Immunological Investigations最新文献

Markers of Endotoxemia and Inflammation are Associated with Digital Ulcers in Systemic Sclerosis Patients. 内毒素血症和炎症标志物与系统性硬化症患者手指溃疡相关。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-08-01 Epub Date: 2025-03-18 DOI: 10.1080/08820139.2025.2478932

Chiara Pellicano, Alessandra Oliva, Amalia Colalillo, Cristina Luceri, Antonietta Gigante, Claudio Maria Mastroianni, Daniela Tornese, Valeria Carnazzo, Valerio Basile, Edoardo Rosato, Umberto Basile

{"title":"Markers of Endotoxemia and Inflammation are Associated with Digital Ulcers in Systemic Sclerosis Patients.","authors":"Chiara Pellicano, Alessandra Oliva, Amalia Colalillo, Cristina Luceri, Antonietta Gigante, Claudio Maria Mastroianni, Daniela Tornese, Valeria Carnazzo, Valerio Basile, Edoardo Rosato, Umberto Basile","doi":"10.1080/08820139.2025.2478932","DOIUrl":"10.1080/08820139.2025.2478932","url":null,"abstract":"Background: The aim of this study was to evaluate the possible role of lipopolysaccharide-binding protein (LBP) and interleukin 6 (IL-6) in the development of digital ulcers (DUs) in Systemic sclerosis (SSc).Methods: 60 SSc patients were enrolled and tested for serum levels of LBP and IL-6. The development of DUs was assessed in a 12-month follow-up period.Results: Median LBP and IL-6 were 107.445 ng/mL and 10.8 pg/mL whilst 33.3% patients had LBP ≥ 11995 ng/mL and 51.7% patients had IL-6 ≥ 12.5 pg/mL. DUs history were present in 41.7% SSc patients and at follow-up 23.3% patients developed new DUs. Baseline LBP (14105 ng/mL vs 10355 ng/mL, p < .001) and IL-6 (195 pg/mL vs 9.4 ng/mL, p < .001) were higher in SSc patients with new DUs. The ROC curves showed a good diagnostic accuracy for a cut-off of LBP ≥ 11995 ng/mL [AUC = 0.804 (95% CI = 0.656-0.951), p < .001] and for a cut-off of IL-6 ≥ 12.5 pg/mL [AUC = 0.897 (95% CI = 0.783-1.000), p < .001]. Free survival from new DUs was shorter in SSc patients with increased LBP (p < .001) or IL-6 (p = .003).Conclusions: LPB or IL-6 could play a role in digital microvascular damage of SSc patients.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"795-808"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Mechanistic Insights into HOTAIR-Driven ADAM17/NF-Κb Activation and Endothelial Dysfunction in LPS-Challenged HUVECs. hotair驱动的ADAM17/NF-Κb在lps挑战的HUVECs中激活和内皮功能障碍的机制研究

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-08-01 Epub Date: 2025-05-14 DOI: 10.1080/08820139.2025.2503174

Junbing He, Zixuan Shao, Zhuoji Li, Yufu He, Jingqi Zhang, Haotian Zhong, Jiekai Li, Qinghua Liu, Yiming Shao

{"title":"Mechanistic Insights into HOTAIR-Driven ADAM17/NF-Κb Activation and Endothelial Dysfunction in LPS-Challenged HUVECs.","authors":"Junbing He, Zixuan Shao, Zhuoji Li, Yufu He, Jingqi Zhang, Haotian Zhong, Jiekai Li, Qinghua Liu, Yiming Shao","doi":"10.1080/08820139.2025.2503174","DOIUrl":"10.1080/08820139.2025.2503174","url":null,"abstract":"Introduction: HOX transcript antisense intergenic RNA (HOTAIR) has been implicated in inflammation and vascular pathology, but its role in regulation of ADAM17 and sepsis-induced endothelial injury remains unclear.Methods: LPS-treated human umbilical vein endothelial cells (HUVECs) modeled sepsis-induced endothelial injury, which were assessed via qRT-PCR, western blot and immunofluorescence. HOTAIR-knockout mice were treated with cecal ligation and perforation to establish sepsis model.Results: LPS-stimulation increased expression of HOTAIR and ADAM17 and decreased miR-326 levels in HUVECs. HOTAIR-knockdown by antisense oligonucleotides (ASOs) decreased ADAM17, TNF-α production and NF-κB activities; it also alleviated endothelial inflammation, VE-cadherin integrity damage, apoptosis and barrier dysfunction, while miR-326 inhibition reversed these effects. MiR-326 inhibited TNF-α/NF-κB via targeting ADAM17. Further experiments demonstrated recombinant TNF-α reversed the inhibitory effect of HOTAIR-ASOs on LPS-triggered TNF-α/NF-κB activation and downstream endothelial injury, which were further mitigated by NF-κB or p38 MAPK inhibitors. In-vivo experiments in HOTAIR-knockout mice confirmed the role of HOTAIR/miR-326/ADAM17 in regulating NF-κB and p38 MAPK inflammation, with improved lung injury and survival following sepsis.Discussion: The HOTAIR/miR-326/ADAM17 axis is a key regulator of inflammation, endothelial injury and barrier dysfunction during sepsis via modulation of TNF-α/NF-κB signaling, providing new insights into the mechanisms underlying endothelial injury in sepsis.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"867-893"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

