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World Journal of Hepatology 2015年第3期7卷 344-361页

作者： Francesca De Nard Monica Todoerti Vittorio Grosso Sara Monti Silvia Breda Silvia Rossi Carlomaurizio Montecucco Roberto Caporali IRCCS Policlinico San Matteo Foundation Chair and Division of Rheumatology University of Pavia

Hepatitis B virus(HBV) reactivation in rheumatoid arthritis(RA) patients undergoing biological therapy is not infrequent. This condition can occur in patients with chronic hepatitis B as well as in patients with resolved HBV infection. Current recommendations are mainlyfocused on prevention and management strategies of viral reactivation under tumor necrosis factor-α inhibitors or chimeric monoclonal antibody rituximab. In recent years, growing data concerning HBV reactivation in RA patients treated with newer biological drugs like tocilizumab and abatacept have cumulated. In this review, epidemiology, pathogenesis and natural history of HBV infection have been revised first, mainly focusing on the role that specific therapeutic targets of current biotechnological drugs play in HBV pathobiology; finally we have summarized current evidences from scientific literature, including either observational studies and case reports as well, concerning HBV reactivation under different classes of biological drugs in RA patients. Taking all these evidences into account, some practical guidelines for screening, vaccination, prophylaxis and treatment of HBV reactivation have been proposed.

关键词： Rheumatoid arthritis Hepatitis B virus Biologics Anti-TNF Rituximab Tocilizumab Abatacept

Successful rescue of acute liver failure and hemophagocytic lymphohistiocytosis following varicella infection: A case report and review of literature

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World Journal of Clinical Cases 2018年第13期6卷 659-665页

作者： Li-Na Zhang Wei Guo Ji-Hong Zhu Yang Guo Department of rheumatology and Immunology Peking University People’s Hospital Department of Emergency Peking University People’s Hospital

Herein we report a case of acute liver failure(ALF) and hemophagocytic lymphohistiocytosis(HLH) induced by varicella infection, successfully rescued by a combination therapy of acyclovir, supportive care, and immunosuppression with dexamethasone and etoposide. A previously healthy 16-year-old boy presented with generalized rash, fever, severe abdominal pain, and abnormal liver function within 4 d. Chickenpox was suspected, and acyclovir and intravenous immunoglobulin were started on admission. However, the patient's condition deteriorated overnight with soaring transaminases, severe coagulopathy and encephalopathy. On the fourth day of admission, pancytopenia emerged, accompanied by hypofibrinogenemia and hyperferritinemia. The patient was diagnosed with ALF. He also met the diagnostic criteria of HLH according to the HLH-2004 guideline. Polymerase chain reaction(PCR) amplifications of varicella-zoster virus(VZV) were positive, confirming that VZV was a causative trigger for ALF and HLH. In view of the devastating immune activation in HLH, immunosuppression therapy with dexamethasone and etoposide was administered, in addition to high dose acyclovir. The patient's symptoms improved dramatically and he finally made a full recovery. To our knowledge, this is only the second report of a successful rescue of ALF associated with HLH, without resorting to liver transplantation. The first case was reported in a neonate infected by herpes simplex virus-1. However, survival data in older children and adults are lacking, most of whom died or underwent liver transplantation. Our report emphasizes the clinical vigilance for the possible presence of HLH, and the necessity of extensive investigation for underlying etiologies in patients presenting with indeterminate ALF. Early initiation of specific therapy targeting the underlying etiology, and watchful immunosuppression such as dexamethasone and etoposide, together with supportive therapy, are of crucial importance in this life

关键词： Acute liver failure Immune dysregulation Hyperferritinemia Hemophagocytic lymphohistiocytosis Varicella infection Skin rash

Logistic Regression Analysis of Damp-Heat and Cold Damp Impeding Syndrome of Rheumatoid Arthritis:A Perspective in Chinese Medicine

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Chinese Journal of Integrative Medicine 2012年第8期18卷 575-581页

作者：王志中方勇飞王勇牟方祥陈军邹庆华钟兵李景怡柏干苹张荣华 Department of rheumatology Southwest HospitalThird Military Medical University Department of Health Statistics Third Military Medical University

