Immunobiology最新文献_第2页

Lymphocyte subpopulations in healthy Ukrainian men: local reference ranges, long temporal stability, and exercise-induced variability 乌克兰健康男性的淋巴细胞亚群：当地参考范围、长期稳定性和运动引起的变异性

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-03-01 Epub Date: 2026-02-22 DOI: 10.1016/j.imbio.2026.153170

Dariia Zabara , Iryna Kozeretska , Ivan Klapoushenko , Yaroslava Anoshko , Ievgen Dubrovskyi , Boris Dons'koi

Reliable interpretation of lymphocyte immunophenotyping depends on population-specific reference ranges that account for demographic and environmental factors. However, such reference data are currently lacking for the Ukrainian population. This study aimed to establish local reference ranges for lymphocyte subpopulations in healthy adult men and to assess their temporal stability and variability following physical exercise.

Peripheral blood samples from 100 clinically healthy men aged 22–55 years were analyzed by flow cytometry to quantify T lymphocytes (CD3⁺, CD3⁺CD4⁺, CD3⁺CD8⁺), B lymphocytes (CD3⁻CD19⁺), and NK cells (CD3⁻CD56⁺, CD3⁻CD56⁺NKp46⁺). Temporal stability was evaluated in 24 participants monitored during a one-year Antarctic expedition, while acute immune responses were assessed in 19 men before and after a modified Cooper test. The established reference ranges were as follows: CD3⁺ (54.0–82.2%), CD3⁺CD4⁺ (29.3–54.0%), CD3⁺CD8⁺ (11.2–39.6%), CD3⁻CD19⁺ (3.7–20.1%), CD3⁻CD56⁺ (4.2–30.0%), and CD3⁻CD56⁺NKp46⁺ (2.7–24.3%).

Comparison with published studies revealed differences in several parameters, whereas discrepancies relative to reference values used by local laboratories were observed across multiple measures. Following a one-year Antarctic expedition, lymphocyte subset distributions remained largely stable despite a significant expansion of monocytes, whereas short-term physical exercise elicited pronounced, subset-selective increases in NK cells and monocytes, accompanied by concurrent elevations in cortisol and testosterone levels. The differences observed across populations and laboratories underscore the need for harmonized, population-based reference intervals.

淋巴细胞免疫分型的可靠解释取决于考虑人口统计学和环境因素的人群特异性参考范围。但是，乌克兰人口目前缺乏这种参考数据。本研究旨在建立健康成年男性淋巴细胞亚群的局部参考范围，并评估其在体育锻炼后的时间稳定性和变异性。本文采用流式细胞术对100例22 ~ 55岁临床健康男性外周血进行了T淋巴细胞（CD3+、CD3+CD4+、CD3+CD8+）、B淋巴细胞（CD3- cd19 +）和NK细胞（CD3- cd56 +、CD3- cd56 +NKp46+）的定量分析。在为期一年的南极考察中，对24名参与者的时间稳定性进行了评估，同时对19名男性的急性免疫反应进行了改进的库珀测试前后的评估。建立的参考范围为：CD3+(54.0-82.2%)、CD3+CD4+(29.3-54.0%)、CD3+CD8+(11.2-39.6%)、CD3- cd19 +(3.7-20.1%)、CD3- cd56 +(4.2-30.0%)、CD3- cd56 +NKp46+(2.7-24.3%)。与已发表研究的比较揭示了几个参数的差异，而在多个测量中观察到相对于当地实验室使用的参考值的差异。经过一年的南极考察，淋巴细胞亚群分布基本保持稳定，尽管单核细胞显著增加，而短期体育锻炼引起NK细胞和单核细胞的亚群选择性明显增加，同时皮质醇和睾酮水平升高。不同人群和实验室之间观察到的差异强调了建立统一的、基于人群的参考区间的必要性。

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引用次数: 0

Clinical value of CTCs combined with serum tumor markers/inflammatory cytokines for the early diagnosis of non-small cell lung cancer ctc联合血清肿瘤标志物/炎症因子对非小细胞肺癌早期诊断的临床价值

