Cytokine最新文献

{"title":"Role of macrophages reprogramming in pathogenesis of gestational diabetes mellitus","authors":"K.L. Milan,&nbsp;R. Adhi Shree,&nbsp;N. Nandana,&nbsp;R. Leela,&nbsp;K.M. Ramkumar","doi":"10.1016/j.cyto.2025.157041","DOIUrl":"10.1016/j.cyto.2025.157041","url":null,"abstract":"<div><div>Gestational diabetes mellitus (GDM) is a pregnancy-associated condition resulting from glucose intolerance affecting approximately 14 % of pregnant women worldwide and contributing to both maternal and neonatal complications. Macrophages, essential components of the innate immune system, exist in three main polarization states: M0 (resting), M1 (pro-inflammatory), and M2 (anti-inflammatory). In normal pregnancy, a proper balance between M1 and M2 phenotypes is critical for successful placentation and fetal development. Although this classification provides a useful framework, emerging evidence indicates that macrophages exist along a dynamic continuum of activation states with overlapping functional characteristics rather than discrete polarization categories. Recent studies further reveal that macrophage behavior in pregnancy involves context-dependent and plastic responses that cannot be fully captured by the M1/M2 paradigm alone. However, in GDM, hyperglycaemia significantly influences macrophage reprogramming toward a pro-inflammatory phenotype. The manuscript examines how dysregulated macrophage polarization contributes to insulin resistance, placental dysfunction, and adverse pregnancy outcomes. Emerging evidence suggests that hyperglycaemia induces trained immunity in macrophages, characterized by persistent expression of pro-inflammatory genes. In the GDM placenta, research indicates an altered M1/M2 ratio, though findings vary regarding specific polarization patterns. This review highlights promising therapeutic strategies targeting macrophage repolarization from M1 toward M2 phenotypes, including pharmacological approaches, RNA-based therapies, and <em>ex vivo</em> macrophage manipulation. Understanding macrophage reprogramming in GDM presents novel opportunities for interventions that may improve maternal-fetal outcomes and long-term metabolic health.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157041"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205069","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":"2025-12-01","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":"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":"2025-12-01","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":"Serum endocan as a dual-function biomarker in Kawasaki disease: early diagnostic potential and prediction of coronary arterial aneurysms","authors":"Chang Liu,&nbsp;Yi Wei,&nbsp;Fengchuan Jing ,&nbsp;Qijian Yi","doi":"10.1016/j.cyto.2025.157052","DOIUrl":"10.1016/j.cyto.2025.157052","url":null,"abstract":"<div><h3>Background</h3><div>Kawasaki disease (KD), an acute vasculitis of unclear etiology, is an important contributor to childhood-acquired heart disease due to coronary arterial aneurysms (CAAs). Current diagnosis lacks specific biomarkers, risking delayed treatment. Endocan, a proteoglycan implicated in vascular inflammation, may address this gap. This study evaluates serum endocan in acute KD for its utility in early KD diagnosis and CAA risk prediction.</div></div><div><h3>Method</h3><div>This prospective cohort study enrolled 79 KD patients and 48 healthy controls. The KD group was further divided into KD with CAA (KD-CAA) and KD non-CAA (KD-NCAA) subgroups. Serum endocan levels were quantified via enzyme-linked immunosorbent assay. Clinical parameters including inflammatory markers were systematically analyzed using SPSS and GraphPad Prism.</div></div><div><h3>Results</h3><div>Serum endocan levels were significantly elevated in KD patients compared to HCs (median [25th–75th percentile], 1803.69 pg/ml [1478.97–2038.87] vs. 931.73 [815.57–1138.72] pg/ml, <em>P</em> &lt; 0.001), with higher concentrations in KD-CAA versus KD-NCAA (mean ± SD, 1962.43 ± 321.48 vs. 1702.46 ± 458.54 pg/ml, <em>P</em> = 0.024).</div><div>Endocan demonstrated excellent performance in distinguishing KD patients from HCs (AUC = 0.915, 95 % CI: 0.863–0.968; sensitivity 88.6 %, specificity 85.4 %). It also showed a modest but statistically significant predictive value for CAAs within the KD cohort (AUC = 0.675, 95 % CI: 0.548–0.801; sensitivity 73.7 %, specificity 58.3 %).</div></div><div><h3>Conclusion</h3><div>Serum endocan is a high-performance biomarker for differentiating KD from HCs. Despite modest performance in predicting CAAs and undetermined specificity, it may serve as a valuable supportive tool for risk stratification in KD patients.