripheral helper t(tph)cells.Unlike t follicular helper(tfh)cells,which interact with B cells within lymphoid organs,tph cells provide help to B cells within inflamed tissues.tph cells share many B helper-associated functions with tfh cells and induce B cell differentiation toward antibody-producing cells.the differentiation mechanism is also partly shared between tph and tfh cells in humans,and both tfh and tph cells can be found within the same tissues,including cancer tissues.However,tph cells display features distinct from those of tfh cells,such as the expression of chemokine receptors associated with tph cell localization within inflamed tissues and a low Bd-6/Blimp1 ratio.Unlike that of tfh cells,current evidence shows that the target of tph cells is limited to memory B cells.In this review,we first summarize recent findings on human tph cells and discuss how tph and tfh cells play shared and distinct roles in human diseases.

关键词： peripheral helper t cells t follicular helper cells CXCL13,Autoantibodies autoimmune diseases

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IL-10-producing regulatory B cells restrain the t follicular helper cell response in primary Sjögren’s syndrome

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Cellular & Molecular Immunology 2019年第12期16卷 921-931页

作者： Xiang Lin Xiaohui Wang Fan Xiao Kongyang Ma Lixiong Liu Xiaoqi Wang Dong Xu Fei Wang Xiaofei Shi Dongzhou Liu Yan Zhao Liwei Lu Department of Pathology and Shenzhen Institute of Research and Innovation The University of Hong KongHong KongChina Department of Rheumatology and Immunology Second Clinical Medical College of Jinan UniversityShenzhen People’s HospitalShenzhenChina Department of Rheumatology Peking Union Medical College HospitalBeijingChina Department of Rheumatology The First Affiliated Hospital and College of Clinical MedicineHenan University of Science and TechnologyLuoyangChina

Increased numbers of t follicular helper(tfh)cells have been implicated in the development of autoimmune diseases including primary Sjögren’s syndrome(pSS),but how the tfh cell response is regulated during autoimmune pathogenesis remains largely unclear.Here,we first found negative correlations between IL-10^(+)regulatory B(Breg)cell numbers and tfh cell responses and disease activity in patients with pSS and mice with experimental Sjögren’s syndrome(ESS).Moreover,we detected high expression of IL-10 receptor on tfh cells and their precursors in both humans and mice.In culture,IL-10 suppressed human and murine tfh cell differentiation by promoting StAt5 phosphorylation.By using an adoptive transfer approach and two-photon live imaging,we found significantly increased numbers of tfh cells with enhanced t cell homing into B cell follicles in the draining cervical lymph nodes of RAG-2−/−mice transferred with IL-10-deficient B cells during ESS development compared with those of RAG-2−/−mice transferred with wild-type B cells.In ESS mice,CD19^(+)CD1d^(hi)CD5^(+)Breg cells with decreased IL-10 production exhibited severely impaired suppressive effects on t cell proliferation.Consistently,CD19^(+)CD24^(+)CD38^(hi) Breg cells from pSS patients showed significantly reduced IL-10 production with defective inhibitory function in the suppression of autologous tfh cell expansion.Furthermore,the adoptive transfer of IL-10-producing Breg cells markedly suppressed the tfh cell response and ameliorated ESS progression in ESS mice.together,these findings demonstrate a critical role for IL-10-producing Breg cells in restraining the effector tfh cell response during pSS development.

关键词： Primary Sjögren’s syndrome t follicular helper cells Breg cells

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Characterization of t follicular helper cells during normal and aborted pregnancies

Characterization of T follicular helper cells during normal ...

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第十一届全国免疫学学术大会

作者： Zeng Weihong Liu Zhicui Zhang Siming Lin Yi Institute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao tong University School of Medicine the International Peace Maternity & Child Health Hospital Shanghai Jiao Tong University School of Medicine Department of Dermatology Ruijin Hospital Shanghai Jiaotong University School of Medicine

Background:A deeper understanding of the immunological events during pregnancy will provide novel insights into the pathogenesis of pregnancy complications.the fundamental function of t follicular helper(tfh)cells is to provide cognate help to B cells and dysregulations of tfh-cell function and/or development can result in various immunological diseases.However,the role and characteristics of tfh cells during pregnancy remain unknown.

关键词： t follicular helper cells allogeneic-normal-pregnancy PDL1 aborted pregnancy

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transcription tipping points for t follicular helper cell and t-helper 1 cell fate commitment

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Cellular & Molecular Immunology 2021年第3期18卷 528-538页

作者： Amania A.Sheikh Joanna R.Groom Divisions of Immunology and Molecular Immunology Walter and Eliza Hall Institute of Medical ResearchParkvilleVIC 3052Australia Department of Medical Biology University of MelbourneParkvilleVIC 3010Australia