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-03-01 Epub Date: 2026-01-24 DOI: 10.1016/j.imbio.2026.153161

Xiuxue Gu , Lingling Wan

Objective: This study investigates the clinical utility of circulating tumor cells (CTCs) in combination with serum tumor markers/inflammatory cytokines for the diagnosis of early-stage non-small cell lung cancer (NSCLC). Methods: A retrospective analysis was conducted on the clinical data of 43 NSCLC patients (stage I-IIA) who underwent surgical treatment at the Fourth Hospital of Hebei Medical University between November 2021 and December 2022. A control group of 50 healthy individuals was also included. Comparative analyses of CTCs, serum tumor markers, and inflammatory cytokine levels were performed between the two groups. The clinical diagnostic value was assessed using receiver operating characteristic (ROC) curve analysis. Results: The median concentrations of CTCs, carcinoembryonic antigen (CEA), Cytokeratin 19 fragment (CYFRA21-1), neuron-specific enolase (NSE), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), and interleukin-17 A (IL-17 A) were significantly elevated in the NSCLC cohort compared to the healthy control cohort, while interleukin-2 (IL-2) levels were reduced (P < 0.05). ROC curve analysis revealed that CTCs exhibited a sensitivity of 65.12%, specificity of 100.00%, and an area under the curve (AUC) of 0.826 for the diagnosis of early-stage NSCLC. The combined diagnostic sensitivity of CTCs, CEA, CYFRA21-1, and NSE reached 86.05%, with 100.00% specificity and an AUC of 0.945. Among the seven inflammatory cytokines evaluated, IL-17 A exhibited the highest diagnostic efficacy for early-stage NSCLC, with an AUC of 0.871, sensitivity of 93.02%, and specificity of 75.00%. The combination of IL-17 A and CTCs achieved an AUC of 0.953, with a sensitivity of 86.05% and specificity of 90.00%. Conclusion: The integration of CTCs with serum tumor markers and/or inflammatory cytokines provides high sensitivity and specificity for the diagnosis of early-stage NSCLC, highlighting its significant clinical potential.

目的：探讨循环肿瘤细胞（CTCs）联合血清肿瘤标志物/炎症因子在早期非小细胞肺癌（NSCLC）诊断中的临床应用价值。方法：回顾性分析2021年11月至2022年12月在河北医科大学第四医院行手术治疗的43例I-IIA期非小细胞肺癌患者的临床资料。另外还包括一个由50名健康个体组成的对照组。比较分析两组患者ctc、血清肿瘤标志物和炎症细胞因子水平。采用受试者工作特征（ROC）曲线分析评估临床诊断价值。结果：NSCLC组CTCs、癌胚抗原（CEA）、细胞角蛋白19片段（CYFRA21-1）、神经元特异性烯醇酶（NSE）、白细胞介素-4 （IL-4）、白细胞介素-6 （IL-6）、白细胞介素-10 （IL-10）、肿瘤坏死因子-α (TNF-α)、白细胞介素- 17a （il - 17a）的中位浓度较健康对照组显著升高，白细胞介素-2 （IL-2）水平降低(P)。CTCs与血清肿瘤标志物和/或炎症细胞因子的结合为早期NSCLC的诊断提供了高敏感性和特异性，突出了其重要的临床潜力。

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引用次数: 0

BCL3 drives an immunosuppressive tumor microenvironment in esophageal cancer by promoting M2 macrophage polarization via STAT3 activation BCL3通过STAT3激活促进M2巨噬细胞极化，在食管癌中驱动免疫抑制肿瘤微环境。

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-03-01 Epub Date: 2026-02-10 DOI: 10.1016/j.imbio.2026.153164

Yushuai Geng , Haowen Ma , Minghang Liu , Tairan Feng , Yang Lv , Zhiqiang Li , Shujun Ma , Hui Wang , Yuna Niu

Introduction

The progression of esophageal cancer is closely linked to the establishment of an immunosuppressive tumor microenvironment. Although B-cell leukemia/lymphoma 3 (BCL3) is dysregulated in various cancers, its specific role and mechanism in shaping the immune microenvironment of esophageal cancer, particularly in macrophage polarization, remain elusive.