Objective： To investigate a method for quantitative differential diagnosis of damp-heat and cold-damp impeding syndrome of rheumatoid arthritis （RA） in Chinese medicine （CM）. Methods： Laboratory parameters were collected from 306 patients with RA. The clinical symptoms and laboratory parameters were compared between patients with these two syndromes （158 with RA of damp-heat impeding syndrome, and 148 with RA of cold-damp impeding syndrome）, and a regression equation was established to facilitate discrimination of the two RA syndromes. Results： There were significant differences in disease activity score in 28 joints [DAS28 （4）], erythrocyte sedimentation rate （ESR）, white blood cell count （WBC）, C-reactive protein （CRP）, platelet count （PLT）, albumin （ALB） and globulin （GLB） between the two syndrome of RA （P〈0.05）. Logistic regression analysis showed that the parameters ESR, WBC, CRP, joint pyrexia, joint cold, thirst, sweating, aversion to wind and cold, and cold extremities were statistically useful to discriminate damp-heat from cold-damp impeding syndrome. The regression equation was as follows： P=1/{1＋exp[-（3.0-0.021X1-0.196X2-0.163X3- 1.559X4＋1.504X5-0.927X6-1.039X7＋1.070X8＋1.330X9）]}. The independent variables X1-X9 were ESR, WBC, CRP, hot joint, cold joint, thirst, sweating, aversion to wind and cold, and cold limbs. A P value 〉 0.5 signified cold-damp impeding syndrome, and a P value 〈 0.5 signified damp-heat impeding syndrome. The accuracy was 90.2%. Conclusion： The regression equation may be useful for discriminating damp-heat from cold-damp impeding syndrome of RA.

关键词： logistic regression damp-heat impeding syndrome cold-damp impeding syndrome rheumatoid arthritis quantitative diagnosis

Cellular and molecular mechanisms breaking immune tolerance in inborn errors of immunity

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Cellular & Molecular Immunology 2021年第5期18卷 1122-1140页

作者： Georgios Sogkas Faranaz Atschekzei Ignatius Ryan Adriawan Natalia Dubrowinskaja Torsten Witte Reinhold Ernst Schmidt Department of rheumatology and Immunology Hannover Medical SchoolHanoverGermany Hannover Medical School Cluster of Excellence RESIST(EXC 2155)HanoverGermany

In addition to susceptibility to infections,conventional primary immunodeficiency disorders(PIDs)and inborn errors of immunity(IEI)can cause immune dysregulation,manifesting as lymphoproliferative and/or autoimmune *** can be the prominent phenotype of PIDs and commonly includes cytopenias and rheumatological diseases,such as arthritis,systemic lupus erythematosus(SLE),and Sjogren’s syndrome(SjS).Recent advances in understanding the genetic basis of systemic autoimmune diseases and PIDs suggest an at least partially shared genetic background and therefore common pathogenic ***,we explore the interconnected pathogenic pathways of autoimmunity and primary immunodeficiency,highlighting the mechanisms breaking the different layers of immune tolerance to self-antigens in selected IEI.

关键词： Inborn errors of immunity Primary immunodeficiencies Autoimmunity Rheumatic diseases

TGF-β-induced CD4+FoxP3+regulatory T cell-derived extracellular vesicles modulate Notch1 signaling through miR-449a and prevent collagen-induced arthritis in a murine model

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Cellular & Molecular Immunology 2021年第11期18卷 2516-2529页

作者： Jingrong Chen Feng Huang Yuluan Hou Xiaorong Lin Rongzhen Liang Xiaojiang Hu Jun Zhao Julie Wang Nancy Olsen Song Guo Zheng Department of Clinical Immunology The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdongChina Department of Internal Medicine Division of RheumatologyThe Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdongChina Division of rheumatology Department of MedicinePenn State University Hershey Medical CenterHersheyPAUSA

CD4^(+)FOXP3^(+)Treg cells are central to the maintenance of self-tolerance and can be defective in *** autoimmune rheumatic diseases,dysfunctional self-tolerance,is to a large extent,caused by insufficient Treg-cell *** nTregs have therapeutic effects in vivo,their relative scarcity and slow rate of in vitro expansion hinder the application of nTreg *** was previously reported that EVs contribute significantly to the suppressive function of FOXP3^(+)Treg *** that the stability and plasticity of nTregs remain major challenges in vivo,we established EVs derived from in vitro TGF-β-induced Treg cells(iTreg-EVs)and assessed their functions in a murine model of autoimmune *** results demonstrated that iTreg-EVs preferentially homed to the pathological joint and efficiently prevented the imbalance in Th17/Treg cells in arthritic ***,we found that miR-449a-5p mediated Notch1 expression modulation and that miR-449a-5p knockdown abolished the effects of iTreg-EVs on effector T cells and regulatory T cells in vitro and in *** together,our results show that iTreg-EVs control the inflammatory responses of recipient T cells through miR-449a-5p-dependent modulation of Notch1 and ameliorate the development and severity of arthritis,which may provide a potential cell-free strategy based on manipulating iTreg-EVs to prevent autoimmune arthritis.