IL-37 Alleviates Sepsis-Induced Lung Injury by Inhibiting Inflammatory Response Through the TGF-β/Smad3 Pathway. IL-37通过TGF-β/Smad3途径抑制炎症反应减轻脓毒症诱导的肺损伤

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-08-01 Epub Date: 2025-04-24 DOI: 10.1080/08820139.2025.2495958

Yufang Guo, Feifei Deng, Yali Jiang, Guodong Cao, Yixin Zhang, Gaowu Liu, Mayinur Alimujiang, Mairhaba Ayati, Yufeng Chen, Lili Chen, Su Lv, Xueqin Dou

{"title":"IL-37 Alleviates Sepsis-Induced Lung Injury by Inhibiting Inflammatory Response Through the TGF-β/Smad3 Pathway.","authors":"Yufang Guo, Feifei Deng, Yali Jiang, Guodong Cao, Yixin Zhang, Gaowu Liu, Mayinur Alimujiang, Mairhaba Ayati, Yufeng Chen, Lili Chen, Su Lv, Xueqin Dou","doi":"10.1080/08820139.2025.2495958","DOIUrl":"10.1080/08820139.2025.2495958","url":null,"abstract":"Introduction: Sepsis is caused by an uncontrolled inflammatory response and immune dysfunction, with lung injury being the most common complication and one of the leading causes of death in clinically ill patients. Interleukin 37 (IL-37) is a multifunctional cytokine that plays a vital role in various pathophysiological processes, including inflammation, infection, and immunity.Methods: The study involved both clinical and animal experiments (establishing an animal model of sepsis-induced lung injury). Firstly, 50 patients with sepsis-induced lung injury and 50 healthy controls were included. In addition, a more in-depth study was conducted using animal models.Results: IL-37, IL-6, PCT, and CRP levels were significantly higher in the sepsis-induced lung injury group. Correlation analysis revealed that IL-37 significantly correlated with IL-6, PCT, and CRP levels. In animal experiments, IL-37 significantly attenuated CLP-induced pulmonary edema and cellular injury while reducing the levels of inflammatory factors IL-6 and TNF-α, as well as sepsis-related inflammatory markers PCT and CRP. Moreover, IL-37 significantly downregulated the expression levels of genes and proteins of apoptosis-related molecules Caspase-3 and Bax and pathway molecules TGF-β and Smad3.Discussion: The TGF-β/Smad3 pathway is involved in the process of IL-37 inhibiting inflammatory response and ameliorating sepsis-induced lung injury.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"809-823"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Aflatoxin B₁ Instigated Redox Imbalance is Accompanied by Amplified Indoleamine 2,3-Dioxygenase/tryptophan Catabolism in the Spleen and Erythrocyte of Male Wistar Rats: Protective Influence of Dietary Rutin. 黄曲霉毒素B1引起的氧化还原失衡伴随着雄性Wistar大鼠脾脏和红细胞吲哚胺2,3-双加氧酶/色氨酸分解代谢的增强：饮食芦丁的保护作用

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-08-01 Epub Date: 2025-05-27 DOI: 10.1080/08820139.2025.2503171

Azubuike Peter Ebokaiwe, Nworie Okoro, Doris Olachi Alilonu, Euslar Nnenna Onu, Jacinta Nkechi Obimma, ChinazomMartina Eze, Olusanya Olasehinde

