European Journal of Immunology最新文献

Short-Chain Fatty Acid Sodium Butyrate Suppresses Protective Humoral Immunity by Inhibiting Follicular T Helper Cell Differentiation 短链脂肪酸丁酸钠通过抑制滤泡T辅助细胞分化抑制保护性体液免疫。

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-17 DOI: 10.1002/eji.70076

Bhushan Nikam, Someshwar Nath Jha, Yatish Thakare, Poonam Coshic, Nimesh Gupta

{"title":"Short-Chain Fatty Acid Sodium Butyrate Suppresses Protective Humoral Immunity by Inhibiting Follicular T Helper Cell Differentiation","authors":"Bhushan Nikam, Someshwar Nath Jha, Yatish Thakare, Poonam Coshic, Nimesh Gupta","doi":"10.1002/eji.70076","DOIUrl":"10.1002/eji.70076","url":null,"abstract":"<div>\u0000 \u0000 The gut microbiome and its metabolites are critical regulators of intestinal homeostasis, with emerging evidence highlighting their influence on humoral immune responses and vaccine efficacy. The development of effective humoral immunity depends on the magnitude and quality of germinal centers (GCs), which are driven by follicular T helper (Tfh) cells. Here, we investigate the role of short-chain fatty acids (SCFAs) in shaping humoral immunity, with a particular focus on Tfh cells. In ex vivo assays, we found that sodium butyrate, not sodium acetate or sodium propionate, directly suppresses Tfh cells differentiation and helper functions. Using antigen-specific and influenza virus infection models, we further demonstrate that sodium butyrate impairs Tfh cell differentiation, leading to diminished GC B cell responses and compromised humoral immunity during systemic infection. Notably, mice treated with sodium butyrate succumbed to virus infection, underscoring its effect on impairing protective immunity. Mechanistically, our findings reveal that sodium butyrate mediates these suppressive effects on Tfh cells via histone deacetylase (HDAC) inhibition. Together, our findings establish sodium butyrate as a negative regulator of humoral immunity by directly suppressing the Tfh-cell differentiation and Tfh-derived GC responses. These insights provide a mechanistic link between gut microbiome-derived metabolites and humoral immunity, with potential implications for vaccine efficacy and therapeutic interventions.\u0000 </div>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145311910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TEAMwork: Interplay of Post-Transcriptional Mechanisms, Epigenetics and Metabolism in (Auto-)Immunity 团队合作：（自身）免疫中转录后机制、表观遗传学和代谢的相互作用。

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-08 DOI: 10.1002/eji.70064

Francesca Rossi, Martin Turner

{"title":"TEAMwork: Interplay of Post-Transcriptional Mechanisms, Epigenetics and Metabolism in (Auto-)Immunity","authors":"Francesca Rossi, Martin Turner","doi":"10.1002/eji.70064","DOIUrl":"10.1002/eji.70064","url":null,"abstract":"Changes in transcript abundance and isoforms, mediated by epigenetic and post-transcriptional mechanisms, are a hallmark of the development, activation, and effector functions of immune cells. How epigenetic and post-transcriptional processes are orchestrated to regulate transcription and pre-mRNA processing, and their interplay with metabolism, is emerging as important for immunity. DNA and histone modifications recruit RNA-binding proteins (RBPs) to mediate co-transcriptional RNA processing at specific chromatin loci. Simultaneously, RBPs influence the deposition of epigenetic modifications by regulating the expression of chromatin-modifying enzymes and enzymes that control the amounts of metabolites. These are used as substrates by chromatin-modifying enzymes and can influence RBP activity; thus, modulation of metabolic pathways represents a mechanism to regulate the epigenetic landscape and pre-mRNA processing. A body of work identifies emerging regulatory principles that address the interplay between epigenetics and RBPs in the nucleus, and of cytoplasmic post-transcriptional mechanisms that regulate metabolism and epigenetics. In this review, we focus on the interconnections between RBP-mediated processes, chromatin modifications, and metabolic pathways, highlighting the role that such circuits have in T- and B-lymphocytes, and in autoimmunity.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12505208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145243369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Exosome miR-6990-5p from MMP14high Macrophage Promotes Fibrosis Through Th17 Cell Differentiation in Hypersensitivity Pneumonia 来自mmp14高巨噬细胞的外泌体miR-6990-5p通过Th17细胞分化促进过敏性肺炎纤维化。

