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Oxidized galectin-1 in SLE fails to bind the inhibitory receptor VSTM1 and increases reactive oxygen species levels in neutrophils

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Cellular & Molecular Immunology 2023年第11期20卷 1339-1351页

作者： Xu Jiang Xinyue Xiao Hao Li Yiyi Gong Min Wang Huaxia Yang Lidan Zhao Ying Jiang Yanping Wei Chongchong Zhao Jin Li Yuling Chen Shan Feng Haiteng Deng Shiliang Ma Yue Xu Yudong Liu George C.Tsokos Minghong Jiang Xuan Zhan Medical Research Center State Key Laboratory of Complex Severe and Rare DiseasesPeking Union Medical College HospitalDepartment of RheumatologyBeijing HospitalNational Center of GerontologyInstitute of Geriatric MedicineChinese Academy of Medical SciencesBeijingChina Department of rheumatology Key Laboratory of MyositisChina-Japan Friendship HospitalBeijingChina Department of Medicine Beth Israel Deaconess Medical CenterHarvard Medical SchoolBostonMAUSA Medical Research Center Peking Union Medical College HospitalChinese Academy of Medical SciencesBeijingChina Department of rheumatology Beijing HospitalNational Center of GerontologyInstitute of Geriatric MedicineClinical Immunology CenterChinese Academy of Medical SciencesBeijingChina Department of rheumatology and Clinical Immunology Peking Union Medical College HospitalClinical Immunology CenterChinese Academy of Medical Sciences and Peking Union Medical CollegeThe Ministry of Education Key LaboratoryBeijingChina Department of rheumatology Xiangya HospitalCentral South UniversityHunanChina MOE Key Laboratory of Bioinformatics Center for Synthetic&Systems BiologySchool of Life SciencesTsinghua UniversityBeijingChina Key Laboratory of Structural Biology of Zhejiang Province School of Life SciencesWestlake UniversityHangzhouZhejiangChina State Key Laboratory of Common Mechanism Research for Major Diseases Institute of Basic Medical Sciences Chinese Academy of Medical SciencesSchool of Basic Medicine Peking Union Medical CollegeBeijingChina

Inhibitory immune receptors set thresholds for immune cell activation,and their deficiency predisposes a person to autoimmune responses.However,the agonists of inhibitory immune receptors remain largely unknown,representing untapped sources of treatments for autoimmune diseases.Here,we show that V-set and transmembrane domain-containing 1(VSTM1)is an inhibitory receptor and that its binding by the competent ligand soluble galectin-1(Gal1)is essential for maintaining neutrophil viability mediated by downregulated reactive oxygen species production.However,in patients with systemic lupus erythematosus(SLE),circulating Gal1 is oxidized and cannot be recognized by VSTM1,leading to increased intracellular reactive oxygen species levels and reduced neutrophil viability.Dysregulated neutrophil function or death contributes significantly to the pathogenesis of SLE by providing danger molecules and autoantigens that drive the production of inflammatory cytokines and the activation of autoreactive lymphocytes.Interestingly,serum levels of glutathione,an antioxidant able to convert oxidized Gal1 to its reduced form,were negatively correlated with SLE disease activity.Taken together,our findings reveal failed inhibitory Gal1/VSTM1 pathway activation in patients with SLE and provide important insights for the development of effective targeted therapies.

关键词： Systemic lupus erythematosus ROS VSTM1 Galectin-1 Glutathione

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A Common Functional Variant at the Enhancer of the Rheumatoid Arthritis Risk Gene ORMDL3 Regulates its Expression Through Allele-Specific JunD Binding

Phenomics

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Phenomics 2023年第5期3卷 485-495页

作者： Wenjing Ye Yiyun Yu Xiaoxia Zhu Weiguo Wan Yun Liu Hejian Zou Zaihua Zhu Division of rheumatology and Immunology Huashan HospitalFudan UniversityShanghai 200040China institute of rheumatology Immunology and AllergyFudan UniversityShanghai 200040China The Ministry of Education Key Laboratory of Metabolism and Molecular Medicine Department of Biochemistry and Molecular BiologySchool of Basic Medical SciencesFudan UniversityShanghai 200032China