Results

BCL3 was significantly overexpressed in esophageal cancer tissues, demonstrated good diagnostic value (AUC = 0.75, P < 0.01), and its high expression was significantly associated with poor patient prognosis (P < 0.05). Immune infiltration analysis revealed that high BCL3 expression correlated with increased M2 macrophage infiltration. In vitro experiments confirmed that knocking down BCL3 suppressed M2 macrophage polarization. Mechanistic studies indicated that BCL3 drives M2 polarization by enhancing the phosphorylation of STAT3.

Conclusion

Our study unveils a novel mechanism whereby BCL3 promotes an immunosuppressive tumor microenvironment in esophageal cancer by facilitating M2 macrophage polarization via the STAT3 signaling pathway. BCL3 represents a potential prognostic biomarker and a promising therapeutic target for immunotherapy in esophageal cancer.

食管癌的发展与免疫抑制肿瘤微环境的建立密切相关。虽然b细胞白血病/淋巴瘤3 （BCL3）在多种癌症中失调，但其在塑造食管癌免疫微环境，特别是巨噬细胞极化中的具体作用和机制尚不清楚。结果：BCL3在食管癌组织中显著过表达，具有良好的诊断价值（AUC = 0.75， P）。结论：本研究揭示了BCL3通过STAT3信号通路促进M2巨噬细胞极化，从而促进食管癌肿瘤微环境免疫抑制的新机制。BCL3是一种潜在的预后生物标志物，也是食管癌免疫治疗的一个有希望的治疗靶点。

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引用次数: 0

Preface to the special issue for the 30th International Complement Workshop Brisbane 2025. 2025年布里斯班第30届国际补体研讨会特刊前言。

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-03-01 Epub Date: 2025-12-19 DOI: 10.1016/j.imbio.2025.153149

Barbara E Rolfe, John D Lee, Trent M Woodruff

This Immunobiology special issue commemorates the 30th International Complement Workshop, held for the first time in Australia. Reflecting the global reach of complement research, the Workshop brought together delegates from 24 countries and showcased a diverse range of topics including: Structural insight into complement function; Mechanisms of activation and regulation; Cell-autonomous and intracellular complement; Novel and non-canonical roles; Complement in infection and disease; and Biomarkers, diagnostics and therapeutics. In addition to invited reviews and an original research article, this issue includes all accepted abstracts from the Workshop. Together, these contributions provide a compelling snapshot of a rapidly evolving field, one that continues to expand in scope and deepen mechanistic understanding. They highlight the dynamic, interdisciplinary and collaborative nature of complement research, and set the stage for future discoveries that will translate into clinical benefit.

本免疫生物学特刊纪念第30届国际补体研讨会，首次在澳大利亚举行。研讨会汇集了来自24个国家的代表，反映了补体研究的全球影响力，并展示了一系列不同的主题，包括：补体功能的结构洞察；激活与调控机制；细胞自主补体和细胞内补体；新颖和非规范的角色；感染和疾病的补体；生物标志物，诊断和治疗。除了特邀评论和一篇原创研究文章外，本期还包括研讨会所有已接受的摘要。总之，这些贡献提供了一个引人注目的快速发展领域的快照，一个继续扩大范围和深化机制的理解。它们突出了补体研究的动态、跨学科和协作性质，并为未来的发现奠定了基础，这些发现将转化为临床效益。

引用次数: 0

Unraveling SLAN+/− monocytes transcriptomics in lupus and extracellular vesicles effects 揭示狼疮中SLAN+/−单核细胞转录组学和细胞外囊泡效应

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-03-01 Epub Date: 2025-12-26 DOI: 10.1016/j.imbio.2025.153153

Paula X. Losada , Juan Antonio Villatoro-García , Julio Jaramillo , Lina Serrato , Karen Álvarez , Daniel Rodriguez , Juan Camilo Diaz , Ricardo Pineda , Pedro Carmona-Saez , Mauricio Rojas , Gloria Vásquez

Objective

Lupus Nephritis (LN) is a common and serious complication in patients with Systemic Lupus Erythematosus (SLE), an immune complex-mediated disease. Extracellular Vesicles (EVs) can carry autoantigens recognized by circulating antibodies, forming immune complexes (ICs) that may deposit in the kidney and be detected by inflammatory cells like monocytes in LN class III/IV. The SLAN marker identifies a subset of non-classical monocytes considered highly inflammatory and migratory. However, the interactions between these blood components in the context of LN remain incompletely understood. We aimed to analyze the transcriptional profiles of circulating SLAN+/− monocytes from LN patients and assess the influence of patient-derived EVs on SLAN− monocyte gene expression.

