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Navigating the Complexities of Pemphigus Vulgaris: A Comprehensive Iranian Study 导航寻常性天疱疮的复杂性:一项全面的伊朗研究。
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-02-04 DOI: 10.1002/iid3.70317
Delaram Moosavi, Seyed Mohammad Mahdi Khadem, Afsaneh Sadeghzadeh Bazargan, Kambiz Kamyab Hesari, Mehrnaz Azh, Hamed Zarei Sharif, Nasrin Shayanfar, Azadeh Goodarzi

Introduction

Pemphigus vulgaris (PV) is a rare, severe autoimmune disorder characterized by the production of autoantibodies that cause blistering of the skin and mucous membranes, often presenting with oral lesions in 50%–70% of cases. It has a global incidence of 0.5–3.2 per 100,000 people, with variations across regions, and in Iran, the rate is about 1 per 100,000 annually. PV affects both sexes equally and typically manifests in the sixth decade of life, though the age of onset varies internationally, tending to be younger in India and Western countries.

Methodology

In this cross-sectional study, data were collected from 63 patients diagnosed with PV via telephone interviews. This project was approved by the Research Ethics Committee of Iran University of Medical Sciences. Statistical analyses were performed using SPSS software, version 22.0 (IBM Corp., Armonk, NY, USA).

Results

Among 63 PV patients, 56% were female, and 44% were male, with an average age of 50.17 years and a mean age of onset of 44.91 years (SD = 14.77). Most patients (70%) initially presented with mucosal symptoms, and the average time to diagnosis was approximately 17 months. Common misdiagnoses included aphthous ulcers, lichen planus, and allergic reactions. After diagnosis, most patients (82%) received multiple medications. The most frequently used medications were prednisolone (50 patients, 84.75%), methylprednisolone (10 patients, 16.9%), and rituximab (34 patients, 57.63%).

Discussion

PV in this cohort most often began with mucosal symptoms and was frequently preceded by consultations with non-dermatology clinicians, contributing to diagnostic delays. Such delays may negatively affect.

寻常型天疱疮(Pemphigus vulgaris, PV)是一种罕见的、严重的自身免疫性疾病,其特征是产生自身抗体,导致皮肤和粘膜起泡,通常在50%-70%的病例中表现为口腔病变。全球发病率为每10万人中有0.5-3.2例,各地区有所不同,在伊朗,发病率约为每年每10万人中有1例。PV对两性的影响是平等的,通常在生命的第六个十年出现,尽管发病年龄在国际上有所不同,在印度和西方国家往往更年轻。方法:在这项横断面研究中,通过电话访谈收集了63名确诊为PV的患者的数据。本项目获得伊朗医科大学研究伦理委员会批准。统计学分析采用SPSS软件,version 22.0 (IBM Corp., Armonk, NY, USA)。结果:63例PV患者中女性占56%,男性占44%,平均年龄50.17岁,平均发病年龄44.91岁(SD = 14.77)。大多数患者(70%)最初表现为粘膜症状,平均诊断时间约为17个月。常见的误诊包括口腔溃疡、扁平苔藓和过敏反应。确诊后,大多数患者(82%)接受了多种药物治疗。最常用的药物是强的松龙(50例,84.75%)、甲基强的松龙(10例,16.9%)和美罗华(34例,57.63%)。讨论:该队列中的PV最常以粘膜症状开始,并且在此之前经常咨询非皮肤科临床医生,导致诊断延迟。这种延误可能会产生负面影响。
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引用次数: 0
Advances in the Role of Adipose Tissue in Promoting Injury Repair and Resist Infection 脂肪组织促进损伤修复和抗感染作用的研究进展。
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-02-04 DOI: 10.1002/iid3.70341
Xi Duan, Run Li, Lei Fu, Jiali Yang, Zhean Zhan

Background

In recent years, adipose tissue (AT) transplantation has increasingly been noticed by many people in the field of tissue repair and regeneration. Accumulating evidence demonstrates that AT exerts dual functions in promoting tissue repair and conferring anti-infective properties, with distinct biological effects attributed to its heterogeneous components.

Objective

This review systematically examines the distribution of AT and its components, including adipocytes, extracellular matrix (ECM), immune cells, stromal vascular fraction (SVF), and adipokines. Distinct AT components mediate tissue repair and infection resistance through unique molecular mechanisms.

Results

Functionally, adipocytes and immune cells secrete various cytokines, including adiponectin, leptin, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), antimicrobial peptides, and IL-17, which coordinate inflammatory signaling and enhance host defense mechanisms. The main function of the ECM is to provide structural support for cells. SVF cell populations exhibit dual functionality: accelerating neural and cutaneous regeneration while suppressing fibrotic pathways to minimize scar formation.

Conclusion

Recommendations are proposed to guide future investigations into AT-mediated immune functions. This review highlights potential strategies for advancing AT-based clinical therapeutics and suggests novel directions for foundational studies on AT's anti-infective mechanisms.