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-06 DOI: 10.1002/eji.70048

Dan Peng, Juan Li, Bomiao Qin, Anying Xiong, Qin Ran, Lingling Bai, Xiang He, Xiaolan Li, Lei Zhang, Madeeha Arooj, Guoping Li

{"title":"Exosome miR-6990-5p from MMP14high Macrophage Promotes Fibrosis Through Th17 Cell Differentiation in Hypersensitivity Pneumonia","authors":"Dan Peng, Juan Li, Bomiao Qin, Anying Xiong, Qin Ran, Lingling Bai, Xiang He, Xiaolan Li, Lei Zhang, Madeeha Arooj, Guoping Li","doi":"10.1002/eji.70048","DOIUrl":"10.1002/eji.70048","url":null,"abstract":"<div>\u0000 \u0000 Th17 cells contribute to pulmonary fibrosis, but the mechanisms driving their differentiation remain unclear. Using single-cell RNA sequencing (scRNA-seq) and a decision tree model, we identify IL17A as a key marker in mice exposed to Saccharopolyspora rectivirgula antigen (SR-Ag). Trajectory and T cell receptor (TCR) analyses reveal IL17A⁺ CD4 T cells as terminally differentiated and clonally expanded. Blocking IL17A reduces SR-Ag–induced lung inflammation and fibrosis. Exosomal miR-6990-5p from MMP14-overexpressing macrophages promotes Th17 differentiation and fibroblast-to-myofibroblast transition (FMT) in vitro. It directly targets STAT1, as confirmed by luciferase assays. Co-immunoprecipitation (Co-IP) and docking analyses show STAT1 interacts with ROR-γt and RUNX1. STAT1 knockdown upregulates ROR-γt, IL17A, and RUNX1 in co-cultures with naïve CD4 T cells. In vivo, miR-6990-5p exacerbates fibrotic hypersensitivity pneumonitis (FHP) in SR-Ag-exposed mice. These findings indicate that miR-6990-5p induces Th17 cell differentiation through the STAT1/RUNX1/ROR-γt/IL17A pathway, contributing to FMT and fibrosis progression. This highlights miR-6990-5p as a potential therapeutic target for FHP.\u0000 </div>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anti-SARS-CoV-2 Spike IgA2 Induces Inflammation by Human Macrophages 抗sars - cov -2刺突IgA2诱导人巨噬细胞炎症

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-06 DOI: 10.1002/eji.70068

Lynn Mes, Jennifer Veth, Julie Van Coillie, Jim B. D. Keijser, Elise Mantel, Richard van der Mast, Theo Rispens, Gestur Vidarsson, Marjolein van Egmond, Jeroen den Dunnen, Hung-Jen Chen

{"title":"Anti-SARS-CoV-2 Spike IgA2 Induces Inflammation by Human Macrophages","authors":"Lynn Mes, Jennifer Veth, Julie Van Coillie, Jim B. D. Keijser, Elise Mantel, Richard van der Mast, Theo Rispens, Gestur Vidarsson, Marjolein van Egmond, Jeroen den Dunnen, Hung-Jen Chen","doi":"10.1002/eji.70068","DOIUrl":"10.1002/eji.70068","url":null,"abstract":"Severe COVID-19 is an immunological disorder characterized by a hyper-inflammatory reaction of the immune system. SARS-CoV-2 anti-spike antibodies of the IgG isotype are known to strongly contribute to this hyperinflammation by overactivation of alveolar macrophages. However, while the pathogenic function of IgG has been extensively studied, very little is known about the function of IgA, the most abundant immunoglobulin isotype in the airways. Although IgA is generally considered noninflammatory, in this study, we show that anti-spike IgA induces pronounced proinflammatory responses. We demonstrate that stimulation of macrophages with anti-spike IgA immune complexes in combination with a viral stimulus amplifies proinflammatory cytokine production. This IgA-induced inflammation is particularly driven by IgA2, the IgA subclass that is increased in the plasma of severely ill COVID-19 patients. We identified that IgA2-induced inflammation is predominantly dependent on FcαRI-Syk signaling. Mechanistically, IgA2-induced inflammation is linked to enhanced glycolysis and altered mitochondrial function, indicating subclass-specific immunometabolic reprogramming. Taken together, these data indicate a pathogenic role for IgA2 in severe COVID-19 and highlight its signaling cascades and metabolic pathways as potential druggable targets to counteract hyperinflammation in severe coronavirus infections, such as COVID-19, SARS, MERS, and potential future outbreaks.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12501405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Abundant Yet Aberrant T Helper Cell Responses to Candida albicans Underlie Mucosal Candidiasis in Humans and Mice 丰富而异常的辅助性T细胞对白色念珠菌的反应是人类和小鼠粘膜念珠菌病的基础。