Genome-wide association studies(GWASs)have identified over 100 loci associated with rheumatoid arthritis(RA);how-ever,the functionally affected genes and the underlying molecular mechanisms contributing to these associations are often unknown.In this study,we conducted an integrative genomic analysis incorporating multiple“omics”data and identified a functional regulatory DNA variant,rs56199421,and a plausible mechanism by which it regulates the expression of a puta-tive RA risk gene,ORMDL Sphingolipid Biosynthesis Regulator 3(ORMDL3).The T allele of rs56199421,located in the enhancer region of ORMDL3,exhibited stronger direct binding ability than the other C allele of rs56199421 did in vitro with the transcription factor JunD and demonstrated higher transcriptional activity.Moreover,the T allele of rs56199421 is associated with elevated RA risk,and ORMDL3 expression is increased in RA patients.Thus,these findings suggest that the T allele of rs56199421 enhances JunD transcription factor binding,increases enhancer activity,and elevates the expression of the RA risk gene ORMDL3.

关键词： Rheumatoid arthritis Genome-wide association study Enhancer ORMDL Sphingolipid Biosynthesis Regulator 3

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Epigenetic regulation of B cells and its role in autoimmune pathogenesis

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Cellular & Molecular Immunology 2022年第11期19卷 1215-1234页

作者： Fan Xiao Ke Rui Xiaofei Shi Haijing Wu Xiaoyan Cai Kathy O.Lui Qianjin Lu Esteban Ballestar Jie Tian Hejian Zou Liwei Lu Department of Pathology Shenzhen Institute of Research and Innovation and Shenzhen HospitalThe University of Hong KongHong KongChongqing International Institute for ImmunologyChongqingChina institute of Medical Immunology Affiliated Hospital of Jiangsu UniversityZhenjiangChina Department of rheumatology and Immunology The First Affiliated Hospital and School of MedicineHenan University of Science and TechnologyLuoyangChina Department of Dermatology Second Xiangya HospitalCentral South UniversityHunan Key Laboratory of Medical EpigenomicsChangshaHunanChina Department of rheumatology Guangzhou First People’s HospitalSchool of MedicineSouth China University of TechnologyGuangzhouChina Department of Chemical Pathology Faculty of MedicinePrince of Wales HospitalThe Chinese University of Hong KongHong KongChina Epigenetics and Immune Disease Group Josep Carreras Research InstituteBadalona08916 BarcelonaSpain Epigenetics in Inflammatory and Metabolic Diseases Laboratory Health Science CenterEast China Normal UniversityShanghaiChina Department of rheumatology Huashan HospitalFudan UniversityShanghaiChina Centre for Oncology and Immunology Hong Kong Science ParkHong KongChina

B cells play a pivotal role in the pathogenesis of autoimmune diseases.Although previous studies have shown many genetic polymorphisms associated with B-cell activation in patients with various autoimmune disorders,progress in epigenetic research has revealed new mechanisms leading to B-cell hyperactivation.Epigenetic mechanisms,including those involving histone modifications,DNA methylation,and noncoding RNAs,regulate B-cell responses,and their dysregulation can contribute to the pathogenesis of autoimmune diseases.Patients with autoimmune diseases show epigenetic alterations that lead to the initiation and perpetuation of autoimmune inflammation.Moreover,many clinical and animal model studies have shown the promising potential of epigenetic therapies for patients.In this review,we present an up-to-date overview of epigenetic mechanisms with a focus on their roles in regulating functional B-cell subsets.Furthermore,we discuss epigenetic dysregulation in B cells and highlight its contribution to the development of autoimmune diseases.Based on clinical and preclinical evidence,we discuss novel epigenetic biomarkers and therapies for patients with autoimmune disorders.

关键词： B cells Epigenetic regulation Autoimmune disease Biomarker Therapy

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Beyond interleukin-17-targeted therapy: Complexity of environment-genetics-immunology needs to be addressed

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Chinese Medical Journal 2022年第5期135卷 511-512页

作者： Xin Wu Huji Xu Chen Dong Department of rheumatology and Immunology Changzheng HospitalSecond Military Medical UniversityShanghai 200003China Shanghai Immune Therapy institute Shanghai Jiaotong University School of Medicine-affiliated Renji HospitalShanghai 200127China

Ankylosing spondylitis(AS)is a prototype of spondyloarthritis(SpA)with long-term joint inflammation of the spine.SpA manifestations also include psoriasis,uveitis,and inflammatory bowel disease,which suggest these dis... 详细信息

关键词： inflammation diseases targeted

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3D Bioprinting for Biomedical Applications

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Biomedical Engineering Frontiers 2023年第1期4卷 199-202页