背景:近年来,脂肪组织(AT)移植在组织修复和再生领域越来越受到人们的关注。越来越多的证据表明,AT在促进组织修复和赋予抗感染特性方面具有双重功能,由于其成分的异质性,具有不同的生物学效应。目的:本综述系统地研究了脂肪细胞、细胞外基质(ECM)、免疫细胞、基质血管组分(SVF)和脂肪因子等AT及其组分的分布。不同的AT成分通过独特的分子机制介导组织修复和感染抵抗。结果:在功能上,脂肪细胞和免疫细胞分泌多种细胞因子,包括脂联素、瘦素、肿瘤坏死因子-α (TNF-α)、白细胞介素-6 (IL-6)、抗菌肽和IL-17,协调炎症信号,增强宿主防御机制。ECM的主要功能是为细胞提供结构支持。SVF细胞群表现出双重功能:加速神经和皮肤再生,同时抑制纤维化途径以减少疤痕形成。结论:为进一步研究at介导的免疫功能提出了建议。这篇综述强调了推进AT临床治疗的潜在策略,并为AT抗感染机制的基础研究提出了新的方向。
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引用次数: 0
Investigating the Role of A20 in Respiratory Syncytial Virus Immunopathogenesis in a BALB/c Mouse Model 在BALB/c小鼠模型中研究A20在呼吸道合胞病毒免疫发病机制中的作用。
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-02-04 DOI: 10.1002/iid3.70337
Alireza Tahamtan, Mohammad Yasaghi, Saeed Samadizadeh, Hadi Razavi Nikoo, Ahad Yamchi, Vahid Salimi

Background

Respiratory syncytial virus (RSV) is a leading cause of acute respiratory tract infections in children and the elderly worldwide. RSV pathogenesis is largely driven by exaggerated host immune responses that result in lung injury. In this study, we examined the role of A20 (TNFAIP3), a key regulator of immune signaling, in RSV infection using a BALB/c mouse model.

Methods

Recombinant lentiviruses encoding TNFAIP3 (A20) or A20-specific shRNA were generated and administered to BALB/c mice. Animals received intravenous lentivectors, challenged intranasally with RSV-A2, and sacrificed on Day 5 postinfection. A20 expression, cytokine and chemokine levels, lung pathology, and viral load were assessed using real-time polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and histopathological analysis.

Results

RSV infection significantly induced A20 expression in bronchoalveolar (BAL) cells. Lentivector-mediated modulation of A20 expression produced distinct outcomes: A20 downregulation amplified inflammatory responses, increased immune cell infiltration, and elevated pro-inflammatory mediator secretion in BAL fluid, leading to aggravated lung pathology. In contrast, A20 upregulation did not markedly alter immune cell recruitment, cytokine production, or histopathological changes following RSV infection.

Conclusion

A20 downregulation exacerbates inflammation and lung injury following RSV infection, highlighting its critical role in immune regulation during the virus infection. Further studies employing targeted molecular delivery systems and human airway organoid models are warranted to evaluate the therapeutic potential of modulating A20 in RSV disease.

背景:呼吸道合胞病毒(RSV)是全世界儿童和老年人急性呼吸道感染的主要原因。RSV的发病机制主要是由过度的宿主免疫反应引起的,从而导致肺损伤。在这项研究中,我们使用BALB/c小鼠模型检测了A20 (TNFAIP3)在RSV感染中的作用,这是免疫信号的关键调节因子。方法:制备编码TNFAIP3 (A20)或A20特异性shRNA的重组慢病毒,并给予BALB/c小鼠。动物接受慢体载体静脉注射,鼻内感染RSV-A2,感染后第5天处死。采用实时聚合酶链反应(RT-PCR)、酶联免疫吸附试验(ELISA)和组织病理学分析评估A20表达、细胞因子和趋化因子水平、肺部病理和病毒载量。结果:RSV感染显著诱导支气管肺泡(BAL)细胞A20表达。慢载体介导的A20表达调节产生了不同的结果:A20下调放大炎症反应,增加免疫细胞浸润,BAL液中促炎介质分泌升高,导致肺部病理加重。相比之下,A20上调并没有显著改变RSV感染后的免疫细胞募集、细胞因子产生或组织病理学变化。结论:A20下调可加重RSV感染后的炎症和肺损伤,凸显其在病毒感染过程中免疫调节的重要作用。有必要进一步研究靶向分子传递系统和人类气道类器官模型,以评估调节A20在RSV疾病中的治疗潜力。
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引用次数: 0
Epidemiology of Mycoplasma genitalium Infections of the Genitourinary Tract Among Attendees of STI Clinic in Hangzhou, China. 杭州地区性病门诊患者生殖道支原体感染流行病学分析
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-02-01 DOI: 10.1002/iid3.70357
Xinmin Qiu, Jiazhen Shi, Hongqin Gu, Jifeng Liu

Objective: This study aimed to investigate the prevalence, associated clinical manifestations, and co-infection patterns of Mycoplasma genitalium (MG) infection among patients attending Venereal Disease, Urology, and Gynecology clinics in Hangzhou, China. The findings provide foundational evidence to guide sexually transmitted infection (STI) screening in patients with genitourinary tract conditions.

