Clinical immunology最新文献_第6页

Glial-derived neurotrophic factor promotes aberrant basal cell hyperplasia in nasal polyps 神经胶质源性神经营养因子促进鼻息肉异常基底细胞增生。

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-10-10 DOI: 10.1016/j.clim.2025.110604

Yilin Hou , Lin Sun , Mengqi Su , Weiqiang Yang , Lingchao Ji , Yaqi Zhou , Xiaochan Lu , Na Yin , Jiaqi Zhao , Zihan Qiu , Yi Wei , Weiping Wen , HongYi Hu

{"title":"Glial-derived neurotrophic factor promotes aberrant basal cell hyperplasia in nasal polyps","authors":"Yilin Hou , Lin Sun , Mengqi Su , Weiqiang Yang , Lingchao Ji , Yaqi Zhou , Xiaochan Lu , Na Yin , Jiaqi Zhao , Zihan Qiu , Yi Wei , Weiping Wen , HongYi Hu","doi":"10.1016/j.clim.2025.110604","DOIUrl":"10.1016/j.clim.2025.110604","url":null,"abstract":"<div><h3>Background</h3><div>Neurotrophins are elevated in nasal polyps (NPs) and/or allergies, exerting neurogenic inflammatory effects. Non-classical glial-derived neurotrophic factor (GDNF) family ligands (GFLs) remain poorly understood in chronic rhinosinusitis with NP (CRSwNP).</div></div><div><h3>Methods</h3><div>GDNF expression was analyzed in 67 nasal fluids (NFs) and 44 tissues via proteomic, transcriptomic, and immunohistochemical assays. Immunofluorescence co-staining identified GDNF and p63 + basal cells (BCs). Functional studies in human nasal epithelial cells (HNECs) assessed GDNF's affects on proliferation and barrier integrity. Bioinformatics identified regulatory networks and drug candidates.</div></div><div><h3>Results</h3><div>GDNF existed in NFs and tissues of CRSwNP, with higher abundance in eosinophilic NPs. P63 + BCs expression positively correlates with GDNF levels. GDNF potently activated MAPK/PI3K/Akt signaling in HNECs and induced Ki-67+/p63 + cells proliferation, while reduced distribution of claudin-1 at junctions. miR-204-5p/211-5p and two FDA-approved neuroactive drugs were predicted as GDNF modulators.</div></div><div><h3>Conclusions</h3><div>GDNF drives aberrant epithelial remodeling in CRSwNP via MAPK/PI3K signaling, highlighting its therapeutic potential for refractory disease.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110604"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regarding the “Efgartigimod versus standard of care in new-onset AChR subtype generalized myasthenia gravis: A prospective cohort study” 关于“依夫加替莫德与标准护理相比治疗新发AChR亚型广泛性重症肌无力：一项前瞻性队列研究”。

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-09-11 DOI: 10.1016/j.clim.2025.110603

Hai-Feng Li , Shi-Min Hu , Wei Han , Yan-Su Guo

引用次数: 0

Hydrogen protects against autoimmune myocarditis by inhibiting necroptosis via the TNF/TNFR1 signalling pathway 氢通过TNF/TNFR1信号通路抑制坏死下垂，从而保护自身免疫性心肌炎

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-08-12 DOI: 10.1016/j.clim.2025.110577

Shuang Pan , Mengshu Yu , Bowei Fan , Bin Wang , Xinrui Yang , Jiawen Zhang , Xiaoqi Liu , Xiaojian Hong , Wei Yang

