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Firsekibart versus compound betamethasone in acute gout patientsunsuitable for standard therapy: A randomized phase 3 trial 认领 引用 被引量：9
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作者 Yu Xue Tianshu Chu +15 位作者 Jiankang Hu Wei Gou Ning Zhang Juan Li Jing Yu Rongping Li Rongbin Li Long Qian Xinwang Duan Lihua Duan Xu Zhang Yuling Lian Yi Li Chuang Qi Dongzhe Huang Hejian Zou 《The Innovation》 EI 2025年第8期30-37,29,共8页
This phase 3 trial evaluated the efficacy and safety of Firsekibart,a novel,fully human anti-interleukin-1βmonoclonal antibody,in patients with frequent acute gout flares unsuitable for standard therapy.Pa-tients wer... This phase 3 trial evaluated the efficacy and safety of Firsekibart,a novel,fully human anti-interleukin-1βmonoclonal antibody,in patients with frequent acute gout flares unsuitable for standard therapy.Pa-tients were randomized(1:1,stratified by baseline pain visual analog scale[VAS])to the Firsekibart(200 mg)or compound betamethasone(CB;7 mg)group.Co-primary endpoints included change in pain inten-sity in the target joint at 72 h(non-inferiority testing)and time to first new flare within 12 weeks(superiority testing).The non-inferiority margin was 10 mm.The full analysis set included 311 patients(Firseki-bart:N=156;CB:N=155).At 72 h,the least squares mean change in pain VAS scores from baseline was-57.09 mm(95%confidence in-terval[CI]:-60.08 to-54.10)for Firsekibart and-53.77 mm(95%CI:-56.77 to-50.77)for CB,with treatment difference of-3.32 mm(95%CI:-7.56 to 0.91),establishing non-inferiority.The median time to first new flare was not reached within 12 weeks in the Firsekibart group compared with 45.0 days(95%CI:28.00 to 63.00)in the CB group.Firsekibart significantly reduced the risk of new flare by 90%vs.CB(haz-ard ratio:0.10;95%CI:0.06 to 0.17;stratified log rank p<0.0001).Effi-cacy was consistent across subgroups.Treatment-emergent adverse events occurred in 71.2%of Firsekibart-treated patients and 69.9%of those receiving CB.In conclusion,Firsekibart is effective and well toler-ated for acute gout flares in patients unsuitable for standard therapy,demonstrating non-inferiority in rapid pain relief and significant superi-ority in preventing flare compared with CB. 展开更多
关键词 compound betamethasone cb firsekibart non inferiority change pain standard therapypa tients pain visual analog scale vas compound betamethasone acute gout
Cholinergic B cells:New players in immune regulation and tissue homeostasis 认领 引用
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作者 Fan Xiao Lam Ng +5 位作者 Kongyang Ma Chong Deng Xiaoxia Zhu Hejian Zou Haijing Wu Liwei Lu 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2025年第7期696-698,共3页
As key players in humoral immunity,B cells play diverse roles in immune responses and disease development.Although early studies focused on the hallmark features of antibody production in B cells,increasing evidence h... As key players in humoral immunity,B cells play diverse roles in immune responses and disease development.Although early studies focused on the hallmark features of antibody production in B cells,increasing evidence has demonstrated the effector functions of cytokine secretion and antigen presentation by B cells in the development of various human diseases.Recent studies on the interactions of immune cells and nerve systems through neurotransmitters,including acetylcholine(ACh),have revealed novel functions of B cells in immune regulation and tissue homeostasis.Two newly published studies in Nature Immunology and Immunity demonstrated that B cells produce ACh to modulate antiviral inflammatory responses and liver regeneration after injury[1,2].These pivotal findings suggest the existence of a new functional subset of ACh-producing B cells,termed“cholinergic B cells”,which are characterized by their ability to synthesize ACh via high expression of choline acetyltransferase(ChAT).Cholinergic B cells span both innate B1 and conventional B2 cells and play a unique role in bridging neuroimmune crosstalk.Thus,elucidation of the functional features of cholinergic B cells will open new avenues for therapeutic intervention in acute inflammatory and regenerative disorders. 展开更多
关键词 cholinergic b cells nerve systems immune regulation b cells humoral immunity b cellsincreasing cytokine secretion immune cells
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B1-cell-produced anti-phosphatidylserine antibodies contribute to lupus nephritis development via TLR-mediated Syk activation 认领 引用 被引量：7