Methods: Between January 2020 and December 2023, 12,934 outpatients from Hangzhou Third People's Hospital were tested for MG using isothermal amplification targeting the 16S rRNA gene. Concurrent testing for Neisseria gonorrhoeae (NG), Chlamydia trachomatis (CT), and Ureaplasma urealyticum (UU) was performed.

Results: Of these 12,934 patients, 589 tested positive for MG, yielding an overall prevalence of 4.55% (589/12,934). Prevalence was significantly higher in males (416/7915, 5.26%) than in females (173/5,019, 3.44%). Significant age-related differences were observed (p < 0.001), with the highest prevalence in patients ≤ 20 years 7.83% and the lowest in those > 60 years 0.57%. Of 416 MG-positive males, 295 (70.91%) exhibited symptoms of urethritis, prostatitis, and epididymitis. whereas 49.71% (86/173) of MG-positive females exhibited vaginitis, cervicitis, or pelvic inflammatory disease (p < 0.001). Symptomatic infection rates were significantly higher in males than in females. Co-infections were found in 44.31% (261/589) of MG-positive patients, with MG + UU co-infection being the most frequent 22.92% (135/589).

Conclusions: MG infection prevalence in Hangzhou is substantial, with significantly higher rates among males and young adults (≤ 20 years). Females exhibit markedly lower symptomatic infection rates. MG demonstrates frequent co-infection, predominantly with UU, underscoring the necessity of multipathogen testing to prevent missed diagnoses.

目的:了解杭州地区性病、泌尿科、妇科门诊患者生殖道支原体(MG)感染的流行情况、相关临床表现及共感染模式。本研究结果为指导泌尿生殖系统疾病患者的性传播感染筛查提供了基础依据。方法:于2020年1月至2023年12月,采用针对16S rRNA基因的等温扩增技术,对杭州市第三人民医院12934例门诊患者进行MG检测。同时检测淋病奈瑟菌(NG)、沙眼衣原体(CT)和解脲原体(UU)。结果:在这12,934例患者中,589例MG检测呈阳性,总体患病率为4.55%(589/12,934)。男性患病率(416/7915,5.26%)明显高于女性(173/ 5019,3.44%)。观察到显著的年龄相关差异(p 60 - 0.57%)。416例mg阳性男性中,295例(70.91%)表现出尿道炎、前列腺炎和附睾炎的症状。49.71%(86/173)的女性MG阳性表现为阴道炎、宫颈炎或盆腔炎(p)。结论:杭州MG感染流行率较高,男性和年轻人(≤20岁)感染率较高。女性表现出明显较低的症状性感染率。MG表现出频繁的合并感染,主要与UU,强调了多病原体检测的必要性,以防止漏诊。
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引用次数: 0
The Progress of Ferroptosis of Immune Cells in the Tumor Microenvironment and Its Impact on Tumorigenesis and Development 肿瘤微环境中免疫细胞铁下垂的进展及其对肿瘤发生发展的影响。
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-01-20 DOI: 10.1002/iid3.70333
Fenfen Zhan, Yanyan Hu, Xiang Jiang, Zejun Fang

Background

The immune cells within the tumor microenvironment (TME) play important roles in tumorigenesis. Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by the accumulation of lipid peroxides. The interplay between ferroptosis and the tumor immune microenvironment significantly influences the outcome of cancer immunotherapy. The study aims to elucidate the dual effects of ferroptosis on cancer progression and immune responses, particularly in the context of enhancing the efficacy of tumor immunotherapy.

Methods

An extensive literature review was conducted using PubMed to identify studies related to ferroptosis and immune cells in the TME, emphasizing translational research outcomes published within the last 5 years.

Results

The study reviews the literature on the mechanisms of ferroptosis and its interactions with various components of the TME, including immune cells such as CD8+ T cells, dendritic cells, natural killer cells, regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages. It also examines the impact of ferroptosis inducers and inhibitors on these interactions, alongside the potential synergistic effects of combining ferroptosis induction with current immunotherapies. Ferroptosis plays a dual role in the TME by both promoting and inhibiting tumor growth through its effects on immune cell function. Activation of ferroptosis in tumor cells can enhance the immunogenicity of cancer cells, thereby improving the effectiveness of immunotherapies. Conversely, ferroptosis in immune cells can lead to immune cell dysfunction and contribute to immunotherapy resistance. The study identifies several therapeutic strategies that harness the induction of ferroptosis to overcome resistance to immune checkpoint inhibitors and enhance the anti-tumor immune response. Inducing ferroptosis in tumor cells and immunosuppressive cells, while preventing ferroptosis in effector immune cells, emerges as a promising strategy to enhance the efficacy of immunotherapy.