关键词： EVs iTreg Arthritis Th17 MicroRNA Notch1

Correlation of Thl7 cells and CD4＋CD25＋ regulatory T cells with clinical parameters in patients with systemic sclerosis

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Chinese Medical Journal 2014年第20期127卷 3557-3561页

作者： Jiang Nan Li Mengtao Zeng Xiaofeng Department of Internal Medicine Department of rheumatology

Background Systemic sclerosis （SSc） is an autoimmune disease that has three major components： inflammation, fibrosis, and vasculopathy. T-helper 17 cell （Th17） and regulatory T cell （Treg） are considered to be critical for autoimmune disease pathogenesis. The role of Th17 and Treg in SSc is still unclear. The aim of this study was to detect the presence of Th17s and CD4＊CD25~ Tregs in peripheral blood samples from SSc patients and to investigate the possible roles of these two T cell subsets in SSc pathogenesis. Methods Th17s （CD4 and IL-17 positive） and CD4＊CD25~ Tregs （CD4, CD25 and Foxp3 positive） in the peripheral blood mononuclear cells of 53 SSc patients and 27 healthy controls were counted by flow cytometry. The differences between SSc and control patients were analyzed. Clinical parameters, including disease duration, duration of the second symptoms, Modified Rodnan Skin Score （MRSS）, anti-topoisomerase I antibody, anti-U1 ribonucleoprotein （RNP） antibody, systemic involvements, pulmonary function test （PFT） and high resolution computed tomography （HRCT） score were prospectively collected following EUSTAR （EULAR scleroderma trial and research group） protocols. The correlations between the experimental and clinical data were investigated. Results The ratio of Th17 in SSc patients was significantly elevated compared to healthy controls （8.74% vs. 4.41%, P 〈0.001）. The amount of Th17 was positively correlated with disease duration （R=-0.531, P=-0.013） and duration of the second symptoms （R=-0.505, P=0.023）. The ratio of CD4＊CD25＊ Treg in SSc patients also significantly differed from the healthy controls （3.04% vs. 2.24%, P=0.018）. Elevated Tregs were more frequently observed in patients with a high interstitial lung disease （ILD） score on computed tomography （24/36） compared with patients with normal ILD scores （4/12, ,P=-0.043）. Elevated Tregs were also more often observed in patients with low carbon monoxide diffusing capacity （DLCO）（24/34） compared with pat

关键词： scleroderma, systemic Thl 7 cells T-lymphoeytes, regulatory

Effect of cream, prepared with Tripterygium wilfordii Hook F and other four medicinals, on joint pain and swelling in patients with rheumatoid arthritis: a double-blinded, randomized, placebo controlled clinical trial

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Journal of Traditional Chinese Medicine 2019年第1期39卷 89-96页

作者： Jiao Juan Wei Chengchung Tang Xiaopo Gong Xun Yin Haibo Jiang Quan Department of rheumatology Guang'anmen Hospital Affiliated to China Academy of Chinese Medical SciencesBeijing 100053China Division of Allergy Immunology and RheumatologyChung Shan Medical University HospitalInstitute of MedicineChung Shan Medical UniversityGraduate Institute of Intergrated MedicineChina Medical UniversityTaichung 40201Taiwan China

OBJECTIVE: To investigate the effectiveness a cream onjoint pain and swelling in patients with rheumatoid arthritis(RA). The cream, topically used, in was prepared with Tripterygium wilfordii Hook F(TwHF), Mangxiao(Nalrii Sulfas), Chuanxiong(Rhizoma Chuanxiong), stir-frying with liquid adjuvant Ruxiang(Olibanum), and stir-frying with liquid adjuvant Moyao(Myrrh).METHODS: Patients were 1∶1 randomized to addon TwHF cream twice a day or placebo for 4 *** primary endpoint was achievement rate of20% improvement in American College of Rheuma-tology criteria(ACR20) at week 4. Secondary endpoints were ACR50, 28-joint count Disease Activity Score(DAS28) improvement and safety *** analyses were performed using intention to treat analysis(ITT) ***: A total of 70 active RA patients were enrolled. At week 4, the ACR20 was 34.3%(12/35) in TwHF cream group and 11.4%(4/35) in placebo group(P = 0.015). Similarly, a higher ACR50 responder proportion was seen in TwHF cream group with 17.1%(6/35) comparing to it in placebo group with 2.9%(1/35)(P = 0.046). The TwHF cream group also had more improvement than the placebo group on DAS28-ESR(1.1 vs 0.5, P = 0.001), DAS28-CRP(1.4 vs 0.7, P = 0.001), tender joint count(5.5 vs2.6, P = 0.018), swollen joint count(3.5 vs 1.6, P =0.003) and Physician's global assessment(25.8 vs13.0, P = 0.002), as well as C-reactive protein(11.2 vs 2.7, P = 0.048). Except 2 skin allergy events in TwHF cream group, no other substantive adverse events were ***: On the short term, TwHF cream is likely to be an effective and safety complimentary treatment in patients with active RA.