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作者 Kongyang Ma Wenhan Du +19 位作者 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 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2023年第8期881-894,共14页
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 develop... 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. 展开更多
关键词 B1 cell Anti-phosphatidylserine antibodies Lupus nephritis TLR Syk
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Epigenetic regulation of B cells and its role in autoimmune pathogenesis 认领 引用 被引量：5
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作者 Fan Xiao Ke Rui +8 位作者 Xiaofei Shi Haijing Wu Xiaoyan Cai Kathy O.Lui Qianjin Lu Esteban Ballestar Jie Tian Hejian Zou Liwei Lu 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2022年第11期1215-1234,共20页
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,pr... 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. 展开更多
关键词 B cells Epigenetic regulation Autoimmune disease Biomarker Therapy
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Aryl hydrocarbon receptor activation drives polymorphonuclear myeloid-derived suppressor cell response and efficiently attenuates experimental Sjögren’s syndrome 认领 引用 被引量：6
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作者 Yanxia Wei Na Peng +13 位作者 Chong Deng Futao Zhao Jie Tian Yuan Tang Sulan Yu Yacun Chen Yu Xue Fan Xiao Yingbo Zhou Xiaomei Li Hejian Zou Ke Rui Xiang Lin Liwei Lu 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2022年第12期1361-1372,共12页
Myeloid-derived suppressor cells(MDSCs)comprise heterogeneous myeloid cell populations with immunosuppressive capacity that contribute to immune regulation and tolerance induction.We previously reported impaired MDSC ... Myeloid-derived suppressor cells(MDSCs)comprise heterogeneous myeloid cell populations with immunosuppressive capacity that contribute to immune regulation and tolerance induction.We previously reported impaired MDSC function in patients with primary Sjögren’s syndrome(pSS)and mice with experimental SS(ESS).However,the molecular mechanisms underlying MDSC dysfunction remain largely unclear.In this study,we first found that aryl hydrocarbon receptor(AhR)was highly expressed by human and murine polymorphonuclear MDSCs(PMN-MDSCs).Indole-3-propionic acid(IPA),a natural AhR ligand produced from dietary tryptophan,significantly promoted PMN-MDSC differentiation and suppressive function on CD4+T cells.In contrast,feeding a tryptophan-free diet resulted in a decreased PMN-MDSC response,a phenotype that could be reversed by IPA supplementation.The functional importance of PMN-MDSCs was demonstrated in ESS mice by using a cell-depletion approach.Notably,AhR expression was reduced in PMN-MDSCs during ESS development,while AhR antagonism resulted in exacerbated ESS pathology and dysregulated T effector cells,which could be phenocopied by a tryptophan-free diet.Interferon regulatory factor 4(IRF4),a repressive transcription factor,was upregulated in PMN-MDSCs during ESS progression.Chromatin immunoprecipitation analysis revealed that IRF4 could bind to the promoter region of AhR,while IRF4 deficiency markedly enhanced AhR-mediated PMN-MDSC responses.Furthermore,dietary supplementation with IPA markedly ameliorated salivary glandular pathology in ESS mice with restored MDSC immunosuppressive function.Together,our results identify a novel function of AhR in modulating the PMN-MDSC response and demonstrate the therapeutic potential of targeting AhR for the treatment of pSS. 展开更多
关键词 myeloid-derived suppressor cell Sjogren's syndrome Aryl hydrocarbon receptor
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Coming of age:the formation and function of age-associated B cells 认领 引用 被引量：2
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作者 Ke Rui Nan Che +3 位作者 Kongyang Ma Hejian Zou Fan Xiao Liwei Lu 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2024年第4期311-312,共2页
B cells are generated in the bone marrow during ontogeny and migrate to peripheral lymphoid organs,where they encounter antigens to elicit humoral immunity.During the past decade,many novel B-cell subsets with distinc... B cells are generated in the bone marrow during ontogeny and migrate to peripheral lymphoid organs,where they encounter antigens to elicit humoral immunity.During the past decade,many novel B-cell subsets with distinct phenotypes and functions have been identified,and among these subsets,age-associated B cells(ABCs)were first characterized as a B-cell subset that accumulates with age[1]. 展开更多
关键词 organs lymphoid migrate
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Association of visceral adipose tissue with gout:Observational and Mendelian randomization analyses 认领 引用 被引量：1