Conclusion

This review highlights the potential of targeting ferroptosis as a sensitization approach to improve cancer treatment outcomes, underscoring the need for further research to fully understand the regulatory mechanisms of ferroptosis in tumor immunity.

背景:肿瘤微环境(tumor microenvironment, TME)内的免疫细胞在肿瘤发生中起重要作用。铁下垂是一种铁依赖性的非凋亡细胞死亡形式,其特征是脂质过氧化物的积累。铁下垂与肿瘤免疫微环境的相互作用显著影响肿瘤免疫治疗的效果。该研究旨在阐明铁下垂对癌症进展和免疫反应的双重影响,特别是在增强肿瘤免疫治疗疗效的背景下。方法:在PubMed上进行广泛的文献综述,找出TME中铁下垂与免疫细胞相关的研究,重点关注近5年内发表的转化研究成果。结果:本研究回顾了有关铁死亡机制及其与TME各成分相互作用的文献,包括CD8+ T细胞、树突状细胞、自然杀伤细胞、调节性T细胞、髓源性抑制细胞和肿瘤相关巨噬细胞等免疫细胞。它还研究了铁下垂诱导剂和抑制剂对这些相互作用的影响,以及将铁下垂诱导与当前免疫疗法相结合的潜在协同效应。铁下垂在TME中发挥双重作用,通过影响免疫细胞功能促进和抑制肿瘤生长。激活肿瘤细胞中的铁下垂可以增强癌细胞的免疫原性,从而提高免疫治疗的有效性。相反,免疫细胞中的铁下垂可导致免疫细胞功能障碍并有助于免疫治疗抵抗。该研究确定了几种利用诱导铁下垂来克服对免疫检查点抑制剂的耐药性并增强抗肿瘤免疫反应的治疗策略。诱导肿瘤细胞和免疫抑制细胞的铁下垂,同时防止效应免疫细胞的铁下垂,是提高免疫治疗效果的一种有前景的策略。结论:本综述强调了靶向铁下垂作为一种增敏方法改善癌症治疗效果的潜力,强调需要进一步研究以充分了解铁下垂在肿瘤免疫中的调节机制。
{"title":"The Progress of Ferroptosis of Immune Cells in the Tumor Microenvironment and Its Impact on Tumorigenesis and Development","authors":"Fenfen Zhan,&nbsp;Yanyan Hu,&nbsp;Xiang Jiang,&nbsp;Zejun Fang","doi":"10.1002/iid3.70333","DOIUrl":"10.1002/iid3.70333","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The immune cells within the tumor microenvironment (TME) play important roles in tumorigenesis. Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by the accumulation of lipid peroxides. The interplay between ferroptosis and the tumor immune microenvironment significantly influences the outcome of cancer immunotherapy. The study aims to elucidate the dual effects of ferroptosis on cancer progression and immune responses, particularly in the context of enhancing the efficacy of tumor immunotherapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>An extensive literature review was conducted using PubMed to identify studies related to ferroptosis and immune cells in the TME, emphasizing translational research outcomes published within the last 5 years.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The study reviews the literature on the mechanisms of ferroptosis and its interactions with various components of the TME, including immune cells such as CD8+ T cells, dendritic cells, natural killer cells, regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages. It also examines the impact of ferroptosis inducers and inhibitors on these interactions, alongside the potential synergistic effects of combining ferroptosis induction with current immunotherapies. Ferroptosis plays a dual role in the TME by both promoting and inhibiting tumor growth through its effects on immune cell function. Activation of ferroptosis in tumor cells can enhance the immunogenicity of cancer cells, thereby improving the effectiveness of immunotherapies. Conversely, ferroptosis in immune cells can lead to immune cell dysfunction and contribute to immunotherapy resistance. The study identifies several therapeutic strategies that harness the induction of ferroptosis to overcome resistance to immune checkpoint inhibitors and enhance the anti-tumor immune response. Inducing ferroptosis in tumor cells and immunosuppressive cells, while preventing ferroptosis in effector immune cells, emerges as a promising strategy to enhance the efficacy of immunotherapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This review highlights the potential of targeting ferroptosis as a sensitization approach to improve cancer treatment outcomes, underscoring the need for further research to fully understand the regulatory mechanisms of ferroptosis in tumor immunity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12820353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146009703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Paeoniflorin Ameliorates Spinal Cord Injury by Controlling Apoptosis and Ferroptosis in H2O2-Damaged PC12 Cells 芍药苷通过调控h2o2损伤的PC12细胞凋亡和铁凋亡改善脊髓损伤
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-01-20 DOI: 10.1002/iid3.70324
Zongyu Zhang, Zhijing Zhou, Peng Zhang, Yongfeng Huo

Background

Spinal cord injury (SCI) leads to severe neurological dysfunction. Current therapeutic strategies remain limited, with poor recovery rates. Oxidative stress and ferroptosis are key mechanisms underlying secondary SCI. Paeoniflorin has anti-inflammatory, antioxidant, and neuroprotective properties; however, its role in regulating apoptosis and ferroptosis after SCI remains unclear.