{"title":"Hydrogen protects against autoimmune myocarditis by inhibiting necroptosis via the TNF/TNFR1 signalling pathway","authors":"Shuang Pan , Mengshu Yu , Bowei Fan , Bin Wang , Xinrui Yang , Jiawen Zhang , Xiaoqi Liu , Xiaojian Hong , Wei Yang","doi":"10.1016/j.clim.2025.110577","DOIUrl":"10.1016/j.clim.2025.110577","url":null,"abstract":"<div><div>Autoimmune myocarditis refers to the inflammation of myocardial tissue caused by innate and adaptive immune responses, characterized by elevated levels of tumour necrosis factor-α (TNF-α), a classic pro-inflammatory factor. Although hydrogen exhibits anti-inflammatory and antioxidant properties, its therapeutic effects in autoimmune myocarditis have not been evaluated. Therefore, the present study aimed to explore whether hydrogen can alleviate autoimmune myocarditis via TNF-α. An experimental autoimmune myocarditis (EAM) model was established in BALB/c mice via subcutaneous injection of pig-derived myocardial myoglobin emulsified with complete Freund's adjuvant. The treatment group received 2 % hydrogen inhalation twice a day (3 h each time) for 21 days. CD4+ T cell expression was higher in the EAM group than in the Control group, and this increase was attenuated following treatment with hydrogen. Additionally, the levels of TNF-α and related inflammatory factors were substantially higher in the EAM group than in the Control group, and these changes were reversed following hydrogen treatment. Echocardiography assessments demonstrated a significant improvement in heart function following treatment with hydrogen compared to that in the EAM group. Pathological results revealed significant inflammatory cell infiltration and fibrosis in the hearts of the untreated EAM group. Tissue immunofluorescence and protein immunoblotting indicated elevated necroptosis markers in the EAM group, which were downregulated after treatment with hydrogen. This study demonstrates that hydrogen effectively ameliorated autoimmune myocarditis by modulating necroptosis via the TNF/TNFR1 signalling pathway, making it a promising novel therapeutic strategy for myocarditis.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110577"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144830395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Primary immunodeficiency diseases, inflammation and mitochondrial dysfunction 原发性免疫缺陷疾病，炎症和线粒体功能障碍。

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-09-02 DOI: 10.1016/j.clim.2025.110595

Salvatore Nesci , Francesca Oppedisano , Giovanni Romeo , Silvia Granata

{"title":"Primary immunodeficiency diseases, inflammation and mitochondrial dysfunction","authors":"Salvatore Nesci , Francesca Oppedisano , Giovanni Romeo , Silvia Granata","doi":"10.1016/j.clim.2025.110595","DOIUrl":"10.1016/j.clim.2025.110595","url":null,"abstract":"<div><div>Primary immunodeficiency diseases (PIDs) are a heterogeneous group of inherited disorders characterized by impaired immune function, leading to increased susceptibility to infections, autoimmunity, and malignancies. While traditionally defined by immune cell defects, emerging evidence highlights the critical role of inflammation in PID pathogenesis. This review explores the intricate relationship between mitochondrial dysfunction and inflammation in PIDs. We examine how genetic defects in PIDs disrupt immune homeostasis, promoting pro-inflammatory states through cytokine dysregulation. Additionally, we discuss the vicious cycle involving oxidative stress, mitochondrial dysfunction, and inflammation, emphasizing the contribution of mitochondrial ROS production, mtDNA damage, and inflammasome activation in sustaining chronic inflammation. Furthermore, we propose that impaired mitochondrial function —potentially through mechanisms involving calcium signalling, ATP synthase regulation, and mitochondrial permeability transition pore formation — may serve as a central link between immune deficiency and hyperinflammation in PIDs. Understanding these complex interactions may provide new insights into the pathogenesis of PIDs and open avenues for targeted therapeutic strategies to improve patient outcomes.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110595"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144999887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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LncRNA MEG3 as a biomarker and therapeutic target in rheumatoid arthritis: Insights from gene polymorphisms, expression patterns, and functional mechanisms LncRNA MEG3作为类风湿性关节炎的生物标志物和治疗靶点：来自基因多态性、表达模式和功能机制的见解

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-08-28 DOI: 10.1016/j.clim.2025.110590

Sha-Sha Tao , Hai-Fen Wei , Shu-Zhen Xu , Xiao-Xiao Li , Yan-Yu Zhu , Jian Tang , Wen-Jie Li , Yu-Wan Chang , Zhu Chen , Hai-Feng Pan

