细胞与分子免疫学杂志最新文献

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[Progress in the application of bronchoalveolar lavage fluid in the diagnosis of infectious lung diseases]. [支气管肺泡灌洗液在感染性肺病诊断中的应用进展]。
细胞与分子免疫学杂志 Pub Date : 2026-09-01
Shumin Zhang, Li Xiao, Guoxin Mo
{"title":"[Progress in the application of bronchoalveolar lavage fluid in the diagnosis of infectious lung diseases].","authors":"Shumin Zhang, Li Xiao, Guoxin Mo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Bronchoalveolar lavage fluid (BALF) contains diverse cellular components and pathogens, directly reflecting the local immune status at sites of pulmonary infection. By detecting pathogens such as bacteria, fungi, and viruses within these samples and analyzing changes in the immune cell composition and cytokine levels, it will help to assess the immune microenvironment of infected lung regions and to predict disease prognosis. In recent years, the application of artificial intelligence in BALF analysis has significantly enhanced the efficiency of cell classification and counting. Combined with molecular diagnostic methods such as metagenomic next-generation sequencing, this approach deeply explores the diagnostic value of immune cells, pathogens, and their molecular characteristics in BALF for infectious lung diseases. It will provide more precise support for early disease identification, personalized treatment, and clinical decision-making.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"844-850"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Detection of anti-Dia antibody in patients with cervical space-occupying lesions following massive blood transfusion]. [大量输血后宫颈占位性病变患者抗dia抗体检测]。
细胞与分子免疫学杂志 Pub Date : 2026-09-01
Ying Li, Yang Chen, Chen Wang, Lin Yang, Shiming Yang, Longfei Yang
{"title":"[Detection of anti-Di<sup>a</sup> antibody in patients with cervical space-occupying lesions following massive blood transfusion].","authors":"Ying Li, Yang Chen, Chen Wang, Lin Yang, Shiming Yang, Longfei Yang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To analyze the identification of serum anti-Di<sup>a</sup> in a patient with cervical space-occupying lesion following massive transfusion, and summarize clinical nursing measures for blood transfusion. Methods The specificity of irregular antibodies in the patient's blood type and serum was confirmed through blood type identification, irregular antibody screening and specificity identification, identification of corresponding blood type antigens and absorption and release test verification, direct immunoglobulin test (DAT) and other blood type serological testing methods. Resluts The patient's ABO blood type is type A, Rh blood type phenotype is CcDEe, and DAT is negative. There is the IgG-type anti-Di<sup>a</sup> in the patient's serum, with an antibody titer of 1:16 and an agglutination strength of 2+. Conclusion The presence of anti-Di<sup>a</sup> in patient's serum is the main cause of positive antibody screening and cross matching mismatch. Performing irregular antibody screening, specificity identification, and cross matching tests on patients before blood transfusion, and then selecting blood units with negative homologous blood group antigens for transfusion is an important monitoring measure to prevent hemolytic transfusion reactions.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 9","pages":"808-812"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Research progress of neutrophil extracellular traps in septic coagulopathy]. 脓毒性凝血病中性粒细胞胞外陷阱的研究进展。
细胞与分子免疫学杂志 Pub Date : 2026-08-01
Zhuowen Dai, Qiong Wang
{"title":"[Research progress of neutrophil extracellular traps in septic coagulopathy].","authors":"Zhuowen Dai, Qiong Wang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Sepsis-induced coagulopathy (SIC) ranks among the most dangerous coagulation disorders in intensive care units, with an incidence rate of up to 67.9% in China. This high mortality is mainly attributed to vascular endothelial cell injury and coagulation dysfunction caused by sepsis. Neutrophil extracellular traps (NETs) are reticular complexes formed by activated neutrophils in infected organisms through the release of DNA, proteases, cytokines, and other components. Recent studies have demonstrated that NETs can trigger systemic hemostatic imbalance in sepsis patients by mediating vascular endothelial damage, promoting immunothrombosis, and disrupting the coagulation-fibrinolysis balance, ultimately leading to the development of SIC. Therefore, this article reviews the mechanistic role of NETs in SIC and discusses recent advances in their potential as diagnostic biomarkers and therapeutic targets.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"749-754"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Therapeutic prospects of miRNA-mediated regulation of NLRP3 inflammasome-targeted synovial cell pyroptosis in bone destruction of rheumatoid arthritis]. [mirna介导的NLRP3炎性小体靶向滑膜细胞焦亡在类风湿关节炎骨破坏中的治疗前景]。