Methods

An in vitro SCI model was established by treating PC12 cells with 300 μM H₂O₂ for 24 h, followed by intervention with various concentrations of paeoniflorin. Cell viability was assessed using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay, apoptosis was analyzed by flow cytometry, lipid reactive oxygen species (ROS) levels were detected by immunofluorescence, and cysteine (Cys), glutathione (GSH), and glutathione peroxidase 4 (GPX4) levels were measured using enzyme-linked immunosorbent assay (ELISA) kits. Western blotting and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were performed to evaluate the expression of sirtuin 3 (SIRT3), B-cell lymphoma-2 (Bcl-2), and BCL2-Associated X (Bax). In addition, the SIRT3-specific inhibitor, 3-TYP, was used to validate the role of SIRT3 in paeoniflorin-mediated protection.

Results

Paeoniflorin increased cell viability; reduced apoptosis; suppressed ROS accumulation; and restored Cys, GSH, and GPX4 levels in a dose-dependent manner. Paeoniflorin significantly upregulated SIRT3 mRNA and protein expression. Co-treatment with 3-TYP attenuated the protective effects of paeoniflorin, indicating that the role of paeoniflorin is mediated through activation of the SIRT3 pathway.

Conclusion

Paeoniflorin exerts significant neuroprotective effects against SCI-induced injury by activating the SIRT3 signaling pathway and regulating apoptosis, oxidative stress, and ferroptosis, offering a novel potential therapeutic target for SCI treatment.

背景:脊髓损伤(SCI)导致严重的神经功能障碍。目前的治疗策略仍然有限,治愈率很低。氧化应激和铁下垂是继发性脊髓损伤的主要机制。芍药苷具有抗炎、抗氧化和神经保护作用;然而,其在脊髓损伤后调节细胞凋亡和铁下垂中的作用尚不清楚。方法:用300 μM H₂O₂处理PC12细胞24 H,再用不同浓度的芍药苷干预,建立体外脊髓损伤模型。采用3-(4,5 -二甲基噻唑-2-酰基)- 2,5 -二苯基溴化四唑(MTT)法评估细胞活力,流式细胞术分析细胞凋亡,免疫荧光法检测脂质活性氧(ROS)水平,酶联免疫吸附试验(ELISA)试剂盒检测半胱氨酸(Cys)、谷胱甘肽(GSH)和谷胱甘肽过氧化物酶4 (GPX4)水平。采用Western blotting和逆转录定量聚合酶链反应(RT-qPCR)检测sirtuin 3 (SIRT3)、b细胞淋巴瘤-2 (Bcl-2)和BCL2-Associated X (Bax)的表达。此外,SIRT3特异性抑制剂3-TYP被用来验证SIRT3在芍药苷介导的保护中的作用。结果:芍药苷能提高细胞活力;减少细胞凋亡;抑制ROS积累;并以剂量依赖的方式恢复Cys、GSH和GPX4水平。芍药苷显著上调SIRT3 mRNA和蛋白的表达。与3-TYP共处理可减弱芍药苷的保护作用,说明芍药苷的作用是通过激活SIRT3通路介导的。结论:芍药苷通过激活SIRT3信号通路,调控细胞凋亡、氧化应激和铁凋亡,对脊髓损伤具有显著的神经保护作用,为脊髓损伤治疗提供了新的潜在靶点。
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引用次数: 0
Integrated Analysis of the Immune Infiltration Pattern and Novel Diagnostic Biomarkers in Septic Cardiomyopathy 脓毒性心肌病免疫浸润模式及新诊断生物标志物的综合分析
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-01-19 DOI: 10.1002/iid3.70311
Wei Liu, Xi Zheng, Dong Wang, Jingyi Wang, Xincheng Li, Fei Li, Wenxiong Li, Jin Zhang

Purpose

In this study, various informatics analyses were employed to identify the hub genes associated with septic cardiomyopathy (SCM) onset and investigate their immune infiltration status.

Methods

High-throughput sequencing data of myocardial tissue samples from mice with SCM were obtained from the GEO database and our previously published articles. The Limma and weighted gene co-expression network analysis (WGCNA) packages were used to identify the hub genes associated with SCM onset. GSEA and the DAVID database were employed for gene enrichment analysis. Additionally, the CIBERSORT database was used to analyze the immune infiltration in SCM. Finally, the multiMiR package was used to analyze the microRNAs acting as ceRNAs for the hub genes. Receiver operating characteristic (ROC) curves and Mendelian randomization analysis were used to evaluate the predictive value of hub genes for SCM.