{"title":"Aflatoxin B1 Instigated Redox Imbalance is Accompanied by Amplified Indoleamine 2,3-Dioxygenase/tryptophan Catabolism in the Spleen and Erythrocyte of Male Wistar Rats: Protective Influence of Dietary Rutin.","authors":"Azubuike Peter Ebokaiwe, Nworie Okoro, Doris Olachi Alilonu, Euslar Nnenna Onu, Jacinta Nkechi Obimma, ChinazomMartina Eze, Olusanya Olasehinde","doi":"10.1080/08820139.2025.2503171","DOIUrl":"10.1080/08820139.2025.2503171","url":null,"abstract":"Introduction: Rutin, a dietary flavonoid, exhibits anti-inflammatory, antioxidant, and immunomodulatory properties. The underlying mechanism of protection of rutin against Aflatoxin B1 (AFB1)-induced immunotoxicity is not completely elucidated. This study investigated the protective effect of rutin against Aflatoxin B1 (AFB1)-induced immunotoxicity in male Wistar rats, supported by molecular docking and dynamics simulations.Methods: Forty male Wistar rats were grouped into five: control (corn oil), AFB1 (0.75 mg/kg bwt), AFB1 (1.5 mg/kg bwt), rutin (50 mg/kg bwt), and AFB1 (1.5 mg/kg bwt) + Rutin (50 mg/kg bwt) orally for 30 days.Results: AFB1 exposure increased (p < 0.05) oxidative and inflammatory markers, altered hematological indices, and caused histological damage in the spleen and bone marrow. Elevated indoleamine 2,3-dioxygenase (IDO) activity, reduced CD4+ T cells, and unchanged tryptophan 2,3-dioxygenase (TDO) activity were also observed. Docking revealed strong binding affinities for AFB1 (-9.5 kcal/mol), rutin (-9.7 kcal/mol), and AFB1-rutin (-10.4 kcal/mol) with IDO. Rutin co-treatment restored oxidative, inflammatory, and hematological indices, mitigated histological damage, and normalized CD4+ T cells and IDO activity, as supported by computational studies.Discussion: The activities/expression of immunosuppressive indoleamine 2, 3-dioxygenase is mostly regulated by inflammation and oxidative stress. This study provides new insights into the mechanisms underlying the modulation of immunotoxicity of AFB1 by dietary rutin.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"844-866"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

FOXM1 Enhances Transcription of S1PR1 and Promotes Pro-Inflammatory Activation of Kupffer Cells in Alcoholic Hepatitis. FOXM1增强S1PR1转录并促进酒精性肝炎Kupffer细胞的促炎激活

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-08-01 Epub Date: 2025-05-21 DOI: 10.1080/08820139.2025.2503167

Ping Lu, Tianfeng Sun

{"title":"FOXM1 Enhances Transcription of S1PR1 and Promotes Pro-Inflammatory Activation of Kupffer Cells in Alcoholic Hepatitis.","authors":"Ping Lu, Tianfeng Sun","doi":"10.1080/08820139.2025.2503167","DOIUrl":"10.1080/08820139.2025.2503167","url":null,"abstract":"Background: Following the bioinformatics predictions, this investigation delves into the function of FOXM1 in the phenotype of macrophages and inflammatory responses in alcoholic hepatitis (AH).Methods: A mouse model of AH was generated using the Lieber-DeCarli method, and mouse Kupffer cells (KCs) were treated with lipopolysaccharide and ethanol. Expression of FOXM1 and S1PR1 in mouse liver tissues or KCs was determined using RT-qPCR, immunofluorescence, or western blot assays. Loss- or gain-of-function assays of FOXM1 and S1PR1 were performed, followed by histopathological staining of the liver tissues, examination of the inflammatory cytokines, and assessment of macrophage phenotype.Results: FOXM1 exhibited heightened expression in the mouse liver tissues and KCs in AH models. Silencing FOXM1 reduced pathological injury, hepatic steatosis, alanine aminotransferase and aspartate aminotransferase levels, inflammatory cytokine production, and pro-inflammatory (M1) polarization markers of macrophages. This condition also alleviated M1 polarization of KCs in vitro. FOXM1 promoted transcription and expression of S1PR1 by binding to its promoter. The additional upregulation of S1PR1, in the presence of FOXM1, rescued M1 skewing of macrophages both in vitro and in vivo, thus aggravating inflammatory responses.Conclusion: This study identifies that FOXM1-mediated transcriptional upregulation of S1PR1 promotes pro-inflammatory activation of macrophages and augments liver injury in AH.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"824-843"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

The Power of Antibodies: Advancing Biomarker-Based Disease Detection and Surveillance. 抗体的力量：推进基于生物标志物的疾病检测和监测。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-08-01 Epub Date: 2025-04-21 DOI: 10.1080/08820139.2025.2492246