Methods

SLAN+/− monocytes were isolated from female LN patients, and controls were matched by similar age. Plasma-derived EVs from LN patients were co-incubated with SLAN-monocytes from controls. Next-generation RNA sequencing was employed to evaluate gene expression profiles and changes induced by EVs, followed by bioinformatic analysis to identify differential gene expression and functional pathways.

Results

Monocytes from LN patients exhibited an inflammatory profile characterized by elevated interferon response genes. The SLAN+ fraction displayed biological processes relevant to renal pathology, including cellular stress response, differentiation, and migration pathways. EVs elicited an inflammatory response with differentiation potential in non-SLAN monocytes.

Conclusions

These findings suggest that EVs transport antigenic molecules and induce transcriptional changes in monocytes toward inflammatory and migratory states, implicating them in LN pathogenesis and highlighting their potential as therapeutic targets.

目的：狼疮性肾炎（LN）是一种免疫复合物介导的系统性红斑狼疮（SLE）患者常见且严重的并发症。细胞外囊泡（EVs）可以携带被循环抗体识别的自身抗原，形成免疫复合物（ic），可沉积在肾脏中，并被LN III/IV类的单核细胞等炎症细胞检测到。SLAN标记识别非经典单核细胞被认为是高度炎症和迁移的子集。然而，在LN的情况下，这些血液成分之间的相互作用仍然不完全清楚。我们的目的是分析LN患者循环SLAN+/ -单核细胞的转录谱，并评估患者源性ev对SLAN -单核细胞基因表达的影响。方法从女性LN患者和年龄相近的对照组中分离sslan +/−单核细胞。来自LN患者的血浆源性ev与来自对照组的slan单核细胞共孵育。采用新一代RNA测序技术评估ev诱导的基因表达谱和变化，然后通过生物信息学分析确定差异基因表达和功能途径。结果LN患者单核细胞表现出以干扰素反应基因升高为特征的炎症谱。SLAN+部分显示了与肾脏病理相关的生物学过程，包括细胞应激反应、分化和迁移途径。ev在非slan单核细胞中引发了具有分化潜力的炎症反应。结论这些发现表明，ev转运抗原分子并诱导单核细胞向炎症和迁移状态的转录变化，暗示其参与LN的发病机制，并突出其作为治疗靶点的潜力。

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引用次数: 0

Chlamydia psittaci inclusion membrane protein CPSIT_0844 elicits inflammatory IL-6 and IL-8 production in human monocytes via TLR2/TLR4 signaling pathways 裸热衣原体包膜蛋白CPSIT_0844通过TLR2/TLR4信号通路诱导人单核细胞炎症性IL-6和IL-8的产生

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-03-01 Epub Date: 2026-01-19 DOI: 10.1016/j.imbio.2026.153160

Xiaoliang Yan , Buwei Wang , Kang Zheng , Dan Luo , Yumeng Li , Jian Xiao , Yuqing Chen , Zhangping He , Yating Wen , Chuan Wang , Yimou Wu

The respiratory disease caused by Chlamydia psittaci (C. psittaci) infection is often characterized by significant inflammation. In the present study, we demonstrated that the C. psittaci inclusion membrane protein CPSIT_0844 induced THP-1 cells to express IL-6 and IL-8. However, silencing of the Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) genes by using small interfering RNA (siRNA) and transfection with the dominant negative plasmid encoding MyD88 (pDeNy-hMyD88) were found to reduce the expression of IL-6 and IL-8 in THP-1 cells stimulated with CPSIT_0844. Furthermore, CPSIT_0844 induces IL-6 and IL-8 production by signaling pathways involving JNK, p38, and NF-κB in monocytes. Collectively, our findings identify CPSIT_0844 as a proinflammatory virulence factor that triggers IL-6 and IL-8 expression via a TLR2/TLR4-MyD88-dependent mechanism, culminating in the activation of MAPK and NF-κB pathways. This work provides crucial molecular insight into the inflammatory pathogenesis of C. psittaci infection.