{"title":"LncRNA MEG3 as a biomarker and therapeutic target in rheumatoid arthritis: Insights from gene polymorphisms, expression patterns, and functional mechanisms","authors":"Sha-Sha Tao , Hai-Fen Wei , Shu-Zhen Xu , Xiao-Xiao Li , Yan-Yu Zhu , Jian Tang , Wen-Jie Li , Yu-Wan Chang , Zhu Chen , Hai-Feng Pan","doi":"10.1016/j.clim.2025.110590","DOIUrl":"10.1016/j.clim.2025.110590","url":null,"abstract":"<div><div>Maternally expressed gene 3 (<em>MEG3</em>) is implicated in autoimmunity, but its role in rheumatoid arthritis (RA) is unclear. This study aimed to investigate gene polymorphisms, expression patterns, and functional mechanisms of <em>MEG3</em> in RA pathogenesis and its clinical associations. <em>MEG3</em> single nucleotide polymorphisms (SNPs) were genotyped in 551 RA patients and 595 controls, finding no association with RA susceptibility. <em>MEG3</em> expression was downregulated in peripheral blood mononuclear cells (PBMCs) from RA patients, particularly in ACPA-positive cases, but increased with NSAID use. In fibroblast-like synoviocytes (FLS), <em>MEG3</em> was downregulated. Overexpression of <em>MEG3</em> inhibited FLS proliferation and invasion, lowering IL-1β and IL-6 but not TNF-α. Whereas <em>MEG3</em> knockdown enhanced FLS proliferation and invasion, elevating TNF-α and IL-1β without altering IL-6. Collectively, <em>MEG3</em> polymorphisms are not associated with RA susceptibility. <em>MEG3</em> dysregulation correlates with RA clinical indicators and regulates FLS pathogenicity, indicating its potential as a clinical biomarker and therapeutic target in RA.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110590"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144921484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of immune complex antigens that are detected prior to early rheumatoid arthritis symptoms and increase with disease progression: Comprehensive serum immune complexome analysis to identify candidate disease biomarkers in health checkup cohort study 识别早期类风湿关节炎症状前检测到的免疫复合物抗原，并随着疾病进展而增加：在健康检查队列研究中，综合血清免疫复合物组分析确定候选疾病生物标志物

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-08-27 DOI: 10.1016/j.clim.2025.110591

Yuki Jimbayashi Kutsuna , Nozomi Aibara , Junya Hashizume , Sayaka Kawarabayashi , Mami Tamai , Jun Miyata , Hajime Yoshifuji , Hirotaka Miyamoto , Kayoko Sato , Yukinobu Kodama , Mikiro Nakashima , Atsushi Kawakami , Takahiro Maeda , Kaname Ohyama

{"title":"Identification of immune complex antigens that are detected prior to early rheumatoid arthritis symptoms and increase with disease progression: Comprehensive serum immune complexome analysis to identify candidate disease biomarkers in health checkup cohort study","authors":"Yuki Jimbayashi Kutsuna , Nozomi Aibara , Junya Hashizume , Sayaka Kawarabayashi , Mami Tamai , Jun Miyata , Hajime Yoshifuji , Hirotaka Miyamoto , Kayoko Sato , Yukinobu Kodama , Mikiro Nakashima , Atsushi Kawakami , Takahiro Maeda , Kaname Ohyama","doi":"10.1016/j.clim.2025.110591","DOIUrl":"10.1016/j.clim.2025.110591","url":null,"abstract":"<div><div>Although anti-cyclic citrullinated peptide is a biomarker, its contribution to rheumatoid arthritis pathogenesis is unknown, and it has not been a therapeutic target to date. As inflammatory pathology is present from an early stage, and increased immune complexes have been suggested to contribute to pathogenesis, we investigated the presence of disease-related antigens that form immune complexes that increase in abundance with disease progression. Using immune complexome analysis, we analyzed immune complex antigen to disease progression for very-early rheumatoid arthritis (<em>n</em> = 52) and early rheumatoid arthritis (<em>n</em> = 19), in comparison with healthy controls (<em>n</em> = 28). Very-early rheumatoid arthritis was defined as those positive for anti-cyclic citrullinated peptide antibody who did not fulfill the diagnostic criteria for rheumatoid arthritis. Seven antigens increased with disease progression and were detected at significantly higher abundance in early rheumatoid arthritis than in other major autoimmune diseases. Among these, three antigens have previously reported associations with rheumatoid arthritis pathogenesis.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110591"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dual role of plasmablasts as immune regulators or amplifiers in COVID-19 质母细胞在COVID-19中作为免疫调节剂或扩增剂的双重作用

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-10-13 DOI: 10.1016/j.clim.2025.110609

Emmanuel Ledoult , Thomas Guerrier , Sylvain Dubucquoi , Martin Figeac , Céline Villenet , Blanche Daunou , Helene Behal , Mohammad Ryadh Pokeerbux , Thomas Machet , Vincent Koether , Aurore Collet , David Launay , Lille Covid Research network (LICORNE)