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-06 DOI: 10.1002/eji.70065

Camilla Basso, Corinne De Gregorio, Roberta Marzi, Florian Kirchner, Gabor Gyülveszi, Mélanie Migaud, Sinu Paul, Alessandro Sette, Antonio Lanzavecchia, Salomé LeibundGut-Landmann, Jean-Laurent Casanova, Anne Puel, Simone Becattini, Federica Sallusto

{"title":"Abundant Yet Aberrant T Helper Cell Responses to Candida albicans Underlie Mucosal Candidiasis in Humans and Mice","authors":"Camilla Basso, Corinne De Gregorio, Roberta Marzi, Florian Kirchner, Gabor Gyülveszi, Mélanie Migaud, Sinu Paul, Alessandro Sette, Antonio Lanzavecchia, Salomé LeibundGut-Landmann, Jean-Laurent Casanova, Anne Puel, Simone Becattini, Federica Sallusto","doi":"10.1002/eji.70065","DOIUrl":"10.1002/eji.70065","url":null,"abstract":"T helper cell subsets—Th1, Th2, and Th17—coordinate pathogen-specific immune responses. Candida albicans-specific T cells include protective Th17 cells alongside other Th subsets. However, the role of alternative Th subsets remains unclear, particularly in individuals with impaired Th17 responses and recurrent candidiasis. Here, we show that patients with STAT1 gain-of-function mutations and chronic mucocutaneous candidiasis have a numerically normal but functionally altered pool of C. albicans-specific Th cells, skewed toward Th1 and Th2. This imbalance persisted even when assessing responses to the known and the newly identified immunodominant C. albicans antigens MP65 (65-kilodalton mannoprotein), HYR1 (hyphally regulated cell wall protein 1), and SAP4-6 (secreted aspartic proteinases 4–6), suggesting that antigen recognition and priming remain intact despite qualitative defects in T cell polarization. Using mucosal infection mouse models, we demonstrate that C. albicans-specific transgenic Th17 cells are sufficient to control infection, whereas Th1 and Th2 cells fail to protect, even in high numbers. Moreover, co-transfer of Th2 cells with Th17 cells impaired fungal control via an IL-4-dependent mechanism. These findings highlight the essential role of Th17 cells in protective immunity against C. albicans and reveal that non-Th17 responses are ineffective and may contribute to susceptibility in both humans and mice.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12501408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Antigen-Specific Tolerance: Clinical and Preclinical Approaches in Autoimmunity 抗原特异性耐受性：自身免疫的临床和临床前方法。

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-06 DOI: 10.1002/eji.70067

Priscilla P. M. Faas, Stephanie D. Scharmann, Novalia Pishesha

引用次数: 0

From Histology to High-Resolution Mapping: The Rise of Spatial Omics in Immunology 从组织学到高分辨率制图：空间组学在免疫学中的兴起。