由鹦鹉热衣原体感染引起的呼吸道疾病通常以明显的炎症为特征。在本研究中，我们证实了psit_0844包合膜蛋白CPSIT_0844诱导THP-1细胞表达IL-6和IL-8。然而，使用小干扰RNA （siRNA）沉默toll样受体2 （TLR2）和toll样受体4 （TLR4）基因，并转染编码MyD88的显性负质粒（pDeNy-hMyD88），发现在CPSIT_0844刺激的THP-1细胞中，IL-6和IL-8的表达降低。此外，CPSIT_0844通过涉及单核细胞JNK、p38和NF-κB的信号通路诱导IL-6和IL-8的产生。总的来说，我们的研究结果确定CPSIT_0844是一种促炎毒力因子，通过TLR2/ tlr4 - myd88依赖机制触发IL-6和IL-8的表达，最终激活MAPK和NF-κB途径。这项工作为鹦鹉螺杆菌感染的炎症发病机制提供了重要的分子见解。

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引用次数: 0

Unveiling a novel NBAS mutation in common variable immunodeficiency: Expanding the genetic landscape of immunodeficiency disorders. 揭示一种新的NBAS突变在常见的可变免疫缺陷：扩大免疫缺陷疾病的遗传景观。

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-03-01 Epub Date: 2025-11-23 DOI: 10.1016/j.imbio.2025.153144

Theresia Risa Davita, Deepti Naruka, Harry Lesmana, James Fernandez

NBAS, neuroblastoma-amplified sequence, mutations have been linked to multisystem disorders, including immunodeficiency. Common variable immunodeficiency (CVID) represents a heterogeneous group of primary immunodeficiency disorders characterized by hypogammaglobulinemia, lack of functional antibodies, and frequent sinopulmonary or gastrointestinal infections. The exact cause of CVID is often unknown; however, recent studies using gene sequencing have identified disease-causing genes underlying this heterogeneous immune defect. Here, we present a case of a novel NBAS mutation identified in a patient with CVID, revealing the genetic basis of immunodeficiency disorders and emphasizing the importance of comprehensive genetic analysis in clinical practice. This case underscores the need for further investigation into the functional consequences of NBAS mutations and their implications for the management of CVID and related immune conditions.

NBAS，神经母细胞瘤扩增序列，突变与多系统疾病有关，包括免疫缺陷。常见变异性免疫缺陷（CVID）是一种异质性的原发性免疫缺陷疾病，其特征是低γ球蛋白血症、缺乏功能性抗体和频繁的肺或胃肠道感染。CVID的确切原因通常是未知的；然而，最近使用基因测序的研究已经确定了这种异质免疫缺陷的致病基因。在此，我们报告了一例在CVID患者中发现的新型NBAS突变，揭示了免疫缺陷疾病的遗传基础，并强调了综合遗传分析在临床实践中的重要性。该病例强调需要进一步研究NBAS突变的功能后果及其对CVID和相关免疫疾病管理的影响。

引用次数: 0

Screening of kinase-related genes as diagnostic biomarkers and immune infiltration analysis in sepsis 激酶相关基因在脓毒症诊断中的筛选及免疫浸润分析。

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-03-01 Epub Date: 2026-01-17 DOI: 10.1016/j.imbio.2026.153158

Bingqiang Su , Yingwei Ding , Xiuqi Zhu , Laifa Kong

Background

Sepsis is a systemic inflammatory syndrome that can lead to loss of organ function. Kinase-related genes (KRGs) modulate immune diseases by regulating inflammation, immune metabolism, and apoptosis. However, their specific role in Sepsis remains unexplored.