During viral infection,immune cells coordinate the induction of inflammatory responses that clear infection and humoral responses that promote protection.CD4^(+)t-cell differentiation sits at the center of this axis.Differentiation toward t-helper 1(th1)cells mediates inflammation and pathogen clearance,while t follicular helper(tfh)cells facilitate germinal center(GC)reactions for the generation of high-affinity antibodies and immune memory.While th1 and tfh differentiation occurs in parallel,these CD4^(+)t-cell identities are mutually exclusive,and progression toward these ends is determined via the upregulation of t-bet and Bcl6,respectively.these lineage-defining transcription factors act in concert with multiple networks of transcriptional regulators that tip the t-bet and Bd6 axis in CD4^(+)t-cell progenitors to either a th1 or tfh fate.It is now clear that these transcriptional networks are guided by cytokine cues that are not only varied between distinct viral infections but also dynamically altered throughout the duration of infection.thus,multiple intrinsic and extrinsic factors combine to specify the fate,plasticity,and function of th1 and tfh cells during infection.Here,we review the current information on the mode of action of the lineage-defining transcription factors Bcl6 and t-bet and how they act individually and in complex to govern CD4^(+)t-cell ontogeny.Furthermore,we outline the multifaceted transcriptional regulatory networks that act upstream and downstream of Bcl6 and t-bet to tip the differentiation equilibrium toward either a tfh or th1 fate and how these are impacted by dynamic inflammatory cues.

关键词： Cytokines Infection t follicular helper cells t-helper 1 cells transcription factors

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t follicular helper expansion and humoral-mediated rejection are independent of the HVEM/BtLA pathway

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Cellular & Molecular Immunology 2017年第6期14卷 497-510页

作者： Jose-Ignacio Rodriguez-Barbosa Carlos Fernandez-Renedo Ana Maria Bravo Moral Leo Biihler Maria-Luisa del Rio transplantation Immunobiology Section Institute of Biomedicine University of Leon and Castilla and Leon Regional Transplantation Coordination Leon University Hospital Leon Spain Department of Veterinary Clinical Sciences University of Santiago de Compostela Veterinary Faculty Lugo Spain Visceral and transplantation Surgery Department of Surgery University Hospitals of Geneva and Faculty of Medicine Geneva Switzerland

the molecular pathways contributing to humoral-mediated allograft rejection are poorly defined. In this study, we assessed the role of the herpesvirus entry mediator/B- and t-lymphocyte attenuator （HVEM/BtLA） signalling pathway in the context of antibody-mediated allograft rejection. An experimental setting was designed to elucidate whether the blockade of HVEM/BtLA interactions could modulate de novo induction of host antidonor-specific antibodies during the course of graft rejection. to test this hypothesis, fully allogeneic major histocompatibility complex-mismatched skin grafts were transplanted onto the right flank of recipient mice that were treated with isotype control, anti-CD40L or modulatory antibodies of the HVEM/BtLA signalling pathway. the frequencies of CD4 t follicular helper （tfh） cells （B220-, CD4＋ CXCR5＋ PD-lhigh）, extrafollicular helper cells （B220-, CD4＋ CXCR5- PD-1＋ and PD-1-） and germinal centre （GC） B cells （B220＋Fas＋ GL7＋） were analysed by flow cytometry in draining and non-draining lymph nodes at day 10 post transplantation during the acute phase of graft rejection. the host antidonor isotype-specific humoral immune response was also assessed. Whereas blockade of the CD40/CD40L pathway was highly effective in preventing the allogeneic humoral immune response, antibody-mediated blockade of the HVEM/BtLA-interacting pathway affected neither the expansion of tfh cells nor the expansion of GC B cells. Consequently, the course of the host antidonor antibody-mediated response proceeded normally, without detectable evidence of impaired development. In summary, these data indicate that HVEM/BtLA interactions are dispensable for the formation of de novo host antidonor isotype-specific antibodies in transplantation.

关键词： BtLA （CD272） humoral immunity HVEM （tNFRSF14, CD270） t follicular helper cells transplantation

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the ubiquitin ligase Pelil inhibits ICOS and thereby tfh-mediated immunity

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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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Deficiency of tfh cells and Germinal Center in Deceased COVID-19 Patients

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Current Medical Science 2020年第4期40卷 618-624页

作者： Ya-qi DUAN Ming-hui XIA Liang REN Yan-fang ZHANG Qi-lin AO San-peng XU Dong KUANG Qian LIU Bing YAN Yi-wu ZHOU Qian CHU Liang LIU Xiang-Ping YANG Guo-ping WANG Institute of Pathology Tongjii HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Pathology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Immunology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Forensic Medicine Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China State Key Laboratory of Virology Wuhan Institute of VirologyCenter for Biosafety Mega ScienceChinese Academy of SciencesWuhan 430071China Department of Oncology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

Summary:the COVID-19 pandemic caused by SARS-CoV2 is characterized by a remarkable variation in clinical severity ranging from a mild illness to a fatal multi-organ disease.Understanding the dysregulated human immune responses in the fatal subjects is critical for management of COVID-19 patients and the pandemic.In this study,we examined the immune cell compositions in the lung tissues and hilar lymph nodes using immunohistochemistry on 6 deceased COVID-19 patients and 4 focal organizing pneumonia(FOP)patients who underwent lung surgery and served as controls.We found a dominant presence of macrophages and a general deficiency of t cells and B cells in the lung tissues from deceased COVID-19 patients.In contrast to the FOP patients,tfh cells and germinal center formation were largely absent in the draining hilar lymph nodes in the deceased COVID-19 patients.this was correlated with reduced IgM and IgG levels compared to convalescent COVID-19 patients.In summary,our data highlight a defect of germinal center structure in deceased COVID-19 patients leading to an impaired humoral immunity.Understanding the mechanisms of this deficiency will be one of the key points for the management of this epidemic.

关键词： COVID-19 immune responses germinal center t follicular helper cells

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