Cytokine最新文献

{"title":"Sepsis-induced cardiac dysfunction: Gender bias role of allograft inflammatory factor-1","authors":"B.C. Wang ,&nbsp;S. Chaki ,&nbsp;H. Taufiq ,&nbsp;K. Sikder ,&nbsp;S.K. Shukla ,&nbsp;K. Rafiq","doi":"10.1016/j.cyto.2025.157040","DOIUrl":"10.1016/j.cyto.2025.157040","url":null,"abstract":"<div><div>Sepsis-induced cardiac dysfunction is a major contributor to the high morbidity and mortality rates seen in septic patients, with those suffering from concurrent cardiac dysfunction experiencing mortality rates up to 90 %. This study elucidates the role of allograft inflammatory factor-1 (AIF-1) in sepsis-induced cardiac dysfunction, using a cecal ligation and puncture (CLP) model in both wild-type (WT) and AIF-1 knockout (^-/-) C57BL/6 mice. We specifically examined AIF-1's expression across genders and its impact on cardiac function and inflammation.</div><div>Results indicate a significant gender-specific upregulation of AIF-1 in female murine hearts during septic shock, suggesting a protective role of this molecule in mitigating cardiac dysfunction. In contrast, AIF-1 knockout female mice exhibited exacerbated cardiac dysfunction compared to their wild-type counterparts, as evidenced by decreased ejection fraction and fractional shortening, increased expression of pro-inflammatory cytokines (TNF-α, IL-6), and heightened cardiac inflammation. Moreover, AIF-1 deletion reduced macrophage infiltration in the heart, underscoring its role in modulating immune responses during septic challenges.</div><div>These findings highlight the protective effects of AIF-1 in female mice and suggest its potential as a therapeutic target for sepsis-induced cardiac dysfunction. Understanding AIF-1's mechanisms may facilitate the development of gender-specific treatments to improve outcomes in sepsis, particularly by leveraging its role in enhancing cardiac resilience and modulating inflammation.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157040"},"PeriodicalIF":3.7,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145263707","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}

{"title":"Quercetin enhances amphotericin B activity and regulates ROS and cytokine production in human monocytes infected by Leishmania infantum","authors":"Leonardo Lima Cardoso,&nbsp;Delva Fonseca Lamec Thyares,&nbsp;Ana Letícia Monteiro Fernandes,&nbsp;Rosália Santos Ferreira,&nbsp;Shayenne Eduarda Ramos Vanderley,&nbsp;Fernando Cézar Comberlang,&nbsp;Fernanda Silva Almeida,&nbsp;Tatjana de Souza Lima Keesen","doi":"10.1016/j.cyto.2025.157047","DOIUrl":"10.1016/j.cyto.2025.157047","url":null,"abstract":"<div><div><em>Leishmania infantum</em>, the main causative agent of zoonotic visceral leishmaniasis, persists and proliferates within host monocytes and macrophages. Numerous studies have focused on developing innovative therapies, as conventional treatments are hampered by high toxicity, drug resistance, and relapse. In recent decades, anti-leishmanial immunotherapy — aimed at triggering or modulating the host's immune response — has gained momentum, with various immunomodulators being tested in experimental and clinical settings. However, achieving effective immunotherapy remains challenging, as it requires a delicate balance between enhancing protective, parasite-specific immune responses and avoiding harmful hyperinflammation. In this context, we evaluated quercetin, a natural flavonoid with reported immunomodulatory properties, alone and in combination with Amphotericin B (AmB), against <em>Leishmania infantum</em> promastigotes and during human monocyte infection. Infected and non-infected PBMCs were assessed for parasite viability and cytotoxicity; monocyte infection rates, reactive oxygen species (ROS), nitric oxide (NO) production, and cytokine profiles. Quercetin showed significant anti-promastigote activity and, in combination with AmB, enhanced parasite death, indicating synergistic effects. It also reduced monocyte infection rates, enhanced ROS production, and downregulated levels of IL-6, IL-10, and IL-17, without altering NO production. These findings support the concept of quercetin as a dual-action agent, exerting direct anti-leishmanial effects while fine-tuning the host immune response. By promoting beneficial immunological pathways and dampening potentially deleterious cytokines, quercetin exemplifies the “trapeze act” of immunotherapy, suggesting its potential as an adjuvant to conventional chemotherapy in visceral leishmaniasis.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157047"},"PeriodicalIF":3.7,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145256892","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}