作者： Bin Kong Yuanjin Zhao Department of rheumatology and Immunology Institute of Translational MedicineThe Affiliated Drum Tower Hospital of Nanjing University Medical SchoolNanjing 210002China Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine Vision and Brain Health)Wenzhou InstituteUniversity of Chinese Academy of SciencesWenzhouZhejiang 325001China Chemistry and Biomedicine Innovation Center Nanjing UniversityNanjing 210023China

Three-dimensional(3D)printing,referring to a type of additive manufacturing,has emerged as a promising fabrication technique in the past decades since it can create 3D objects with desired architecture by precise control over the deposition of successive layers of various materials.Benefiting from these advantages,3D printing has been extensively applied in varied areas of science and engineering.

关键词： materials printing precise

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Expression of C5aR ( CD88) of synoviocytes isolated from patients with rheumatoid arthritis and osteoarthritis

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Chinese Medical Journal 2003年第9期116卷 1408-1412页

作者：袁国华魏锦周京国胡宏唐中张国元 institute of rheumatology and Immunology Affiliated Hospital of North Sichuan Medical College Nanchong 637000 China

Objective To investigate the expression of anaphylatoxin receptor C5aR (CD88) in synoviocytes from patients with rheumatoid arthritis (RA) and osteoarthritis (OA).Methods The expression of C5aR was assessed in synoviocytes isolated from 27 RA and 12 OA patients using reverse transcription-polymerase chain reactions (RT-PCR), flow cytometry, and immunofluorescence analysis. The effects of C5a on the release of tumor necrosis factor a (TNFα) from synoviocytes were assayed using enzyme-linked immunosorbent assays (ELISA).Results C5aR mRNA was detected in 24 of 27 samples from RA patients, and 10 of 12 samples from OA patients. Flow cytometric analysis and immunofluorescence study demonstrated the cell surface expression of C5aR in a significant proportion of synoviocytes from both RA and OA patients, and the level of C5aR expression in synoviocytes was significantly correlated with joint swelling, erythrocyte sedimentation rate ( ESR) and C-reactive protein ( CRP) in RA patients. Finally, interaction of C5aR with its ligand C5a was shown to enhance lipopolysaccharide (LPS) -induced TNFa release from synoviocytes.Conclusions The expression of C5aR in synoviocytes from inflammatory joint diseases and also the induction of TNFa release in activated synovicytes by the interaction of C5a and C5aR suggest that the C5a/C5aR system may play an important role in joint inflammation process.

关键词： C5a receptor·synoviocytes·arthritis rheumatoid·osteoarthritis

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COVID-19 Induced Mixed Connective Tissue Disease (MCTD)—Case Report

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Case Reports in Clinical Medicine 2022年第9期11卷 393-398页

作者： Cintia Nagy-Kardos Dominique Zö ld László Tihanyi Gábor Veress National Heart institute Balatonfüred National Institute for Rheumatology and Physiotherapy Budapest Hungary

Mixed connective tissue disease (MCTD) is a rare systemic autoimmune disorder that damages multiple organs simultaneously and is associated with chronic inflammation, in which the signs of systemic sclerosis, systemic lupus erythematosus, and polymyositis can co-occur. Its distinctive feature and the basis for the diagnosis of MCTD is the presence of an antibody against the uridine-rich RNP of the cell nucleus (Anti-U1-RNP). It has been observed that intercurrent infections can trigger autoimmune diseases, however, the fact that viral infections—such as SARS-CoV-2—induce them is currently poorly understood. The present study raises the etiological role of the SARS-CoV-2 virus in the development of the disease. Authors describe the case of a 38-year-old patient in good general condition, who was diagnosed with mixed connective tissue disease three months after COVID-19 infection.

关键词： Mixed Connective Tissue Disease (MCTD) Anti-U1-RNP Antibody SARS-CoV-2 COVID-19 Infection Post-COVID Syndrome

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Innate and adaptive immune abnormalities underlying autoimmune diseases:the genetic connections

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Science China(Life Sciences) 2023年第7期66卷 1482-1517页

作者： Xinxin Chi Miaozhen Huang Hailin Tu Bin Zhang Xin Lin Huji Xu Chen Dong Xiaoyu Hu institute for Immunology&School of Medicine Tsinghua UniversityBeijing 100084China Department of rheumatology and Immunology Shanghai Changzheng HospitalThe Second Military Medical UniversityShanghai 200433China Peking-Tsinghua Center for Life Sciences Tsinghua UniversityBeijing100084China Shanghai Immune Therapy institute Shanghai Jiaotong University School of Medicine-affiliated Renji HospitalShanghai 200127China