Woei Kean Ng, Gunasegran Thanusha, Pei Pei Chong, Candy Chuah

{"title":"The Power of Antibodies: Advancing Biomarker-Based Disease Detection and Surveillance.","authors":"Woei Kean Ng, Gunasegran Thanusha, Pei Pei Chong, Candy Chuah","doi":"10.1080/08820139.2025.2492246","DOIUrl":"10.1080/08820139.2025.2492246","url":null,"abstract":"Background: Antibodies have long served as fundamental tools in disease diagnosis and surveillance. Their utility as biomarkers has expanded beyond infectious diseases to encompass a wide range of health conditions.Objectives: This review aims to explore recent advancements in antibody biomarker discovery and their applications in diagnosing and monitoring diverse health conditions. It also examines the role of antibody surveillance in public health and epidemiological studies.Methods: A comprehensive analysis of recent literature was conducted, focusing on studies that identify and characterize disease-specific antibodies. Particular attention was given to their relevance in autoimmune diseases, infections, cancers, and neurological disorders.Content: The review highlights disease-specific antibody biomarkers and their clinical significance. It also discusses the utility and challenges of antibody-based surveillance in assessing disease prevalence, tracking immunity trends, and supporting One Health strategies.Conclusions: Recent advancements in antibody biomarker discovery demonstrate significant potential in improving early diagnosis, personalized treatment, and population-level health management. Antibody surveillance continues to play a pivotal role in guiding public health responses and understanding disease dynamics.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"770-794"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Macrophage Polarization in Lung Diseases: From Mechanisms to Therapeutic Strategies. 巨噬细胞极化在肺部疾病：从机制到治疗策略。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-08-01 Epub Date: 2025-04-11 DOI: 10.1080/08820139.2025.2490898

Jia Wang, Huajie Niu, Junwei Kang, Haiping Liu, Xiaoyang Dong

引用次数: 0

Activation of NF-κB Signaling by a High-Fat and High-Sugar Diet Enhances Macrophage Polarization and Aggravates Postoperative Pain and Inflammatory Responses. 高脂高糖饮食激活NF-κB信号可增强巨噬细胞极化，加重术后疼痛和炎症反应

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-08-01 Epub Date: 2025-05-19 DOI: 10.1080/08820139.2025.2505900

Chenran Zhang, Ming Zhu

{"title":"Activation of NF-κB Signaling by a High-Fat and High-Sugar Diet Enhances Macrophage Polarization and Aggravates Postoperative Pain and Inflammatory Responses.","authors":"Chenran Zhang, Ming Zhu","doi":"10.1080/08820139.2025.2505900","DOIUrl":"10.1080/08820139.2025.2505900","url":null,"abstract":"Objective: To investigate how a high-fat, high-sugar (HFHS) diet influences postoperative pain and inflammation, and to explore the role of NF-κB signaling and macrophage polarization.Methods: Male Sprague Dawley rats were divided into five groups: normal diet (ND), HFHS, ND + surgery (ND + S), HFHS + surgery (HFHS + S), and HFHS + surgery + NF-κB inhibitor (HFHS + S + B). After eight weeks of diet, laparotomy was performed. Pain behavior was assessed using the Rat Grimace Scale. DRG and blood samples were collected for Western blotting, ELISA, flow cytometry, and immunofluorescence.Results: HFHS combined with surgery significantly activated NF-κB signaling, shown by increased p65/IκBα phosphorylation and COX-2 upregulation. NF-κB inhibition reversed these effects and reduced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, MCP-1) and pain scores. HFHS and surgery also increased M1 and decreased M2 macrophages; these changes were reversed by NF-κB blockade. Western blotting confirmed upregulation of iNOS and IL-6 and downregulation of Arg-1 and IL-10 under HFHS conditions.Conclusion: An HFHS diet exacerbates postoperative pain and inflammation via NF-κB activation and M1 macrophage polarization. Inhibiting NF-κB may mitigate diet-induced sensitization.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"894-908"},"PeriodicalIF":2.9,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Protective Effects of Pachymic Acid in a DSS-Induced Mouse Model of Ulcerative Colitis. 厚青酸对dss诱导的小鼠溃疡性结肠炎模型的保护作用。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2025-07-24 DOI: 10.1080/08820139.2025.2536320