{"title":"Long-term storage stability of plasma TNF-α and IL-6 concentrations of psychiatric emergency patients: The Signature Biobank","authors":"Enzo Cipriani ,&nbsp;Charles-Édouard Giguère ,&nbsp;Cécile Le Page ,&nbsp;Helen Findlay ,&nbsp;Janick Boissoneault ,&nbsp;Stéphane Potvin ,&nbsp;Robert-Paul Juster","doi":"10.1016/j.cyto.2025.157033","DOIUrl":"10.1016/j.cyto.2025.157033","url":null,"abstract":"<div><div>Cytokines are increasingly incorporated in psychiatric research. While biobanking provides advantages for different study designs, long-term storage could degrade cytokine quality and introduce bias. To date, reports on cytokine stability are based on small sample sizes (<em>n</em> &lt; 20) and do not address long-term (4+ years) storage effects. This article reports two studies evaluating IL-6 and TNF-α measurements in human plasma samples biobanked for long periods. In the first study, with samples stored between 5 and 139 months (11.6 years), IL-6 concentrations were not significantly correlated with storage length in all available baseline data of the Signature Biobank (n[IL-6] = 1206, n[TNF-α] = 1223). TNF-α correlated negatively with storage length (<em>r</em> = −0.217; <em>p</em> &lt; 0.001) indicating a decrease of concentrations with longer storage. In the second study, IL-6 and TNF-α concentrations were measured twice in the same plasma samples of 50 psychiatric participants from the Signature Biobank stored between analyses from 32 to 45 months. We assessed if storage effects differed between analytes. In IL-6, we observe a relatively good stability in samples stored up to 6 years. For TNF-α, we observed only a moderate stability of measurements (rTNF-α = 0.59; rIL-6 = 0.71) with linear decrease over time. As a potential solution, a corrective equation extracted from Study 1 was applied to TNF-α in the Study 2 sample; however, this did not improve correlation coefficients but might be useful in other settings. Integrating samples' age in statistical analyses and/or more systematic quality controls could mitigate degradation process.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157033"},"PeriodicalIF":3.7,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249116","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}

{"title":"Clinical value of serum TNF-α and IL-2R as treatment predictive and prognostic biomarkers in metastatic colorectal cancer","authors":"Jinxiu Tian ,&nbsp;Jinjia Chang ,&nbsp;Zhujun Chen ,&nbsp;Wenhua Li","doi":"10.1016/j.cyto.2025.157046","DOIUrl":"10.1016/j.cyto.2025.157046","url":null,"abstract":"<div><h3>Background</h3><div>Metastatic colorectal cancer remains a major global health concern, with advanced-stage disease posing significant challenges in terms of treatment and prognosis. Cytokines, key mediators of immune regulation and inflammation, have emerged as potential prognostic biomarkers in CRC. However, their prognostic value in the context of first-line standard therapy remains unclear.</div></div><div><h3>Methods</h3><div>This retrospective observational study included 95 patients with metastatic colorectal cancer who underwent first-line therapy at Fudan University Shanghai Cancer Center between 2020 and 2021. Baseline levels of TNF-α, IL-1β, IL-2R, IL-6, IL-8, and IL-10 before treatment were assessed, and patients were categorized into high and low cytokine expression groups. Survival outcomes were analyzed based on baseline cytokine levels and dynamic changes before and after treatment.</div></div><div><h3>Results</h3><div>Higher baseline levels of TNF-α and IL-2R were associated with poorer progression-free survival outcomes. Dynamic changes of TNF-α and IL-2R before and after treatment were also predictive of survival, with persistently elevated levels associated with worse outcomes. Additionally, clinical characteristics such as liver metastasis and surgical intervention were correlated with cytokine expression levels and survival outcomes.</div></div><div><h3>Conclusions</h3><div>Baseline cytokine levels of TNF-α and IL-2R and their dynamic changes before and after treatment are potential prognostic indicators in patients with metastatic colorectal cancer undergoing first-line standard therapy. Monitoring cytokine profiles may aid in risk stratification and treatment decision-making, ultimately improving patient outcomes.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157046"},"PeriodicalIF":3.7,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249125","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}