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作者 Wenze Xiao Qi Wang +2 位作者 Yining Liu Hui Zhang Hejian Zou 《Chinese Medical Journal》 SCIE CAS CSCD 2024年第19期2351-2357,共7页
Background:The causal relationship between visceral adipose tissue(VAT)and gout is still unclear.We aimed to examine the potential association between them using observational and Mendelian randomization(MR)analyses.M... Background:The causal relationship between visceral adipose tissue(VAT)and gout is still unclear.We aimed to examine the potential association between them using observational and Mendelian randomization(MR)analyses.Methods:In the observational analyses,a total of 11,967 participants(aged 39.5±11.5 years)were included from the National Health and Nutrition Examination Survey.Logistic regression models were used to investigate the association between VAT mass and the risk of gout.In two-sample MR analyses,211 VAT mass-related independent genetic variants(derived from genome-wide association studies in 325,153 UK biobank participants)were used as instrumental variables.The random-effects inverse-variance weighted(IVW)method was used as the primary analysis.Additional sensitivity analyses were also performed to validate our results.Results:Observational analyses found that an increase in VAT mass(per standard deviation)was associated with a higher risk of gout after controlling for confounding factors(odds ratio[OR]=1.27,95%confidence intervals[CI]=1.11-1.45).The two-sample MR analyses demonstrated a causal relationship between increased VAT mass and the risk of gout in primary analyses(OR=1.78,95%CI=1.57-2.03).Sensitivity analyses also showed similar findings,including MR-Egger,weighted median,simple mode,weighted mode,and leave-one-out analyses.Conclusions:Observational analyses showed a robust association of VAT mass with the risk of gout.Meanwhile,MR analyses also provided evidence of a causal relationship between them.In summary,our findings suggested that targeted interventions for VAT mass may be beneficial to prevent gout. 展开更多
关键词 Visceral adipose tissue Gout Observational analyses Mendelian randomization Causal relationship Epidemiology
A Common Functional Variant at the Enhancer of the Rheumatoid Arthritis Risk Gene ORMDL3 Regulates its Expression Through Allele-Specific JunD Binding 认领 引用 被引量：1
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作者 Wenjing Ye Yiyun Yu +4 位作者 Xiaoxia Zhu Weiguo Wan Yun Liu Hejian Zou Zaihua Zhu 《Phenomics》 2023年第5期485-495,共11页
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 assoc... 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. 展开更多
关键词 Rheumatoid arthritis Genome-wide association study Enhancer ORMDL Sphingolipid Biosynthesis Regulator 3
Iron metabolism and arthritis:Exploring connections and therapeutic avenues 认领 引用 被引量：4
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作者 Dachun Zhuo Wenze Xiao +11 位作者 Yulong Tang Shuai Jiang Chengchun Geng Jiangnan Xie Xiaobei Ma Qing Zhang Kunhai Tang Yuexin Yu Lu Bai Hejian Zou Jing Liu Jiucun Wang 《Chinese Medical Journal》 SCIE CAS CSCD 2024年第14期1651-1662,共12页
Iron is indispensable for the viablility of nearly all living organisms,and it is imperative for cells,tissues,and organisms to acquire this essential metal sufficiently and maintain its metabolic stability for surviv... Iron is indispensable for the viablility of nearly all living organisms,and it is imperative for cells,tissues,and organisms to acquire this essential metal sufficiently and maintain its metabolic stability for survival.Disruption of iron homeostasis can lead to the development of various diseases.There is a robust connection between iron metabolism and infection,immunity,inflammation,and aging,suggesting that disorders in iron metabolism may contribute to the pathogenesis of arthritis.Numerous studies have focused on the significant role of iron metabolism in the development of arthritis and its potential for targeted drug therapy.Targeting iron metabolism offers a promising approach for individualized treatment of arthritis.Therefore,this review aimed to investigate the mechanisms by which the body maintains iron metabolism and the impacts of iron and iron metabolism disorders on arthritis.Furthermore,this review aimed to identify potential therapeutic targets and active substances related to iron metabolism,which could provide promising research directions in this field. 展开更多
关键词 Iron metabolism Arthritis Inflammation Immunity Rheumatoid arthritis Psoriatic arthritis Gouty arthritis
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