Methods

mRNA and single-cell sequencing data in sepsis were obtained from the Gene Expression Omnibus. Weighted gene co-expression network analysis (WGCNA) was used to identify gene modules associated with sepsis, which were intersected with KRGs to determine candidate genes. Functional enrichment analyses (GO, KEGG, GSVA) were conducted, followed by biomarker selection using Least Absolute Shrinkage and Selection Operator (LASSO) regression and the Boruta algorithm. Model performance was assessed via receiver operating characteristic (ROC) curves, and immune infiltration was assessed using CIBERSORT and ssGSEA. Consensus clustering defined kinase-associated molecular subtypes of sepsis, while CellChat analysis of single-cell data characterized intercellular communication patterns.

Results

This study employed WGCNA and machine learning analyses to identify four key diagnostic genes for sepsis—ZAP70, TXK, TRRAP, and TRIM28—and constructed a highly accurate diagnostic model (AUC = 0.986). Immune infiltration analysis revealed significant associations with T cells, NK cells, and other cell types. Single-cell data analysis demonstrated increased proportions of platelets and neutrophils in sepsis, highlighted the prominent role of monocytes in intercellular communication, and showed widespread expression of TRIM28 in monocyte subsets. Additionally, two distinct molecular subtypes with significant immune differences were identified.

Conclusion

This study systematically analyzed KRGs in sepsis and identified four clinically valuable biomarkers. By integrating single-cell transcriptomic data, it offers novel insights into the pathogenesis of sepsis and proposes potential biomarkers and therapeutic targets.

背景：败血症是一种全身性炎症综合征，可导致器官功能丧失。激酶相关基因（KRGs）通过调节炎症、免疫代谢和细胞凋亡来调节免疫疾病。然而，它们在脓毒症中的具体作用仍未被探索。方法：从Gene Expression Omnibus获取脓毒症mRNA和单细胞测序数据。加权基因共表达网络分析（WGCNA）用于鉴定与脓毒症相关的基因模块，并将其与KRGs相交以确定候选基因。进行功能富集分析（GO， KEGG， GSVA），然后使用最小绝对收缩和选择算子（LASSO）回归和Boruta算法进行生物标志物选择。通过受试者工作特征（ROC）曲线评估模型性能，使用CIBERSORT和ssGSEA评估免疫浸润。共识聚类定义了激酶相关的脓毒症分子亚型，而CellChat分析单细胞数据表征了细胞间通信模式。结果：本研究通过WGCNA和机器学习分析，确定了脓毒症的4个关键诊断基因——zap70、TXK、TRRAP和trim28，并构建了高度准确的诊断模型（AUC = 0.986）。免疫浸润分析显示与T细胞、NK细胞和其他细胞类型显著相关。单细胞数据分析显示，脓毒症中血小板和中性粒细胞比例增加，单核细胞在细胞间通讯中的突出作用，并显示TRIM28在单核细胞亚群中广泛表达。此外，鉴定出两种具有显著免疫差异的不同分子亚型。结论：本研究系统分析了脓毒症中的KRGs，并鉴定出4个具有临床价值的生物标志物。通过整合单细胞转录组学数据，它为脓毒症的发病机制提供了新的见解，并提出了潜在的生物标志物和治疗靶点。

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引用次数: 0

Advances in research on the complement system and cognitive impairment 补体系统与认知障碍的研究进展

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-01-01 Epub Date: 2026-01-12 DOI: 10.1016/j.imbio.2026.153157

Jie Gao , Zhe Li , Xinyue Zhang, Wenshu Huang, Zhiyu Tian, Chuyu Xiao, Yuanyang Zhen, Fang Yu , Xuezhao Cao

Cognitive impairment is a global health problem with increasing prevalence and mortality rates. The complement system plays a key role in the underlying pathological mechanisms. To explore potential strategies for ameliorating and preventing cognitive impairment through targeted therapies involving the complement system, it is crucial to understand the relationship between the complement system and neuroinflammation, as well as its role in the development of cognitive dysfunction. In recent years, the mechanisms involving the complement system and its targeted treatments have become a major focus of research. This review provides an overview of the physiological functions of the complement system, its association with to neuroinflammation, the mechanisms by which it contributes to cognitive impairment, and the potential applications of complement inhibitors in the treatment of cognitive dysfunction.