{"title":"Therapeutic potential of IFIT2 in human diseases","authors":"Ewura-Esi Manful ,&nbsp;Francis Adu-Amankwaah ,&nbsp;Abhilasha Madhvi ,&nbsp;Kayla Bubb ,&nbsp;Ray-Dean Pietersen ,&nbsp;Bienyameen Baker","doi":"10.1016/j.cyto.2025.157049","DOIUrl":"10.1016/j.cyto.2025.157049","url":null,"abstract":"<div><div>The interferon-induced protein with tetratricopeptide repeats 2 (IFIT2) is a crucial member of the interferon-stimulated gene (ISG) family, widely acknowledged for its antiviral activity. IFIT2 functions primarily through AU-rich RNA binding, aiding in viral suppression by inhibiting protein translation and promoting apoptosis via mitochondrial pathways. While traditionally known for its role in antiviral defence, emerging research highlights its broader significance in cancer, bacterial and fungal infections, autoimmune diseases, neurological disorders, and metabolic and cardiovascular conditions. Notably, IFIT2 is the only IFIT family member with established tumour suppressor properties, demonstrating anti-proliferative effects in multiple cancers, including lung, renal, colorectal, breast, and gallbladder cancers.</div><div>Beyond oncology, IFIT2 has been implicated in the host response to <em>Mycobacterium tuberculosis</em>, <em>Plasmodium</em> spp., <em>Candida albicans</em>, and <em>Treponema pallidum</em>, where it modulates immune responses and infection outcomes. It is upregulated in several autoimmune diseases such as systemic lupus erythematosus, Sjögren's syndrome, and multiple sclerosis, suggesting its potential as a diagnostic and therapeutic biomarker. Furthermore, transcriptomic analyses have linked IFIT2 to disease progression and treatment response in conditions like diabetic ulcers, gestational diabetes, ischaemic cardiomyopathy, schizophrenia, and Alzheimer's disease.</div><div>This review thoroughly examines the molecular structure, regulatory mechanisms, and diverse roles of IFIT2 in human diseases. It addresses its interaction with key immune pathways, its ability to modulate apoptosis and inflammation, and its potential as a prognostic marker and therapeutic target. Although its mechanistic functions in numerous diseases remain only partly understood, IFIT2 emerges as a versatile immune effector with considerable translational promise. Further investigation into its biological roles will be crucial for utilising its therapeutic potential across infectious, inflammatory, metabolic, and neoplastic diseases.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157049"},"PeriodicalIF":3.7,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145218245","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}

