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 Q2 IMMUNOLOGY

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

Background

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).

Methods

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.

Results

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.

Conclusions

GDNF drives aberrant epithelial remodeling in CRSwNP via MAPK/PI3K signaling, highlighting its therapeutic potential for refractory disease.

背景：神经营养因子在鼻息肉（NPs）和/或过敏中升高，发挥神经源性炎症作用。非经典神经胶质源性神经营养因子（GDNF）家族配体（GFLs）在慢性鼻窦炎伴NP （CRSwNP）中的作用尚不清楚。方法：通过蛋白质组学、转录组学和免疫组化分析67种鼻液（NFs）和44种组织中GDNF的表达。免疫荧光共染色鉴定GDNF和p63 + 基底细胞（BCs）。人鼻上皮细胞（HNECs）的功能研究评估了GDNF对增殖和屏障完整性的影响。生物信息学鉴定了监管网络和候选药物。结果：GDNF存在于CRSwNP的NFs和组织中，且在嗜酸性NPs中丰度较高。P63 + BCs表达与GDNF水平呈正相关。GDNF有效激活HNECs中MAPK/PI3K/Akt信号通路，诱导Ki-67+/p63 + 细胞增殖，同时减少连接处cludin -1的分布。预测miR-204-5p/211-5p和两种fda批准的神经活性药物可作为GDNF调节剂。结论：GDNF通过MAPK/PI3K信号驱动CRSwNP异常上皮重塑，突出了其治疗难治性疾病的潜力。

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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 Q2 IMMUNOLOGY

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 Q2 IMMUNOLOGY

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

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.

自身免疫性心肌炎是指由先天和适应性免疫反应引起的心肌组织炎症，其特征是肿瘤坏死因子-α (TNF-α)水平升高，这是一种典型的促炎因子。虽然氢具有抗炎和抗氧化的特性，但其治疗自身免疫性心肌炎的效果尚未得到评价。因此，本研究旨在探讨氢是否能通过TNF-α缓解自身免疫性心肌炎。通过皮下注射经完全弗氏佐剂乳化的猪源性心肌肌红蛋白，建立了BALB/c小鼠实验性自身免疫性心肌炎（EAM）模型。治疗组给予2%氢气吸入，每日2次，每次3 h，连用21 d。EAM组CD4+ T细胞表达高于对照组，氢治疗后这种升高减弱。此外，EAM组的TNF-α和相关炎症因子水平明显高于对照组，这些变化在氢治疗后被逆转。超声心动图评估显示，与EAM组相比，氢治疗后心功能有显著改善。病理结果显示，EAM治疗组心脏有明显的炎症细胞浸润和纤维化。组织免疫荧光和蛋白质免疫印迹显示，EAM组坏死下垂标志物升高，氢治疗后下调。本研究表明，氢通过TNF/TNFR1信号通路调节坏死性下垂，有效改善自身免疫性心肌炎，使其成为治疗心肌炎的一种有前景的新策略。

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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 Q2 IMMUNOLOGY

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

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.

原发性免疫缺陷疾病（pid）是一种异质性的遗传性疾病，其特征是免疫功能受损，导致对感染、自身免疫和恶性肿瘤的易感性增加。虽然传统上由免疫细胞缺陷定义，但新的证据强调了炎症在PID发病机制中的关键作用。本文综述了线粒体功能障碍与炎症之间的复杂关系。我们研究了PIDs中的遗传缺陷如何破坏免疫稳态，通过细胞因子失调促进促炎状态。此外，我们讨论了氧化应激、线粒体功能障碍和炎症的恶性循环，强调了线粒体ROS产生、mtDNA损伤和炎症小体激活在维持慢性炎症中的作用。此外，我们提出线粒体功能受损-可能通过涉及钙信号，ATP合成酶调节和线粒体通透性过渡孔形成的机制-可能是免疫缺陷和PIDs高炎症之间的中心联系。了解这些复杂的相互作用可能为PIDs的发病机制提供新的见解，并为有针对性的治疗策略开辟道路，以改善患者的预后。

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引用次数: 0

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 Q2 IMMUNOLOGY

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

Maternally expressed gene 3 (MEG3) 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 MEG3 in RA pathogenesis and its clinical associations. MEG3 single nucleotide polymorphisms (SNPs) were genotyped in 551 RA patients and 595 controls, finding no association with RA susceptibility. MEG3 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), MEG3 was downregulated. Overexpression of MEG3 inhibited FLS proliferation and invasion, lowering IL-1β and IL-6 but not TNF-α. Whereas MEG3 knockdown enhanced FLS proliferation and invasion, elevating TNF-α and IL-1β without altering IL-6. Collectively, MEG3 polymorphisms are not associated with RA susceptibility. MEG3 dysregulation correlates with RA clinical indicators and regulates FLS pathogenicity, indicating its potential as a clinical biomarker and therapeutic target in RA.

母系表达基因3 （MEG3）与自身免疫有关，但其在类风湿关节炎（RA）中的作用尚不清楚。本研究旨在探讨MEG3在RA发病中的基因多态性、表达模式、功能机制及其临床相关性。在551例RA患者和595例对照中对MEG3单核苷酸多态性（snp）进行了基因分型，未发现与RA易感性相关。在RA患者外周血单个核细胞（PBMCs）中，MEG3表达下调，特别是在acpa阳性病例中，但随着NSAID的使用而升高。在成纤维细胞样滑膜细胞（FLS）中，MEG3下调。MEG3过表达可抑制FLS增殖和侵袭，降低IL-1β和IL-6，但对TNF-α无抑制作用。而MEG3敲低可增强FLS的增殖和侵袭，升高TNF-α和IL-1β，但不改变IL-6。总的来说，MEG3多态性与RA易感性无关。MEG3异常与RA临床指标相关，并调节FLS致病性，提示其可能成为RA的临床生物标志物和治疗靶点。

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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 Q2 IMMUNOLOGY

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

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 (n = 52) and early rheumatoid arthritis (n = 19), in comparison with healthy controls (n = 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.