细胞与分子免疫学杂志 Pub Date : 2026-08-01
Shiyu Ji, Sha Li, Runqing Gao, Wukai Ma, Xueming Yao
{"title":"[Therapeutic prospects of miRNA-mediated regulation of NLRP3 inflammasome-targeted synovial cell pyroptosis in bone destruction of rheumatoid arthritis].","authors":"Shiyu Ji, Sha Li, Runqing Gao, Wukai Ma, Xueming Yao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation and progressive bone destruction. Its pathological core lies in the aberrant activation of fibroblast-like synoviocytes (FLS) and involves a cascade of pyroptosis mediated by the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. This article systematically reviews the pathological patterns of inflammatory bone destruction in RA, with a particular focus on the role of exosomes derived from mesenchymal stem cells (MSC-Exo) in carrying microRNAs (miRNAs). These miRNAs can regulate the NLRP3 inflammasome signaling axis and play a crucial role in inhibiting FLS pyroptosis. This article provides a new perspective for RA treatment by regulating exosome miRNA to intervene in cell pyroptosis. However, the specific molecular targets, clinical translational value, and functional synergism among different non-coding RNAs (ncRNAs) still need further validation.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"743-748"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[A novel extraction method and identification of primary mouse pulmonary artery smooth muscle cells]. [一种新的小鼠原代肺动脉平滑肌细胞提取方法及鉴定]。
细胞与分子免疫学杂志 Pub Date : 2026-08-01
Jiayue Chao, Zhangyu Liu, Qing Yin, Shenqiang Zhao, Hui Shen
{"title":"[A novel extraction method and identification of primary mouse pulmonary artery smooth muscle cells].","authors":"Jiayue Chao, Zhangyu Liu, Qing Yin, Shenqiang Zhao, Hui Shen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To establish an efficient and rapid primary culture protocol for mouse pulmonary artery smooth muscle cell (PASMC). Methods PASMC were isolated from mice using a novel dual-enzyme digestion method. Cell morphology was observed under an inverted phase-contrast microscope, and cell type and purity were identified by immunofluorescence staining for α-smooth muscle actin (α-SMA). Cell growth after passage was assessed using the CCK-8 assay. The migratory response of PASMC to platelet-derived growth factor-BB (PDGF-BB) was evaluated by cell scratch assay. Changes of protein expression in primary PASMC after stimulation of transforming growth factor β1 (TGF-β1) were detected by Western blot. Results Under light microscopy, PASMC showed a long spindle-shaped morphology with a positive rate reaching as high as 98%. The growth curve of passaged cells approximated an \"S\" shape. Primary cultured PASMC showed a significant migratory response to stimulation of PDGF-BB. TGF-β1 stimulation significantly increased the expression of phospho-Smad2 (p-Smad2) in PASMC. Conclusion The novel dual-enzyme digestion method significantly improves the isolation efficiency and viability of primary PASMC, providing a sufficient and phenotypically stable source of high-quality cells for in vitro studies.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"701-707"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Advances in macrophage and neutrophil crosstalk in chronic respiratory diseases]. 慢性呼吸系统疾病中巨噬细胞与中性粒细胞串扰的研究进展
细胞与分子免疫学杂志 Pub Date : 2026-08-01
Shan Jiang, Rongfang Xie, Shiyu Chen, Hui Cheng, Zhihui Lan, Dan Xie
{"title":"[Advances in macrophage and neutrophil crosstalk in chronic respiratory diseases].","authors":"Shan Jiang, Rongfang Xie, Shiyu Chen, Hui Cheng, Zhihui Lan, Dan Xie","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Macrophages serve as tissue-resident immune sentinels, continuously surveying the local microenvironment via pattern recognition receptors (PRRs) to orchestrate inflammation resolution and antigen presentation. In contrast, neutrophils-circulating first responders-mediate rapid pathogen clearance through phagocytosis, degranulation, and neutrophil extracellular trap (NET) formation. Although historically viewed as functionally distinct and largely autonomous, mounting evidence reveals that macrophages and neutrophils engage in dynamic, bidirectional crosstalk across multiple molecular axes-including cytokine signaling, lipid mediators, and cell-cell contact-to jointly shape innate immune responses. Chronic respiratory diseases-including COPD, asthma, idiopathic pulmonary fibrosis, and bronchiectasis-represent a leading cause of global morbidity and mortality, imposing substantial clinical and socioeconomic burdens. Elucidating the mechanistic underpinnings of macrophage-neutrophil interactions is thus critical not only for uncovering fundamental principles of innate immune regulation but also for identifying novel, cell-type-specific therapeutic targets in these complex, heterogeneous disorders. In this review, we synthesize recent advances enabled by single-cell multi-omics, spatial transcriptomics, and functional imaging, contextualized within the pathobiology of chronic respiratory diseases, to provide a systematic and mechanistically grounded overview of the macrophage-neutrophil interaction network and its emerging translational implications for precision immunomodulation.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"735-742"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Construction of a butyrate-producing engineered bacteria and its therapeutic effects on atopic dermatitis]. [一种产丁酸工程菌的构建及其对特应性皮炎的治疗作用]。