{"title":"Extracellular granzyme B and K are associated with endometriosis severity in infertile women","authors":"Fadhil Ahsan ,&nbsp;Budi Santoso ,&nbsp;Nanda Yuli Rahmawati ,&nbsp;Fidyah Nanda Alditia ,&nbsp;Alfin Firasy Mufid ,&nbsp;M.Y. Ardianta Widyanugraha ,&nbsp;Ashon Sa'adi ,&nbsp;Sri Ratna Dwiningsih ,&nbsp;Arif Tunjungseto","doi":"10.1016/j.cyto.2025.157045","DOIUrl":"10.1016/j.cyto.2025.157045","url":null,"abstract":"<div><h3>Background</h3><div>Endometriosis is a chronic inflammatory condition often associated with infertility. The role of granzymes as cytotoxic proteases and immune regulators in endometriosis remains poorly understood. This study evaluated serum and peritoneal fluid levels of granzymes A, B, and K in women with endometriosis and their links to disease severity.</div></div><div><h3>Methodology</h3><div>An observational study of 87 infertile women undergoing diagnostic laparoscopy, including 44 with endometriosis and 43 benign gynecologic controls. Granzyme levels were measured using ELISA and correlated with clinical parameters.</div></div><div><h3>Results</h3><div>Serum GrB and GrK were significantly higher in women with endometriosis, particularly in advanced stages. Peritoneal fluid revealed reduced GrA and increased GrB in the endometriosis group. Serum GrB and GrK levels correlated positively with rASRM adhesion and endometriosis severity scores, while GrB levels correlated inversely with the Endometriosis Infertility Index (EFI) score, indicating their role in predicting infertility. Combining serum GrB and GrK effectively differentiated endometriosis from control, highlighting their diagnostic potential.</div></div><div><h3>Conclusion</h3><div>Elevated serum GrB and GrK levels suggest their involvement in endometriosis pathogenesis and infertility. These findings highlight granzymes as promising biomarkers for disease severity, diagnosis, and targeted therapy in endometriosis management.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157045"},"PeriodicalIF":3.7,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145218247","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}

{"title":"Inhibiting TGF-β signaling pathway for disease therapy: challenges and opportunities","authors":"XiaoYan Gao ,&nbsp;XiuDan Li ,&nbsp;CongYing Zhang ,&nbsp;Jing Zhou ,&nbsp;Kai Gu ,&nbsp;XiaoQiang Liu ,&nbsp;ChunYing Bai","doi":"10.1016/j.cyto.2025.157048","DOIUrl":"10.1016/j.cyto.2025.157048","url":null,"abstract":"<div><div>Transforming growth factor (TGF)-β is a multifunctional cytokine expressed in nearly all human tissues and cell types. The TGF-β signaling pathway is essential for embryonic development, cell and tissue differentiation, and tissue homeostasis in adults. Aberrant regulation of this pathway is closely associated with various diseases, indicating that the TGF-β signaling pathway represents a promising target for therapeutic intervention. Notably, diseases linked to the disruption of the TGF-β signaling pathway include cancer, vascular disorders, wound healing complications, tissue fibrosis, and autoimmune diseases. The development and optimization of selective inhibitors targeting TGF-β could provide viable therapeutic options for the clinical treatment of these conditions. Consequently, targeting the cytokine TGF-β and its signaling pathway may offer a novel and promising treatment strategy for related diseases. This review summarizes recent studies on the role of TGF-β in the pathogenesis and treatment of associated diseases.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157048"},"PeriodicalIF":3.7,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145218246","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}

{"title":"Regulation of TREG/TH17 balance by NK cells pretreated with ESTRIOL and bacterial cells in multiple sclerosis","authors":"Irina Nekrasova ,&nbsp;Natalia Glebezdina ,&nbsp;Irina Maslennikova ,&nbsp;Irina Danchenko ,&nbsp;Sergei Shirshev","doi":"10.1016/j.cyto.2025.157038","DOIUrl":"10.1016/j.cyto.2025.157038","url":null,"abstract":"<div><div>We studied the influence of the pregnancy hormone estriol (E₃) and bacterial strains on the ability of NK cells to modulate levels of T regulatory (Treg) and IL-17-producing (Th17) lymphocytes from patients with multiple sclerosis (MS) and healthy donors. NK cell phenotype and cytokine production in co-cultures with CD4⁺ lymphocytes was also investigated after incubation with the hormone and bacterial cells. Treatment of NK cells with these factors stimulated Treg formation and inhibited Th17 development. Within 24 h, NK cell cytotoxicity and production of IL-2 and IFN-γ were inhibited, while IL-10 secretion increased. This was accompanied by a rise in IL-6 and TNF-α. After three days, NK cells showed increased IL-10 and decreased IL-17 expression. Notably, cells from MS patients were more sensitive to this regulatory influence than those from healthy donors.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157038"},"PeriodicalIF":3.7,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145218248","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}