With the exception of an extremely small number of cases caused by single gene mutations,most autoimmune diseases result from the complex interplay between environmental and genetic factors.In a nutshell,etiology of the common autoimmune disorders is unknown in spite of progress elucidating certain effector cells and molecules responsible for pathologies associated with inflammatory and tissue damage.In recent years,population genetics approaches have greatly enriched our knowledge regarding genetic susceptibility of autoimmunity,providing us with a window of opportunities to comprehensively re-examine autoimmunity-associated genes and possible pathways.In this review,we aim to discuss etiology and pathogenesis of common autoimmune disorders from the perspective of human genetics.An overview of the genetic basis of autoimmunity is followed by3 chapters detailing susceptibility genes involved in innate immunity,adaptive immunity and inflammatory cell death processes respectively.With such attempts,we hope to expand the scope of thinking and bring attention to lesser appreciated molecules and pathways as important contributors of autoimmunity beyond the‘usual suspects’of a limited subset of validated therapeutic targets.

关键词： autoimmune diseases etiology pathogenesis innate immunity adaptive immunity

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Atypical Cogan＇s syndrome associated with coronary disease

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Chinese Medical Journal 2011年第19期124卷 3192-3194页

作者： Ivanovic Branislava Tadic Marijana Damjanov Nemanja Simic Dragan Zlatanovic Maja Clinic for Cardiology Clinical Centre of Serbia Belgrade 11000 Serbia institute of rheumatology Belgrade 11000 Serbia

Cogan＇s syndrome （CS） is a rare inflammatory disorder characterized by interstitial keratitis and vestibuloauditory abnormalities often associated with various systemic manifestations. Involvement of cardiovascular system resembling systemic vasculitis may lead to severe complications and death. The present report describes a case of a female patient with atypical Cogan＇s syndrome presented with systemic manifestations and severe coronary and femoral artery stenosis Despite the clinical improvement after glucocorticoids and cyclophosphamide, the patient required double aortocoronal bypass grafting one year letter. During three years follow-up, she was in stable condition, without stenocardial symptoms and claudication and her inflammatory parameters remain normal. This case highlights the rare involvement of coronary arteries without associated large-vessel vasculitis of the aortic arch in CS.

关键词： Cogan＇s syndrome hearing loss coronary artery disease

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CARs:a new approach for the treatment of autoimmune diseases

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Science China(Life Sciences) 2023年第4期66卷 711-728页

作者： Yeting Sun Yeshuang Yuan Bo Zhang Xuan Zhang Graduate School of Peking Union Medical College Department of RheumatologyBeijing HospitalNational Center of GerontologyInstitute of Geriatric MedicineState Key Laboratory of Complex Severe and Rare DiseasesPeking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China State Key Laboratory of Complex Severe and Rare Diseases Peking Union Medical College HospitalChinese Academy of Medical SciencesBeijing 100730China Department of rheumatology Beijing HospitalNational Center of GerontologyInstitute of Geriatric MedicineClinical Immunology CenterChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China

The development of chimeric antigen receptor(CAR)-based therapeutic interventions represented a breakthrough in cancer treatment.Following the success of the CAR-T-cell strategy,this novel therapeutic approach has been applied to other diseases,including autoimmune diseases.Using CAR-T cells to deplete pathological immune cells(i.e.,B cells,autoreactive B or T cells,and accessory antigen-presenting cells(APCs))has resulted in favorable outcomes in diseases characterized by excessive autoantibody levels or hyperactive lymphocyte cell numbers.The importance of immunosuppressive regulatory Tcells(Tregs)in restoring immune tolerance has been well established,and CAR-Tregs have shown promising therapeutic potential in treating autoimmune diseases.Moreover,prior experience from the cancer field has provided sufficient paradigms for understanding how to optimize the structure and function of CARs to improve their function,persistence,stability and safety.In this review,we describe the potential application of CAR-T cells and CAR-Tregs in the treatment of autoimmune diseases,and we summarize the currently available strategies of gene editing and synthetic biological tools that have improved the practical application of CAR-based therapies.

关键词： autoimmune diseases chimeric antigen receptor regulatory T cells cellular therapy

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