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-06 DOI: 10.1002/eji.70073

Marco De Giovanni, Donato Inverso, Matteo Iannacone

{"title":"From Histology to High-Resolution Mapping: The Rise of Spatial Omics in Immunology","authors":"Marco De Giovanni, Donato Inverso, Matteo Iannacone","doi":"10.1002/eji.70073","DOIUrl":"10.1002/eji.70073","url":null,"abstract":"The immune system is deeply shaped by its anatomical context, with spatial organization emerging as a fundamental principle of immune regulation. Recent advances in spatial omics technologies—encompassing transcriptomics, proteomics, metabolomics, lipidomics, and phosphoproteomics—have revolutionized our ability to study immune processes within intact tissue environments. By preserving spatial coordinates while capturing high-dimensional molecular data, these technologies offer unprecedented insight into how immune cell states and functions are governed by local cues and tissue architecture. In this review, we provide an overview of the major spatial omics platforms, emphasizing methodologies that have gained traction within the immunology community and in our own research. We then illustrate how these tools have begun to elucidate the logic of immune compartmentalization across anatomically complex tissues. While not exhaustive, we highlight selected examples from the intestine, secondary lymphoid organs, and liver to show how spatial omics has uncovered region-specific immune programs, microenvironmental niches, and context-dependent signaling pathways. Together, these studies demonstrate how spatial omics technologies are redefining immunological inquiry—shifting the focus from isolated cell types to their spatially embedded roles in tissue physiology and pathology.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12501406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Equine Asthma Is Characterised by Severity-Dependent Correlations Between Blood Neutrophil Cholesterol Content and NET Formation 马哮喘的特点是血液中性粒细胞胆固醇含量和NET形成之间的严重依赖相关性。

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-06 DOI: 10.1002/eji.70072

Lia K. Meiseberg, AhmedElmontaser Mergani, Julien Delarocque, Rabea Imker, Darleen Köhn, Dalanda Wanes, Marta C. Bonilla, Edwin J. A. Veldhuizen, Maren von Köckritz-Blickwede, Bernhard Ohnesorge, Nicole de Buhr

{"title":"Equine Asthma Is Characterised by Severity-Dependent Correlations Between Blood Neutrophil Cholesterol Content and NET Formation","authors":"Lia K. Meiseberg, AhmedElmontaser Mergani, Julien Delarocque, Rabea Imker, Darleen Köhn, Dalanda Wanes, Marta C. Bonilla, Edwin J. A. Veldhuizen, Maren von Köckritz-Blickwede, Bernhard Ohnesorge, Nicole de Buhr","doi":"10.1002/eji.70072","DOIUrl":"10.1002/eji.70072","url":null,"abstract":"Equine asthma (EA) is the most prevalent chronic lung disease in horses. Neutrophils are the main effector cells in severe EA. Neutrophil extracellular traps (NETs) have been described as contributors to severity in human asthma and chronic obstructive pulmonary disease. Thus, we aimed to investigate if NET-related factors in equine neutrophils, blood and bronchoalveolar lavage fluid (BALF) allow us to differentiate EA severities and to identify NET-related mechanistic insights in EA. We quantified NETs and NET-related factors in the blood and BALF of eight healthy horses and 18 horses with differing EA severities. The proportion of activated cells in BALF increased with EA severity, accompanied by dysregulation of local NET regulators in severe EA. Furthermore, circulating anti-neutrophil cytoplasmic antibodies (ANCAs = NET-autoantibodies) were found elevated in severely diseased horses. In line with these findings, NET formation by circulating neutrophils was found to depend on the severity of EA. Finally, we analysed the cholesterol content of circulating neutrophils and identified an asthma-severity-dependent decrease in cellular cholesterol, which correlated with increased NET formation and hypoxia. Local and systemic modifications—particularly in neutrophil cellular cholesterol content—provide further insight into the partially understood pathogenesis of EA and point to a systemic cholesterol-associated inflammatory component fuelling disease progression.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12501399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Purin Metabolism Is Crucial for Regulatory T Cell Stability and Function 嘌呤代谢对调节性T细胞的稳定性和功能至关重要。

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-06 DOI: 10.1002/eji.70070

Young S. Lee, Marina W. Shirkey, Vikas Saxena, Dejun Kong, Bing Ma, Reza Abdi, Jonathan S. Bromberg