关键词： Tripterygium wilfordii Arthritis,rheumatoid External therapy Randomized controlled trial

Gene mutations and clinical phenotypes in 15 Chinese children with cryopyrin-associated periodic syndrome(CAPS)

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Science China(Life Sciences) 2017年第12期60卷 1436-1444页

作者： Caifeng Li Xiaohua Tan Junmei Zhang Shipeng Li Wenxiu Mo Tongxin Han Weiying Kuang Yifang Zhou Jianghong Deng Department of rheumatology and Immunology Beijing Children's HospitalCapital Medical UniversityNational Center for Children"s HealthBeijing 100045China

The aim of our study is to explore the features of clinical manifestations and genetic mutations in Chinese CAPS patients. Fifteen confirmed patients with CAPS were enrolled. The onset time ranges from 2 days after birth to 6 years and 1 month. Recurrent urticaria rash(93.3%) with fever(100%) were two dominant characteristics of these patients that were presented as either acute or chronic process. Systemic involvements were found in all patients except for one with only rash and fever. The top three symptoms were fever(100%), rash(93.3%) and myalgia(76%). Other clinical manifestations include arthritis(11 cases), lung involvement(seven cases), optical dysfunction(seven cases), nerve deafness(six cases), nervous system involvement(five cases), hepatomegaly, splenomegaly and lymphadenectasis(five cases). Also, four patients had heart involvement and one patient suffered kidney involvement. The laboratory inflammation index such as leukocyte counts, platelet counts, erythrocyte sedimentation rate(ESR), C-reactive protein(CRP), serum amyloid A(SAA) and fibrinogen(FIB) increased significantly at initial stage, but decreased after therapy. As for gene mutation detection, Twelve out of 15 patients were confirmed with mutation in NLRP3, including 11 mutant site: c1789 A>G, c.1703 T>A, c.913 G>A, c.1710 G>C, c.1057 G >T, c.2335 C>T, c.932 T>C,c.296 G>C, c.663 C>T, t.1702 T>A, 299 G>A. Mutation sites c.1703 T>A, c.2335 C>T, c.296 G>C, c.663 C>T, and 299 G>A were newly identified. The association between gene mutation and clinical manifestation shows that D305 N was highly associated with severe organs involvements, and therefore, the time of therapy and regimen were critical for the prognosis of disease. As the largest cohort study of Chinese CAPS patients, we confirmed that all patients presented typical clinical manifestations, identified five new mutation sites on NLRP3 and analyzed the correlation between the genotypes and phenotypes. We also raise concerns for one case

关键词： CAPS genetic mutation clinical phenotTpe NLRP3

nvolvement of collagen-binding heat shock protein 47 in scleroderma-associated fibrosis

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Protein & Cell 2015年第8期6卷 589-598页

作者： Haiyan Chu Ting Wu Wenyu Wu Wenzhen Tu Shuai Jiang Sidi Chen Yanyun Ma Qingmei Liu Xiaodong Zhoua Li Jin Jiucun Wang Ministry of Education Key Laboratory of Contemporary Anthropology and State Key Laboratory of Genetic Engineering Collaborative Innovation Center for Genetics and Development School of Life Sciences and Institutes of Biomedica Sciences Fudan University Shanghai 200438 China Division of Dermatology Huashan Hospital Fudan University Shanghai 200040 China Division of rheumatology Shanghai TCM-Integrated Hospital Shanghai 200082 China Division of rheumatology University of Texas Health Science Center at Houston Houston TX 77030 USA Institute of rheumatology Immunology and Allergy Fudan University Shanghai 20080 China