Results

The SCM group included nine samples, while the control group included ten samples. SCM upregulated 15 genes and downregulated 7. Mt1 and Actc1 were the most significantly upregulated and downregulated, respectively. GO analysis indicated that the most significantly enriched biological process was “response to bacterium,” and the most enriched signaling pathway was “mineral absorption.” Immunoinfiltration analysis revealed decreased T cells CD4 naive, B cells naive, resting mast cells, and M2 macrophage infiltration in the hearts of SCM mice. WGCNA and Limma package analyses identified Clu, Igf1, and Trp53 as hub genes associated with SCM onset. The ROC curves demonstrated a strong correlation and predictive value for Trp53, Igf1, and Clu in the SCM. Moreover, Clu and Igf1 demonstrated predictive values for SCM using Mendelian randomization analysis from the IEU database. Eleven miRNAs formed a ceRNA network with these hub genes.

Conclusion

In summary, our results implicated Igf1 and Clu as the potential candidates involved in SCM pathogenesis.

目的:本研究采用多种信息学分析方法,鉴定与脓毒性心肌病(SCM)发病相关的枢纽基因,并探讨其免疫浸润状况。方法:从GEO数据库和我们先前发表的文章中获得SCM小鼠心肌组织样本的高通量测序数据。使用Limma和加权基因共表达网络分析(WGCNA)包来鉴定与SCM发病相关的枢纽基因。采用GSEA和DAVID数据库进行基因富集分析。此外,利用CIBERSORT数据库对SCM的免疫浸润进行分析。最后,使用multiMiR包分析作为中枢基因cerna的microrna。采用受试者工作特征(ROC)曲线和孟德尔随机化分析评价枢纽基因对SCM的预测价值。结果:SCM组9例,对照组10例。SCM上调15个基因,下调7个。Mt1和Actc1分别表达上调和下调最为显著。氧化石墨烯分析表明,富集程度最高的生物过程是“对细菌的反应”,富集程度最高的信号通路是“矿物质吸收”。免疫浸润分析显示,SCM小鼠心脏中T细胞CD4幼稚、B细胞幼稚、静息肥大细胞和M2巨噬细胞浸润减少。WGCNA和Limma包分析发现,Clu、Igf1和Trp53是与SCM发病相关的枢纽基因。ROC曲线显示Trp53、Igf1和Clu在SCM中具有很强的相关性和预测价值。此外,利用来自IEU数据库的孟德尔随机化分析,Clu和Igf1证明了SCM的预测值。11个mirna与这些中心基因形成了一个ceRNA网络。结论:综上所述,我们的结果提示Igf1和Clu可能是参与SCM发病的潜在候选基因。
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引用次数: 0
MAFG Induces the Methylation of CRYAB to Promote the Activation of A1 Astrocyte After Spinal Cord Injury 脊髓损伤后,MAFG诱导CRYAB甲基化促进A1星形细胞活化。
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-01-19 DOI: 10.1002/iid3.70334
Xuefei Li, Zhuang Zhu, Ying Wang, Hao Wan, Zhiwei Wang, Wanqing Qiao

Purpose

To investigate the effects of MAF bZIP transcription factor G (MAFG) on the transformation of A1/A2 reactive astrocytes and the production of inflammatory factors after spinal cord injury (SCI).

Methods

An SCI model was established using Sprague–Dawley rats. Astrocyte conditioned medium (ACM) and lipopolysaccharide (LPS) were used to induce the generation of type A1 astrocytes. MAFG-, CRYAB-, C3-, and S100A10-positive cells were examined using immunofluorescence. The expression of MAFG, TNF-α, IL-1β, IL-6, C3, Serping1, Sphk1, S100A10, CRYAB, DNMT1, DNMT3a, and DNMT3b was detected through RT-PCR and/or Western blot. The inclined plate test and Basso-Beattie-Bresnahan scores were used to evaluate the motor function in rats. Hematoxylin and eosin and Nissl staining were performed to assess pathological changes in the rat spinal tissues. In rat astrocytes, IL-1β and IL-6 levels were examined via enzyme-linked immunosorbent assay.

Results

A1 astrocyte activation was accompanied by MAFG upregulation in rat spinal cord tissues after SCI. MAFG silencing inhibited the activation of A1 astrocytes and inflammation and improved neurological outcomes and functional recovery in rats after SCI. In ACM-treated rat astrocytes, MAFG silencing inhibited A1 astrocyte activation, inflammation, and CRYAB methylation. Moreover, 5-Aza (an inhibitor of methylation) further inhibited the activation of A1 astrocytes and inflammation, whereas DNMT3b overexpression had the opposite effect.

Conclusion

Silencing MAFG reduced the activation of A1 astrocytes and neuroinflammation and improved functional recovery after SCI, which might be involved in the inhibition of CRYAB methylation.