{"title":"The significance of serum IL-18 levels in Hodgkin lymphoma patients","authors":"Gülden Sincan ,&nbsp;Suat Sincan ,&nbsp;Çağrı Kızıltunç ,&nbsp;Esra Eğilmez","doi":"10.1016/j.cyto.2025.157044","DOIUrl":"10.1016/j.cyto.2025.157044","url":null,"abstract":"<div><h3>Background</h3><div>Inflammation plays a crucial role in the pathogenesis of Hodgkin lymphoma. IL-18 is a proinflammatory cytokine. Therefore, we investigated the serum IL-18 levels and their prognostic significance in Hodgkin lymphoma patients.</div></div><div><h3>Method</h3><div>Serum IL-18 levels were compared between 30 newly diagnosed Hodgkin lymphoma patients and 30 healthy controls. The association between IL-18 levels, clinical findings, prognostic markers, and treatment response was also evaluated in Hodgkin lymphoma patients.</div></div><div><h3>Results</h3><div>The HL group's IL-18 level (29.28 ± 13.48 pg/mL) was significantly higher than that of the control group (16.69 ± 9.33 pg/mL) (<em>p</em> &lt; 0.001). Significant associations were observed between IL-18 levels and extranodal involvement, B symptom presence, performance status, Ann-Arbor stage, bulky mass presence, bone marrow involvement, and treatment response in Hodgkin lymphoma patients (<em>p</em> = 0.013, <em>p</em> = 0.006, <em>p</em> = 0.009, <em>p</em> = 0.003, <em>p</em> = 0.001, <em>p</em> = 0.02, <em>p</em> = 0.03, respectively). IL-18 levels also positively correlated with LDH and beta-2 microglobulin levels (<em>r</em> = 0.37, <em>p</em> = 0.04, <em>r</em> = 0.5, <em>p</em> = 0.005, respectively).</div></div><div><h3>Conclusion</h3><div>Serum IL-18 levels are higher in Hodgkin lymphoma patients compared to healthy individuals. IL-18 levels may serve as a prognostic marker and a predictor of treatment response in Hodgkin lymphoma patients.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157044"},"PeriodicalIF":3.7,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145218249","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}

{"title":"Epitranscriptomic regulation of immunity: The role of m6A in shaping immune response dynamics.","authors":"Devesh Srivastava, Vinayak Nayak, Srijoni Pahari, Gopu Sandeep, Ashish Misra","doi":"10.1016/j.cyto.2025.157011","DOIUrl":"10.1016/j.cyto.2025.157011","url":null,"abstract":"<p><p>N6-methyladenosine (m6A) is the most prevalent internal modification found in eukaryotic mRNAs and plays a critical role in shaping immune response. It acts as a dynamic regulatory step modulating the splicing, stability, degradation and translation of target mRNAs involved in regulating immune outcome. These effects are mediated by the dynamic interplay of m6A methyltransferases (\"writers\"), demethylases (\"erasers\"), and binding proteins (\"readers\") which work in concert to fine-tune immune activation and suppression. m6A modifications modulate both innate and adaptive immune responses by regulating chemokine signaling, inflammation, and guiding the lineage commitment and function of various cells involved in immune regulation. For example, m6A-modified mRNAs encoding interferons and pro-inflammatory cytokines are translated more efficiently, facilitating a swift response to infection, while m6A-mediated degradation of pro-inflammatory transcripts offers a counterbalance, allowing immune cells to fine-tune responses and limit overactivation. In T cells, m6A readers influence antigen responsiveness and immune tolerance, while in regulatory T cells, m6A plays a key role in maintaining immune equilibrium. In this review, we present an in-depth overview of how m6A methylation shapes immune function and outline its potential as a therapeutic target. A detailed understanding of the interplay between m6A and immune regulation may provide valuable insights for developing novel therapies for immune-related diseases.</p>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"194 ","pages":"157011"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144811490","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}