细胞与分子免疫学杂志 Pub Date : 2026-08-01
Yuwen Gao, Xu Yao
{"title":"[Construction of a butyrate-producing engineered bacteria and its therapeutic effects on atopic dermatitis].","authors":"Yuwen Gao, Xu Yao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective Dysregulation of the gut-skin axis caused by intestinal microbiota imbalance is an important contributor to the pathogenesis of atopic dermatitis (AD). This study aims to construct an engineered Escherichia coli Nissle 1917 (EcN) strain capable of efficient and stable butyrate secretion, and evaluate its therapeutic efficacy in a calcipotriol (MC903)-induced mouse model of AD. Methods Using synthetic biology strategies, the core butyrate synthesis gene modules (bcd, but) derived from Faecalibacterium prausnitzii were codon-optimized, cloned into an expression plasmid, and introduced into the probiotic chassis strain Escherichia coli Nissle 1917 (EcN) by electroporation to generate the butyrate-producing engineered strain EcN-But. Butyrate yield was quantified via High-Performance Liquid Chromatography (HPLC), and genetic stability was rigorously assessed. An MC903-induced AD mouse model was established and treated with oral EcN-But. Therapeutic efficacy was evaluated through Eczema Area and Severity Index (EASI) scores, histological analysis (HE staining), serum IgE levels, and RT-qPCR analysis of cutaneous inflammatory cytokines including interleukin 4 (IL-4), IL-13, IL-33, thymic stromal lymphopoietin (TSLP) and tumor necrosis factor α (TNF-α). Results The engineered strain EcN-But was successfully constructed, achieving a stable butyrate secretion of (326.30±19.8)mg/L under anaerobic fermentation without significant metabolic burden on bacterial growth. In vivo, oral administration of EcN-But significantly reduced EASI scores and inhibited epidermal hyperplasia. Furthermore, EcN-But treatment significantly downregulated serum total IgE levels and suppressed the expression of key inflammatory cytokines in skin tissues. Conclusion The engineered strain EcN-But effectively alleviates AD-like inflammation by enabling in situ butyrate secretion in the gut to modulate systemic immune homeostasis, offering a novel live biotherapeutic product strategy for the clinical management of atopic dermatitis.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"673-680"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Exploring the impact of macrophage depletion on influenza viral pneumonia and its mechanism of action through the cGAS-STING pathway]. [探讨巨噬细胞耗竭对流感病毒性肺炎的影响及其通过cGAS-STING通路的作用机制]。
细胞与分子免疫学杂志 Pub Date : 2026-08-01
Jianing Shi, Lan Liu, Mengjuan Li, Zhuolin Liu, Lang Hu, Wanjing Yuan, Qian Ouyang, Qing Zhong, Ling Li
{"title":"[Exploring the impact of macrophage depletion on influenza viral pneumonia and its mechanism of action through the cGAS-STING pathway].","authors":"Jianing Shi, Lan Liu, Mengjuan Li, Zhuolin Liu, Lang Hu, Wanjing Yuan, Qian Ouyang, Qing Zhong, Ling Li","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective This study investigated the impact of macrophage depletion on influenza A virus (IAV)-induced pneumonia and its underlying mechanism. Methods A mouse model of IAV-induced pneumonia with macrophage depletion was created using CL<sub>2</sub>MBP followed by IAV inoculation. Experiments were conducted on days 1, 3, and 5 post-infection. Hematoxylin and eosin (HE) staining was used to assess tissue pathology, and the bicinchoninic acid (BCA) assay was employed to measure protein levels in bronchoalveolar lavage fluid (BALF). ELISA was used to quantify inflammatory factors and cGAMP in lung tissues, and flow cytometry was performed to detect macrophages in BALF. qPCR was used to assess mitochondrial DNA (mtDNA) expression levels. cGAS and STING protein levels in lungs were evaluated by immunohistochemistry. Single-cell sequencing was used to detect the expression levels of IFI16 gene in humans, while immunohistochemical staining was employed to assess IFI204 protein expression in mouse lung tissues. In vitro, RAW264.7 macrophages were treated with STING agonist MSA-2 or inhibitor H-151. Real-time quantitative PCR (qPCR) was used to detect the expression levels of STING, viral nucleoprotein (NP), interleukin 1β (IL-1β), and IFI204 in cells from each group. ResultsFlow cytometry confirmed effective macrophage depletion. BALF protein and inflammatory