目的:探讨MAF bZIP转录因子G (MAFG)对脊髓损伤(SCI)后A1/A2反应性星形细胞转化及炎症因子产生的影响。方法:采用Sprague-Dawley大鼠建立脊髓损伤模型。采用星形细胞条件培养基(ACM)和脂多糖(LPS)诱导A1型星形细胞的生成。免疫荧光法检测MAFG-、CRYAB-、C3-和s100a10阳性细胞。通过RT-PCR和/或Western blot检测MAFG、TNF-α、IL-1β、IL-6、C3、Serping1、Sphk1、S100A10、CRYAB、DNMT1、DNMT3a、DNMT3b的表达。采用斜板试验和Basso-Beattie-Bresnahan评分法评价大鼠运动功能。采用苏木精染色、伊红染色和尼氏染色观察大鼠脊髓组织的病理变化。在大鼠星形胶质细胞中,采用酶联免疫吸附法检测IL-1β和IL-6水平。结果:脊髓损伤后大鼠脊髓组织中A1星形胶质细胞激活并伴有MAFG上调。在脊髓损伤大鼠中,MAFG沉默抑制A1星形胶质细胞的激活和炎症,改善神经预后和功能恢复。在acm处理的大鼠星形胶质细胞中,MAFG沉默抑制A1星形胶质细胞激活、炎症和CRYAB甲基化。此外,5-Aza(一种甲基化抑制剂)进一步抑制A1星形胶质细胞的激活和炎症,而DNMT3b过表达则具有相反的作用。结论:沉默MAFG可降低脊髓损伤后A1星形胶质细胞的活化和神经炎症,改善功能恢复,这可能与抑制CRYAB甲基化有关。
{"title":"MAFG Induces the Methylation of CRYAB to Promote the Activation of A1 Astrocyte After Spinal Cord Injury","authors":"Xuefei Li,&nbsp;Zhuang Zhu,&nbsp;Ying Wang,&nbsp;Hao Wan,&nbsp;Zhiwei Wang,&nbsp;Wanqing Qiao","doi":"10.1002/iid3.70334","DOIUrl":"10.1002/iid3.70334","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>To investigate the effects of MAF bZIP transcription factor G (MAFG) on the transformation of A1/A2 reactive astrocytes and the production of inflammatory factors after spinal cord injury (SCI).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>An SCI model was established using Sprague–Dawley rats. Astrocyte conditioned medium (ACM) and lipopolysaccharide (LPS) were used to induce the generation of type A1 astrocytes. MAFG-, CRYAB-, C3-, and S100A10-positive cells were examined using immunofluorescence. The expression of MAFG, TNF-α, IL-1β, IL-6, C3, Serping1, Sphk1, S100A10, CRYAB, DNMT1, DNMT3a, and DNMT3b was detected through RT-PCR and/or Western blot. The inclined plate test and Basso-Beattie-Bresnahan scores were used to evaluate the motor function in rats. Hematoxylin and eosin and Nissl staining were performed to assess pathological changes in the rat spinal tissues. In rat astrocytes, IL-1β and IL-6 levels were examined via enzyme-linked immunosorbent assay.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A1 astrocyte activation was accompanied by MAFG upregulation in rat spinal cord tissues after SCI. MAFG silencing inhibited the activation of A1 astrocytes and inflammation and improved neurological outcomes and functional recovery in rats after SCI. In ACM-treated rat astrocytes, MAFG silencing inhibited A1 astrocyte activation, inflammation, and CRYAB methylation. Moreover, 5-Aza (an inhibitor of methylation) further inhibited the activation of A1 astrocytes and inflammation, whereas DNMT3b overexpression had the opposite effect.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Silencing MAFG reduced the activation of A1 astrocytes and neuroinflammation and improved functional recovery after SCI, which might be involved in the inhibition of CRYAB methylation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12815693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146003302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Short-Term Change in IgG Antibody Elicited by Omicron BA.5 Infection and Inhaled Ad5-nCoV Vaccine Among Healthcare Workers 医护人员感染Omicron BA.5和吸入Ad5-nCoV疫苗后IgG抗体的短期变化
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-01-19 DOI: 10.1002/iid3.70332
Zhaohui Luo, Ting Zeng, Shi Zhao, Jing Liang, Shengzhi Sun, Yongkang Ni, Chunyan Yan, Liang Yin, Lan Wang, Kai Wang, Zihao Guo

Background

Little is known about the immune response induced by the SARS-CoV-2 Omicron BA.5 variants or the inhaled adenovirus vector vaccine. In this study, we investigated the short-term profile of antireceptor-binding-domain IgG antibody responses elicited by either the virus or the vaccine.

Methods

A cohort of healthcare workers who were infected with Omicron BA.5 or who received the inhaled adenovirus vector vaccine was identified between August and December 2022. Blood samples were collected twice to detect IgG antibodies against the receptor-binding domain of the SARS-CoV-2 spike protein. Baseline characteristics were obtained through questionnaires. Multivariate linear mixed-effect models were applied to assess the changes in IgG antibody levels between the two laboratory test time points, adjusting for baseline covariates.