{"title":"Purin Metabolism Is Crucial for Regulatory T Cell Stability and Function","authors":"Young S. Lee, Marina W. Shirkey, Vikas Saxena, Dejun Kong, Bing Ma, Reza Abdi, Jonathan S. Bromberg","doi":"10.1002/eji.70070","DOIUrl":"10.1002/eji.70070","url":null,"abstract":"Cellular metabolism intricately directs the differentiation, stability, and function of regulatory T cells (Tregs), which are pivotal in immune regulation. Metabolic reprogramming enables Tregs to adapt to diverse tissue environments; however, it can also disturb immune equilibrium, driving their conversion into unfavorable states like exTregs that hinder regulation in autoimmunity and transplantation. Purine metabolism has emerged as a critical but underexplored regulator of Treg biology. Beyond their traditional roles in nucleotide synthesis and energy balance, purine metabolites also serve as potent second messengers shaping Treg phenotype, suppressive capacity, and adaptability in inflammatory, autoimmune, and transplant environments. Extracellular ATP promotes inflammation, while adenosine supports Treg-mediated immunosuppression, highlighting a dual and context-dependent nature of purinergic signaling. This review outlines current findings on intracellular and extracellular purine metabolism in Tregs, emphasizing key enzymes and purinergic receptors that sustain Treg phenotype and resilience. It discusses disruptions in purine signaling compromising Treg functions, identifies knowledge gaps, and proposes future research directions for potential therapeutic strategies in immune-related ailments.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.70070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Significance of miRNA Profile of Regulatory T Cells (Tregs) After Baricitinib Treatment in Rheumatoid Arthritis Patients Baricitinib治疗后类风湿关节炎患者调节性T细胞（Tregs） miRNA谱的意义

IF 3.7 3区医学

European Journal of Immunology Pub Date : 2025-10-06 DOI: 10.1002/eji.70063

Magdalena Massalska, Anna Felis-Giemza, Patrycja Gardias, Tomasz Burakowski, Anna Kornatka, Paulina Klimek, Magdalena Plebanczyk, Marta Marecka-Kuzdub, Weronika Kurowska, Ewa Kuca-Warnawin, Wlodzimierz Maslinski, Marzena Ciechomska

{"title":"Significance of miRNA Profile of Regulatory T Cells (Tregs) After Baricitinib Treatment in Rheumatoid Arthritis Patients","authors":"Magdalena Massalska, Anna Felis-Giemza, Patrycja Gardias, Tomasz Burakowski, Anna Kornatka, Paulina Klimek, Magdalena Plebanczyk, Marta Marecka-Kuzdub, Weronika Kurowska, Ewa Kuca-Warnawin, Wlodzimierz Maslinski, Marzena Ciechomska","doi":"10.1002/eji.70063","DOIUrl":"10.1002/eji.70063","url":null,"abstract":"<div>\u0000 \u0000 Several studies proved that microRNA (miRNA) originated from cells or body fluids can serve as disease-specific biomarkers in many diseases, including rheumatoid arthritis (RA). In this study, we investigated the effects of Janus Kinase (JAK) selective inhibitor—baricitinib treatment on Treg populations and Treg-derived miRNA in context of basic thrombotic parameters. Blood samples from healthy controls (HCs) and RA patients were used for Treg phenotyping and miRNA detection. Thrombotic parameters were investigated in citrated plasma of RA and HCs. KEGG pathways enrichment analysis of selected four miRNAs was performed using DIANA-mirPath databases to predict the interaction between selected miRNAs and their mRNA targets. Baricitinib treatment resulted in significant CD4+Foxp3+ Treg population decrease (4.6 ± 0.4 vs. 5.6 ± 0.4; p = 0.01) and was characteristic of good responders’ patient group. In this group, significantly lower expression of four miRNAs—miRNA-17, miRNA-142, miRNA-146, and miRNA-155—in comparison to moderate responders or HCs was noticed. The expression of all selected miRNA and miRNA-125 negatively correlated with antithrombin III level. KEGG analysis showed that levels of selected miRNA were strongly associated with four pathways regulating immunity and inflammation. We identified a panel of miRNA in Tregs that can serve as biomarkers of good response in baricitinib therapy.\u0000 </div>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0