Hua Zhang, Yunxia Wu, Siyu Li, Danyang Wang, Mei Zheng, Nan Yang

{"title":"Protective Effects of Pachymic Acid in a DSS-Induced Mouse Model of Ulcerative Colitis.","authors":"Hua Zhang, Yunxia Wu, Siyu Li, Danyang Wang, Mei Zheng, Nan Yang","doi":"10.1080/08820139.2025.2536320","DOIUrl":"https://doi.org/10.1080/08820139.2025.2536320","url":null,"abstract":"Objective: This study aimed to investigate the protective effects and underlying mechanisms of pachymic acid (PA), a natural triterpenoid compound, in a dextran sulfate sodium (DSS)-induced murine model of ulcerative colitis (UC).Methods: Disease severity was assessed using the disease activity index (DAI). Histological changes and mucus layer integrity were evaluated via hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining. Inflammatory cytokines and oxidative stress markers were measured using ELISA and biochemical assays. DNA damage was assessed by γH2AX immunofluorescence. Protein expression levels of tight junction markers, apoptosis regulators, and NF-κB signaling components were analyzed by Western blotting.Results: PA administration significantly alleviated colitis symptoms, as indicated by reduced DAI scores, mitigation of colon shortening, preservation of colon histoarchitecture, and restoration of mucus secretion. PA suppressed the expression of pro-inflammatory cytokines and oxidative stress markers, enhanced endogenous antioxidant activity, and decreased γH2AX levels, indicating reduced DNA damage. Moreover, PA restored tight junction protein expression, improved the Bax/Bcl-2 ratio, and inhibited activation of the NF-κB signaling pathway.Conclusion: PA effectively ameliorates colonic inflammation and epithelial barrier dysfunction in DSS-induced colitis, suggesting its potential as a therapeutic candidate for ulcerative colitis.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-13"},"PeriodicalIF":2.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144698444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Differential Methylation Patterns Predict HBsAg Seroconversion in Hepatitis B Virus Reactivation Patients. 不同甲基化模式预测乙型肝炎病毒再激活患者HBsAg血清转化。

IF 2.4 4区医学

Immunological Investigations Pub Date : 2025-07-21 DOI: 10.1080/08820139.2025.2532630

Jayesh Kumar Sevak, Mojahidul Islam, Gayantika Verma, Anoushka Saxena, Preedia Babu E, Shahana Parveen, Ankur Jindal, Manoj Kumar Sharma, Gayatri Ramakrishna, Syed Naqui Kazim, Shiv Kumar Sarin, Nirupama Trehanpati

{"title":"Differential Methylation Patterns Predict HBsAg Seroconversion in Hepatitis B Virus Reactivation Patients.","authors":"Jayesh Kumar Sevak, Mojahidul Islam, Gayantika Verma, Anoushka Saxena, Preedia Babu E, Shahana Parveen, Ankur Jindal, Manoj Kumar Sharma, Gayatri Ramakrishna, Syed Naqui Kazim, Shiv Kumar Sarin, Nirupama Trehanpati","doi":"10.1080/08820139.2025.2532630","DOIUrl":"10.1080/08820139.2025.2532630","url":null,"abstract":"Background: Hepatitis B virus (HBV) modulates immune epigenetic landscape. Therefore, we investigated immune epigenetic landscape in HBsAg seroconverters and non-seroconverters.Methods: Sixteen rHBV patients including seroconverters (SC, n = 7) and non-seroconverters (NSC, n = 9) at baseline and week 24 were recruited. Age matched naïve chronic hepatitis B patients (nCHBV, n = 7) and healthy controls (HC, n = 6) were also included. PBMCs and plasma were subjected to genome-methylation, gene-expression, immunophenotyping, functionality, and cytokines analysis using Reduced Representation Bisulfite Sequencing (RRBS), qRT-PCR, flow-cytometry, and cytokine-bead-array.Results: In rHBV patients, as compared to nCHBV, there is significant hypomethylation (p < .05) of epigenetic remodellers and immune and metabolic genes like KDM2B, NCOR2 and GATA6, TGF-β, IL-6, IRF8, RPTOR, HK3, specifically at CpG islands. At baseline, HBsAg SC had hypomethylation of KDM2B, COX19, IRF8, TLR5, and hypermethylation of LAG3 compare to NSC. By week-24, SC demonstrated hypomethylation of IL17RA, IFN-γ, TGF-β, STAT5B (p < .05) and correlated with increased plasma IL-6 (p = .009) and decreased LAG3 (p = .01). At baseline and 24 weeks, SC depicted differentiation of HBV-specific CD8+, Tfh, and Th1/17 cells.Conclusion: This study identifies hypomethylation of immune genes suggesting enhanced immune response and viral clearance in SC. Conversely, nCHBV and NSC consistently exhibited hypomethylation of LAG3 and TOX, contributing to immune exhaustion.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-21"},"PeriodicalIF":2.4,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144674667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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