{"title":"Dual role of plasmablasts as immune regulators or amplifiers in COVID-19","authors":"Emmanuel Ledoult , Thomas Guerrier , Sylvain Dubucquoi , Martin Figeac , Céline Villenet , Blanche Daunou , Helene Behal , Mohammad Ryadh Pokeerbux , Thomas Machet , Vincent Koether , Aurore Collet , David Launay , Lille Covid Research network (LICORNE)","doi":"10.1016/j.clim.2025.110609","DOIUrl":"10.1016/j.clim.2025.110609","url":null,"abstract":"<div><div>COVID-19 induces a marked plasmablast (PB) expansion, whose functional role remains unclear. We performed B-cell immunophenotyping and multiplex cytokine analysis in a prospective cohort of 50 COVID-19 patients. PB expansion occurred early and correlated with both maximal disease severity and inflammatory markers. A retrospective cohort of 282 steroid-naïve patients was used to validate PB dynamics, model trajectories, and perform transcriptomic profiling. Two PB trajectories emerged: a transient one and a persistent, amplified one, the latter associated with a sixfold increase in 30-day mortality (<em>p</em> < 0.001). In severe cases, PB upregulated purine metabolism genes; in non-severe cases, they expressed interferon and CIITA-mediated MHC-II programs. BAFF levels at day 7 correlated with severity suggesting a role in sustaining PB expansion. PB exhibit functional duality in COVID-19—acting as immune regulators in non-severe cases and as inflammation amplifiers in severe disease. BAFF emerges as a potential therapeutic target in PB-driven immune dysregulation.</div><div><strong>Trial registration.</strong> <span><span>ClinicalTrials.gov</span><svg><path></path></svg></span> <span><span>NCT04327180</span><svg><path></path></svg></span> and <span><span>NCT04341792</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110609"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cerebrospinal fluid exosomal Epstein-Barr virus microRNAs in multiple sclerosis and effects of disease modifying therapies 多发性硬化症脑脊液外泌体爱泼斯坦-巴尔病毒microrna及疾病修饰疗法的效果

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-10-11 DOI: 10.1016/j.clim.2025.110608

Victoria Hyslop Hvalkof, Malene Bredahl Hansen, Sahla El Mahdaoui, Marie Mathilde Hansen, Jeppe Romme Christensen, Sophie Buhelt, Finn Sellebjerg, Helle Bach Søndergaard

{"title":"Cerebrospinal fluid exosomal Epstein-Barr virus microRNAs in multiple sclerosis and effects of disease modifying therapies","authors":"Victoria Hyslop Hvalkof, Malene Bredahl Hansen, Sahla El Mahdaoui, Marie Mathilde Hansen, Jeppe Romme Christensen, Sophie Buhelt, Finn Sellebjerg, Helle Bach Søndergaard","doi":"10.1016/j.clim.2025.110608","DOIUrl":"10.1016/j.clim.2025.110608","url":null,"abstract":"<div><div>Epstein-Barr virus (EBV) may be crucial for development of multiple sclerosis (MS). EBV encodes 44 microRNAs (miRNAs) that are found in exosomes. We investigated EBV miRNAs in cerebrospinal fluid (CSF) exosomes in 50 newly diagnosed people with relapsing-remitting MS (pwRRMS), 24 with clinically isolated syndromes (CIS), 45 symptomatic controls (SC), 15 anti-CD20 antibody-treated 24 natalizumab (NTZ)-treated pwRRMS. miRNAs were measured by quantitative PCR. Plasma anti-EBNA1 antibody and various CSF biomarkers were measured by immunoassays. ebv-miR-BART13-5p and ebv-miR-BART19-3p were reliably measured. ebv-miR-BART19-3p was lower in pwRRMS and correlated with disease severity. In NTZ-treated pwRRMS, ebv-miR-BART19-3p was higher, correlated with treatment duration, and was associated with soluble B-cell maturation antigen, CD27, and zonula occludens-1. No differences were observed in anti-CD20 antibody-treated pwRRMS. These findings may reflect the presence of more exosome recipient cells in pwRRMS, resulting in fewer exosomes as they become internalized in recipient cells along with their EBV miRNA cargo.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110608"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Altered methylation-related genes expression in B cells of systemic lupus erythematosus patients 系统性红斑狼疮患者B细胞甲基化相关基因表达的改变。

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-10-08 DOI: 10.1016/j.clim.2025.110606