Uncontrolled fibrosis of skin and internal organs is the main characteristic of scleroderma, and collagen is a major extracellular matrix protein that deposits in the fibrotic organs. As the chaperone of collagen, heat shock protein 47 （HSP47） is closely related with the development of fbrosis. To explore the potential func- tion of HSP47 in the pathogenesis of scleroderma, the clinical, in vivo and in vitro studies were performed. In clinical, the increased mRNA level of HSP47 was observed in the skin fibroblasts and PBMC from scle- roderma patients, and the enhanced protein level of HSP47 was also detected in the skin biopsy and plasma of the above patients. Unexpectedly, the enhanced levels of HSP47 were positively correlated with the presence of anti-centromere antibody in scleroderma patients. Moreover, a high expression of HSP47 was found in the skin lesion of BLM-induced scleroderma mouse model. Further in vitro studies demonstrated that HSP47 knockdown could block the intracellular and extracellular collagen over-productions induced by exogenous TGF-13. Therefore, the results in this study provide direct evidence that HSP47 is involved in the pathogenesis of scleroderma. The high expression of HSP47 can be detected in the circulatory system of scleroderma patients, indicating that HSP47 maybecome a pathological marker to assess the progres- sion of scleroderma, and also explain the systemic fibrosis of scleroderma. Meanwhile, collagen over-ex- pression is blocked by HSP47 knockdown, suggesting the possibility that HSP47 can be a potential therapeutic target for scleroderma.

关键词： systemic sclerosis fibrosis collagenheat shock protein 47 anti-centromere antibody,therapeutic target

B1-cell-produced anti-phosphatidylserine antibodies contribute to lupus nephritis development via TLR-mediated Syk activation

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Cellular & Molecular Immunology 2023年第8期20卷 881-894页

作者： Kongyang Ma Wenhan Du Shiyun Wang Fan Xiao Jingyi Li Jie Tian Yida Xing Xiaodan Kong Ke Rui Rencai Qin Xiaoxia Zhu Jing Wang Cainan Luo Haijing Wu Yun Zhang Chengping Wen Lan He Dongzhou Liu Hejian Zou Qianjin Lu Lijun Wu Liwei Lu Centre for Infection and Immunity Studies School of MedicineThe Sun Yat-sen UniversityShenzhen518107GuangdongChina Department of Pathology and Shenzhen Institute of Research and Innovation The University of Hong KongHong Kong999077China Department of rheumatology Shenzhen People’s HospitalThe Second Clinical Medical CollegeJinan UniversityShenzhenChina Chongqing International Institute for Immunology Chongqing400038China Department of rheumatology and Immunology Southwest HospitalThe First Hospital Affiliated to Army Medical UniversityChongqing400038China Department of Laboratory Medicine Affiliated Hospital and Institute of Medical ImmunologyJiangsu UniversityZhenjiangChina Department of rheumatology The Second Affiliated Hospital of Dalian Medical UniversityDalianChina Department of rheumatology Huashan HospitalFudan UniversityShanghaiChina Department of rheumatology and Immunology The First Affiliated Hospital of Xi’an Jiaotong UniversityXi’an710061ShaanxiChina Department of rheumatology and Immunology People’s Hospital of Xinjiang Uygur Autonomous RegionUrumqiChina Department of Dermatology Hunan Key Laboratory of Medical EpigenomicsSecond Xiangya HospitalCentral South UniversityChangshaHunanChina Key Laboratory of Chinese Medicine rheumatology of Zhejiang Province Institute of Basic Research in Clinical MedicineCollege of Basic Medical ScienceZhejiang Chinese Medical UniversityHangzhou310053China Centre for Oncology and Immunology Hong Kong Science ParkHong KongChina

Autoantibodies produced by B cells play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). However, both the cellular source of antiphospholipid antibodies and their contributions to the development of lupus nephritis (LN) remain largely unclear. Here, we report a pathogenic role of anti-phosphatidylserine (PS) autoantibodies in the development of LN. Elevated serum PS-specific IgG levels were measured in model mice and SLE patients, especially in those with LN. PS-specific IgG accumulation was found in the kidney biopsies of LN patients. Both transfer of SLE PS-specific IgG and PS immunization triggered lupus-like glomerular immune complex deposition in recipient mice. ELISPOT analysis identified B1a cells as the main cell type that secretes PS-specific IgG in both lupus model mice and patients. Adoptive transfer of PS-specific B1a cells accelerated the PS-specific autoimmune response and renal damage in recipient lupus model mice, whereas depletion of B1a cells attenuated lupus progression. In culture, PS-specific B1a cells were significantly expanded upon treatment with chromatin components, while blockade of TLR signal cascades by DNase I digestion and inhibitory ODN 2088 or R406 treatment profoundly abrogated chromatin-induced PS-specific IgG secretion by lupus B1a cells. Thus, our study has demonstrated that the anti-PS autoantibodies produced by B1 cells contribute to lupus nephritis development. Our findings that blockade of the TLR/Syk signaling cascade inhibits PS-specific B1-cell expansion provide new insights into lupus pathogenesis and may facilitate the development of novel therapeutic targets for the treatment of LN in SLE.

关键词： B1 cell Anti-phosphatidylserine antibodies Lupus nephritis TLR Syk