Results

Among 1146 identified healthcare workers, a total of 419 healthcare workers with known infection status who provided informed consent were eligible for inclusion in the study. The study participants were mostly female (71.8%), had received three doses of intramuscularly injected inactivated vaccine before follow-up (93.8%), and had no comorbidities (94.3%). We estimated that the IgG level increased by 5.1% per week over the 2 months following Omicron BA.5 infection. No significant change in IgG antibody levels in the short term was observed within 1 month after receiving the inhaled adenovirus vector vaccine.

Conclusion

These findings suggested that the inhaled adenovirus vector vaccine may provide modest protection against Omicron BA.5 infection in the healthcare worker population.

背景:目前对SARS-CoV-2 Omicron BA.5变异体或吸入腺病毒载体疫苗诱导的免疫应答知之甚少。在这项研究中,我们研究了由病毒或疫苗引起的抗受体结合域IgG抗体反应的短期概况。方法:选取2022年8月至12月感染欧米克隆ba5或吸入腺病毒载体疫苗的医护人员为研究对象。采集两次血样,检测针对SARS-CoV-2刺突蛋白受体结合域的IgG抗体。通过问卷调查获得基线特征。采用多变量线性混合效应模型评估两个实验室检测时间点之间IgG抗体水平的变化,并对基线协变量进行调整。结果:在确定的1146名医护人员中,共有419名提供知情同意的已知感染状况的医护人员符合纳入研究的条件。研究参与者大多为女性(71.8%),随访前接受过三剂肌肉注射灭活疫苗(93.8%),无合并症(94.3%)。我们估计,在感染欧米克隆BA.5后的2个月内,IgG水平每周增加5.1%。吸入腺病毒载体疫苗接种后1个月内,短期内IgG抗体水平无明显变化。结论:这些结果表明,吸入腺病毒载体疫苗可能对医护人员人群的Omicron BA.5感染有一定的保护作用。
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引用次数: 0
Bilateral Chronic Expanding Hematomas of the Gluteus Maximus Presenting With Gluteal Muscle Contracture: A Case Report 双侧臀大肌慢性扩张性血肿伴臀肌挛缩1例。
IF 2.7 4区 医学 Q3 IMMUNOLOGY Pub Date : 2026-01-15 DOI: 10.1002/iid3.70336
Xi-Qing Pan, Jin-Hui Liu, Jiang-Li Zhang, Ya-Ya Zhang, Jian-Yong Zhang, Lei Shu, Wei Zhao

Background

Chronic expanding hematoma is defined as a progressively enlarging soft tissue mass persisting beyond 1 month, typically resulting from prior trauma or surgical procedures. Although the condition is rare, its occurrence within deep musculature—particularly with bilateral involvement of the gluteus maximus—is exceedingly uncommon. No previously published English-language reports were identified describing bilateral gluteus maximus hematomas associated with gluteal muscle contracture (GMC).

Case Report

This report describes a 29-year-old male presenting with bilateral chronic expanding hematomas involving the gluteus maximus muscles, accompanied by clinical features consistent with GMC.

Conclusion

Chronic expanding hematoma should be considered a potential underlying etiology in individuals presenting with GMC, particularly when involving deep gluteal musculature.

背景:慢性扩张性血肿被定义为持续超过1个月的逐渐扩大的软组织肿块,通常由先前的创伤或外科手术引起。虽然这种情况很少见,但它发生在深层肌肉组织,特别是双侧累及臀大肌,是非常罕见的。没有先前发表的英文报告被确定描述与臀肌挛缩(GMC)相关的双侧臀大肌血肿。病例报告:本报告描述了一名29岁男性,表现为双侧慢性扩张性血肿累及臀大肌,伴有与GMC一致的临床特征。结论:慢性扩张性血肿应被认为是GMC患者的潜在病因,特别是当涉及臀深肌肉组织时。
{"title":"Bilateral Chronic Expanding Hematomas of the Gluteus Maximus Presenting With Gluteal Muscle Contracture: A Case Report","authors":"Xi-Qing Pan,&nbsp;Jin-Hui Liu,&nbsp;Jiang-Li Zhang,&nbsp;Ya-Ya Zhang,&nbsp;Jian-Yong Zhang,&nbsp;Lei Shu,&nbsp;Wei Zhao","doi":"10.1002/iid3.70336","DOIUrl":"10.1002/iid3.70336","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Chronic expanding hematoma is defined as a progressively enlarging soft tissue mass persisting beyond 1 month, typically resulting from prior trauma or surgical procedures. Although the condition is rare, its occurrence within deep musculature—particularly with bilateral involvement of the gluteus maximus—is exceedingly uncommon. No previously published English-language reports were identified describing bilateral gluteus maximus hematomas associated with gluteal muscle contracture (GMC).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Report</h3>\u0000 \u0000 <p>This report describes a 29-year-old male presenting with bilateral chronic expanding hematomas involving the gluteus maximus muscles, accompanied by clinical features consistent with GMC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Chronic expanding hematoma should be considered a potential underlying etiology in individuals presenting with GMC, particularly when involving deep gluteal musculature.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12805526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Immunity, Inflammation and Disease
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