cytokines (TNF-α, IFN-γ) were significantly higher in macrophage-depleted mice. Histopathological damage worsened, with the most severe effects in macrophage-depleted mice. Macrophage depletion reduced mtDNA, cGAMP, and cGAS/STING protein expression in lungs. Elevated IFI16 expression was observed in COVID-19 or IAV-infected patients. Following macrophage depletion, IFI204 expression in mouse lung tissues was significantly reduced. In vitro, MSA-2 increased IFI204 mRNA, suppressed IL-1β, and inhibited IAV NP replication. H-151 reversed these effects and promoted viral NP gene expression. ConclusionMacrophage depletion impairs the cGAS-STING pathway activation in response to IAV infection, disrupting the innate immune response and worsening viral lung injury.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"681-691"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[miR-199a-3p targets PD-L1 to regulate immune evasion in microsatellite stable colorectal cancer]. [miR-199a-3p靶向PD-L1调节微卫星稳定型结直肠癌的免疫逃避]。
细胞与分子免疫学杂志 Pub Date : 2026-08-01
Zhiyuan Luo, Xiangqian Wang, Shujing Zhang, Yuying Zhao, Jiexuan Sun, Caifeng Zhao, Weiqun Chi, Zhuo Gao
{"title":"[miR-199a-3p targets PD-L1 to regulate immune evasion in microsatellite stable colorectal cancer].","authors":"Zhiyuan Luo, Xiangqian Wang, Shujing Zhang, Yuying Zhao, Jiexuan Sun, Caifeng Zhao, Weiqun Chi, Zhuo Gao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective Immune checkpoint inhibitors show limited efficacy in microsatellite-stable (MSS) colorectal cancer (CRC). This study aims to elucidate the molecular mechanisms underlying immune evasion in MSS CRC. Prior miRNA profiling of MSS CRC tissues from anti-programmed death 1 (PD-1) monoclonal antibody responders and non-responders identified miR-199a-3p as a candidate molecule. This study further validates its clinical relevance and investigates its mechanistic role. Methods Quantitative real-time PCR was performed to assess gene expression levels. Dual-luciferase reporter assays were conducted to evaluate the targeting relationship between miR-199a-3p and programmed death-ligand 1 (PD-L1). A co-culture system of MSS CRC cells and peripheral blood mononuclear cells (PBMC) was established to analyze the proportion of CD8<sup>+</sup> T cell and cytokine secretion. Cell proliferation was assessed using Cell Counting Kit-8 (CCK-8) assays and colony formation assays. Cell migration was evaluated by wound healing assays, and apoptosis was measured using Annexin V-FITC/7-AAD staining. Results miR-199a-3p directly targeted PD-L1 and downregulated its expression in MSS SW620 cells. Overexpression of miR-199a-3p relieved the inhibition of CD8<sup>+</sup> T cells, enhanced their cell cytotoxic activity and alleviated immunosuppression in the tumor microenvironment. Furthermore, miR-199a-3p overexpression inhibited cell proliferation and migration while promoting apoptosis in MSS SW620 cells. In contrast, inhibition of miR-199a-3p exerted opposite effects. Conclusion miR-199a-3p mediates immune evasion in MSS CRC by targeting PD-L1. It may serve as a potential noninvasive diagnostic biomarker and therapeutic target, providing a theoretical basis for promoting novel immunotherapeutic strategies.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"715-722"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[From mechanisms to manifestations: Research advances in ACPA-related clinical presentations of rheumatoid arthritis]. [从机制到表现:类风湿性关节炎acpa相关临床表现的研究进展]。
细胞与分子免疫学杂志 Pub Date : 2026-08-01
Chao Yang
{"title":"[From mechanisms to manifestations: Research advances in ACPA-related clinical presentations of rheumatoid arthritis].","authors":"Chao Yang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized primarily by joint destruction. Anti-citrullinated protein antibodies (ACPA) are not only key drivers and major risk factors for the onset and immune persistence of RA but also crucial biomarkers for its clinical diagnosis. Recent studies have demonstrated that ACPA can directly exacerbate the clinical symptoms of RA through various mechanisms, including promoting inflammatory responses, mediating bone erosion, and inducing pain. Therefore, ACPA holds significant value not only for the early diagnosis, prognosis assessment, and treatment monitoring of RA but is also regarded as a highly promising therapeutic target, offering new directions for developing precision treatment strategies for RA. This article reviews the latest research progress on the correlation between ACPA and the core clinical symptoms as well as common complications of RA, aiming to provide a theoretical basis for a deeper understanding of the pathogenesis and the development of personalized treatment plans for ACPA-positive RA patients.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"729-734"},"PeriodicalIF":0.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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