Amin Azizan , Elham Farhadi , Seyedeh Tahereh Faezi , Majid Alikhani , Mahdi Mahmoudi , Ahmadreza Jamshidi , Mohammad Vodjgani

{"title":"Altered methylation-related genes expression in B cells of systemic lupus erythematosus patients","authors":"Amin Azizan , Elham Farhadi , Seyedeh Tahereh Faezi , Majid Alikhani , Mahdi Mahmoudi , Ahmadreza Jamshidi , Mohammad Vodjgani","doi":"10.1016/j.clim.2025.110606","DOIUrl":"10.1016/j.clim.2025.110606","url":null,"abstract":"<div><h3>Background and objective</h3><div>B cells contribute to systemic lupus erythematosus (SLE) pathogenesis through autoantibody production. DNA hypomethylation in B cells is a hallmark of SLE and may be associated with altered expression of key epigenetic regulators. This study investigated the mRNA expression of DNMT1 and UHRF1, which maintain DNA methylation, and TET2 and TET3, which mediate demethylation, in B cells from SLE patients.</div></div><div><h3>Methods</h3><div>Participants included individuals with active SLE, inactive SLE, and healthy controls. Purified B cells were stimulated in vitro with anti-human IgM. Gene expression of DNMT1, UHRF1, TET2, and TET3 was quantified by qRT-PCR</div></div><div><h3>Results</h3><div>At baseline, UHRF1 mRNA expression was significantly decreased, and TET3 expression significantly increased in B cells from active SLE patients compared to controls. Upon anti-IgM activation, further reductions in UHRF1 and increases in TET3 expression were observed in active SLE B cells. DNMT1 and TET2 expression did not differ significantly across groups or conditions.</div></div><div><h3>Conclusion</h3><div>The altered expression of UHRF1 and TET3 mRNA in B cells from active SLE patients may reflect underlying epigenetic dysregulation associated with disease activity. These findings provide preliminary support for further investigation into their potential involvement in the pathobiology of SLE.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110606"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

B cell receptor repertoires identified by next-generation sequencing showed signatures associated with incomplete immune reconstitution in people living with HIV 新一代测序鉴定的B细胞受体谱显示了与HIV感染者不完全免疫重建相关的特征。

IF 3.8 3区医学

Clinical immunology Pub Date : 2025-12-01 Epub Date: 2025-08-31 DOI: 10.1016/j.clim.2025.110594

Yu-Jie Zhan , Wei Liu , Bu-Yi Wang , Bo-Yang Ma , Jia-Ye Wang , Yi-Lin Zhao , Xin-Xin Wang , Yue Jiang , Dan Wang , Li Wang , Hong Ling , Min Zhuang

{"title":"B cell receptor repertoires identified by next-generation sequencing showed signatures associated with incomplete immune reconstitution in people living with HIV","authors":"Yu-Jie Zhan , Wei Liu , Bu-Yi Wang , Bo-Yang Ma , Jia-Ye Wang , Yi-Lin Zhao , Xin-Xin Wang , Yue Jiang , Dan Wang , Li Wang , Hong Ling , Min Zhuang","doi":"10.1016/j.clim.2025.110594","DOIUrl":"10.1016/j.clim.2025.110594","url":null,"abstract":"<div><div>Incomplete immune reconstitution poses a significant challenge for anti-retroviral therapy (ART) in HIV-infected individuals. The role of B cell receptors (BCRs) in immune reconstitution, a critical aspect of the immune system, has not been well elucidated in ART-experienced people. We analyzed the BCR heavy chain repertoire in immune non-responders (INRs) and immune responders (IRs) by next-generation sequencing. The BCR repertoire of INRs was characterized by a higher proportion of longer HCDR3 and reduced frequencies of IGHV1–69, IGHJ2, and IGHV1–69/IGHJ4 and IGHV5–51/IGHJ4 pairings. INRs, rather than IRs, carried HCDR3 genes which were highly homologous to anti-HIV broadly neutralizing antibodies targeting the six-helix bundle (6HB) in envelope gp41. The plasmas of INRs also exhibited an increased reactivity to FPPR-N36, a peptide within 6HB. These findings indicated a potential association between BCR, antibodies to partial gp41, and incomplete immune reconstitution and provided new perspectives for understanding the BCR repertoire and immune reconstitution.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110594"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0