虽然抗环瓜氨酸肽是一种生物标志物，但其在类风湿关节炎发病机制中的作用尚不清楚，并且迄今为止尚未成为治疗靶点。由于炎症病理从早期就存在，并且免疫复合物的增加被认为有助于发病机制，我们研究了疾病相关抗原的存在，这些抗原形成免疫复合物，随着疾病进展而增加。通过免疫复合物组分析，我们分析了极早期类风湿关节炎（n = 52）和早期类风湿关节炎（n = 19）的免疫复合物抗原与疾病进展的关系，并与健康对照（n = 28）进行了比较。早期类风湿关节炎定义为抗环瓜氨酸肽抗体阳性，但不符合类风湿关节炎的诊断标准。7种抗原随着疾病进展而增加，在早期类风湿关节炎中检测到的丰度明显高于其他主要自身免疫性疾病。在这些抗原中，有三种抗原曾被报道与类风湿关节炎的发病机制有关。

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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 Q2 IMMUNOLOGY

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)

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 (p < 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.

Trial registration. ClinicalTrials.gov NCT04327180 and NCT04341792.

COVID-19诱导明显的浆母细胞（PB）扩增，其功能作用尚不清楚。我们对50名COVID-19患者进行了b细胞免疫分型和多重细胞因子分析。PB扩张发生较早，并与最大疾病严重程度和炎症标志物相关。282例steroid-naïve患者的回顾性队列被用来验证PB动力学，模型轨迹，并执行转录组分析。出现了两种PB轨迹：一种是短暂的轨迹，另一种是持续的、放大的轨迹，后者与30天死亡率增加6倍有关

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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 Q2 IMMUNOLOGY

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

Background and objective

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.

Methods

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

Results

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.

Conclusion

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.

背景与目的：B细胞通过自身抗体的产生参与系统性红斑狼疮（SLE）的发病。B细胞中的DNA低甲基化是SLE的一个标志，可能与关键表观遗传调控因子的表达改变有关。本研究研究了SLE患者B细胞中维持DNA甲基化的DNMT1和UHRF1以及介导去甲基化的TET2和TET3的mRNA表达。方法：参与者包括活动性SLE患者、非活动性SLE患者和健康对照。体外用抗人IgM刺激纯化的B细胞。采用qRT-PCR定量检测DNMT1、UHRF1、TET2和TET3基因表达结果：基线时，与对照组相比，活动性SLE患者B细胞中UHRF1 mRNA表达显著降低，TET3表达显著升高。在抗igm激活后，在活动性SLE B细胞中观察到UHRF1的进一步降低和TET3表达的增加。DNMT1和TET2的表达在不同组或不同条件下无显著差异。结论：活动性SLE患者B细胞中UHRF1和TET3 mRNA表达的改变可能反映了与疾病活动性相关的潜在表观遗传失调。这些发现为进一步研究它们在SLE病理生物学中的潜在作用提供了初步支持。

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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 Q2 IMMUNOLOGY

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

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.

eb病毒（EBV）可能对多发性硬化症（MS）的发展至关重要。EBV编码在外泌体中发现的44种microrna （mirna）。我们研究了50例新诊断的复发-缓解型MS (pwRRMS)， 24例临床分离综合征（CIS）， 45例症状对照（SC）， 15例抗cd20抗体治疗的24例纳他珠单抗（NTZ）治疗的pwRRMS患者脑脊液（CSF）外泌体中的EBV mirna。采用定量PCR检测mirna。采用免疫分析法检测血浆抗ebna1抗体和各种脑脊液生物标志物。Ebv-miR-BART13-5p和ebv-miR-BART19-3p的测定是可靠的。Ebv-miR-BART19-3p在pwRRMS中较低，且与疾病严重程度相关。在ntz治疗的pwRRMS中，ebv-miR-BART19-3p更高，与治疗时间相关，并与可溶性b细胞成熟抗原、CD27和小带闭塞-1相关。抗cd20抗体处理的pwRRMS未见差异。这些发现可能反映了pwRRMS中存在更多的外泌体受体细胞，导致外泌体减少，因为它们与EBV miRNA货物一起被内化在受体细胞中。

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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 Q2 IMMUNOLOGY

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

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.

不完全的免疫重建对艾滋病毒感染者的抗逆转录病毒治疗（ART）提出了重大挑战。B细胞受体（BCRs）在免疫重建中的作用是免疫系统的一个关键方面，但在经历过art治疗的人群中尚未得到很好的阐明。我们利用新一代测序技术分析了免疫无应答者（INRs）和免疫应答者（IRs）的BCR重链库。INRs的BCR库的特点是HCDR3较长比例较高，IGHV1-69、IGHJ2、IGHV1-69/IGHJ4和IGHV5-51/IGHJ4配对频率较低。INRs而不是IRs携带HCDR3基因，这些基因与靶向包膜gp41中六螺旋束（6HB）的抗hiv广泛中和抗体高度同源。INRs的血浆也表现出对fpr - n36 （6HB内的肽）的反应性增加。这些发现提示了BCR、部分gp41抗体和不完全免疫重建之间的潜在关联，并为理解BCR库和免疫重建提供了新的视角。

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引用次数: 0