认知障碍是一个全球性的健康问题，发病率和死亡率都在上升。补体系统在潜在的病理机制中起着关键作用。为了探索通过涉及补体系统的靶向治疗来改善和预防认知障碍的潜在策略，了解补体系统与神经炎症之间的关系及其在认知功能障碍发展中的作用至关重要。近年来，补体系统的机制及其靶向治疗已成为研究的热点。本文综述了补体系统的生理功能、与神经炎症的关系、导致认知功能障碍的机制以及补体抑制剂在治疗认知功能障碍中的潜在应用。

引用次数: 0

MiR-210 suppresses Candida albicans-derived β-glucan-induced inflammation in THP-1-derived macrophages via the Syk-NF-κB pathway MiR-210通过Syk-NF-κB途径抑制thp -1来源的巨噬细胞β-葡聚糖诱导的炎症

IF 2.3 4区医学 Q3 IMMUNOLOGY

Immunobiology

Pub Date : 2026-01-01 Epub Date: 2026-01-11 DOI: 10.1016/j.imbio.2026.153156

Junsheng Hou , Min Li

In immunocompromised individuals, infections due to Candida albicans (C. albicans) can be life-threatening. Recognition of the insoluble β-glucan derived from the C. albicans cell wall (CaIG) by Dectin-1 in macrophages initiates an inflammatory reaction that is critical for clearing the fungal infection. However, uncontrolled inflammation may lead to septic shock. Research has established that miR-210 is strongly upregulated in THP-1-derived macrophages (THP-1 macrophages) following CaIG stimulation. MiR-210 has been implicated in the metabolic and immunological responses of macrophages in various infectious and inflammatory disease models. Nevertheless, whether miR-210 modulates Dectin-1-activated inflammation remains unclear. An in vitro inflammation model was established using CaIG-stimulated THP-1 macrophages in the current research. By using miR-210 mimic and inhibitor transfection approaches, we observed that miR-210 overexpression significantly reduced CaIG-induced IL-6 and TNF-α expression, whereas inhibition of endogenous miR-210 enhanced their production. Furthermore, by inhibiting CaIG-triggered spleen tyrosine kinase (Syk) activation and subsequent IκBα phosphorylation, miR-210 effectively prevents the accumulation of NF-κB p65 in the nucleus in THP-1 macrophages. These findings demonstrate that miR-210 participates in negative feedback to limit CaIG-triggered inflammation, primarily through downregulating the Syk-NF-κB signaling cascade. In summary, our findings reveal that miR-210 acts as a precise inflammatory modulator in macrophages, highlighting its therapeutic potential.

在免疫功能低下的个体中，由于白色念珠菌感染（C.白色念珠菌）可能危及生命。巨噬细胞中的Dectin-1识别来自白色念珠菌细胞壁（CaIG）的不溶性β-葡聚糖，引发炎症反应，这对清除真菌感染至关重要。然而，不受控制的炎症可能导致感染性休克。研究已经证实，在CaIG刺激后，miR-210在THP-1来源的巨噬细胞（THP-1巨噬细胞）中被强烈上调。MiR-210参与了各种感染性和炎症性疾病模型中巨噬细胞的代谢和免疫反应。然而，miR-210是否调节dectin -1激活的炎症尚不清楚。本研究采用caig刺激THP-1巨噬细胞建立体外炎症模型。通过使用miR-210模拟物和抑制剂转染方法，我们观察到miR-210过表达显著降低了caig诱导的IL-6和TNF-α的表达，而抑制内源性miR-210则增强了它们的产生。此外，通过抑制caig触发的脾酪氨酸激酶（Syk）激活和随后的i -κB α磷酸化，miR-210有效地阻止了THP-1巨噬细胞核中NF-κB p65的积累。这些发现表明，miR-210主要通过下调Syk-NF-κB信号级联参与负反馈来限制caig引发的炎症。总之，我们的研究结果表明，miR-210在巨噬细胞中作为一种精确的炎症调节剂，突出了其治疗潜力。

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引用次数: 0