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157052"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145353137","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":"IL-6, IFN-γ, IL-17A elevations and glutathione depletion predict severe MODS and mortality in critically ill children with COVID-19 and bacterial sepsis: a prospective cohort study from the Brazilian Amazon","authors":"Emmerson C.F. de Farias ,&nbsp;Patricia B. Carvalho ,&nbsp;Luciana M.P.P. do Nascimento ,&nbsp;Andreza H.O. Pinheiro ,&nbsp;Marília C.B. Alves ,&nbsp;Kíssila M.M. Machado-Ferraro ,&nbsp;Larisse F.Q. Aires ,&nbsp;Luana G. Dias ,&nbsp;Mayara M.M. Machado ,&nbsp;Michaelle J.D. Serrão ,&nbsp;Raphaella R. Gomes ,&nbsp;Sara M.P. de Moraes ,&nbsp;Gabriela C.L. Pontes ,&nbsp;Railana D.F.P. Carvalho ,&nbsp;Elaine B.G.P. Nascimento ,&nbsp;Cristiane T.C. Silva ,&nbsp;Adriana M.B. de Sousa ,&nbsp;Lêda L. da Silva ,&nbsp;Nathália K.F. Barbosa ,&nbsp;Anna L.M. Machado ,&nbsp;Marta C. Monteiro","doi":"10.1016/j.cyto.2025.157043","DOIUrl":"10.1016/j.cyto.2025.157043","url":null,"abstract":"<div><h3>Background</h3><div>Multiple organ dysfunction syndrome (MODS) remains a major cause of morbidity and mortality in pediatric intensive care units (PICUs), particularly when triggered by SARS-CoV-2 or bacterial sepsis. This study aimed to investigate the association between inflammatory and oxidative stress biomarkers and the development and outcome of MODS in critically ill children with confirmed SARS-CoV-2 or bacterial infections.</div></div><div><h3>Methods</h3><div>In this prospective, single-center cohort study (May 2020–December 2024), 62 pediatric patients (29 days to &lt;18 years) were stratified into three groups: SARS-CoV-2 without MODS (<em>n</em> = 22), SARS-CoV-2 with MODS (<em>n</em> = 20), and bacterial MODS (n = 20). Circulating cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-γ, IL-17A) and oxidative stress markers (GSH, TBARS, TEAC) were quantified at PICU admission and on day 5. Associations with organ dysfunction and 28-day mortality were assessed using non-parametric statistical analyses and Kaplan-Meier survival estimates.</div></div><div><h3>Results</h3><div>MODS groups exhibited on day 1 sustained elevations in TNF-α, IFN-γ, and IL-17A—most pronounced in bacterial MODS (Group 3; <em>p</em> &lt; 0.0001). IFN-γ was notably increased in viral MODS (Group 2). Group 3 also showed marked elevations in IL-6, IL-2, and IL-10 (p &lt; 0.0001). By day 5, both MODS groups demonstrated significant reduced GSH and TEAC and elevated TBARS, the most severe in Group 3. In contrast, Group 1 exhibited stable cytokine profiles and preserved antioxidant status throughout. Non-survivors showed persistently elevated IL-6, TNF-α, IFN-γ, and IL-17A, coupled with sustained depletion of GSH and TEAC, and increased TBARS levels (all <em>p</em> &lt; 0.0001). IL-6 and IFN-γ were particularly elevated in non-survivors with bacterial and viral MODS, respectively. Biomarker trajectories diverged between survivors and non-survivors by day 5, with failure to normalize immune-redox profiles associated with mortality. Accessible indices such as NLR, CAR, and VIS correlated with biomarker levels and disease severity. Kaplan–Meier analysis confirmed reduced survival in MODS groups (<em>p</em> = 0.0005).</div></div><div><h3>Conclusions</h3><div>A distinct cytokine and oxidative stress signature—marked by early and sustained elevations in IL-6, TNF-α, IFN-γ, IL-17A, and TBARS, and depletion of GSH and TEAC—is associated with mortality in pediatric MODS. Bacterial MODS was distinguished by the most severe immune-redox imbalance. Integrated immune-redox profiling offers prognostic value and may inform precision-targeted interventions, particularly in resource-limited settings.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157043"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145353182","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":"Inflammation and inflammatory cytokines in cardiac cachexia: an incendiary issue","authors":"Amisha Mahur ,&nbsp;Bhoomika M. Patel","doi":"10.1016/j.cyto.2025.157063","DOIUrl":"10.1016/j.cyto.2025.157063","url":null,"abstract":"<div><div>Cardiac cachexia, a severe consequence of heart failure, is marked by progressive weight loss due to skeletal and cardiac muscle wasting. This complex condition involves nutritional deficiencies, gut dysfunction, hormonal imbalances, and a critical disruption in muscle protein metabolism. However, chronic inflammation in the heart failure is the key driver, triggering the release of cytokines like TNF-α, IL-6, IL-1, IL-10 and TGF-β. These cytokines significantly impact muscle metabolism, promoting protein breakdown while hindering protein synthesis. Elevated TNF-α levels induce anorexia, worsening weight loss, and muscle depletion. IL-6 acts as a potent muscle-wasting agent, upregulating protein degradation via the ubiquitin-proteasome system. Similarly, IL-1 activates pathways that promote protein breakdown and suppress cell proliferation. TGF-β, despite its diverse functions, contributes to muscle atrophy by increasing protein degradation. In contrast, the anti-inflammatory cytokine IL-10 promotes protein synthesis by suppressing pathways that normally inhibit it. Understanding these cytokine actions provides valuable insights into cardiac cachexia and paves the way for targeted therapies aimed at modulating these pathways to prevent or reverse muscle wasting in heart failure. In this review, we will describe the pathophysiology of cardiac cachexia and the role of various cytokines in cardiac cachexia which is released due to inflammation.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157063"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145385471","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":"2025-12-01","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":"Unveiling IL-41: A novel biomarker for polymyositis and dermatomyositis diagnosis","authors":"Zhi Li ,&nbsp;Wen Qin ,&nbsp;Xiudi Wu ,&nbsp;Mingcai Li ,&nbsp;Yan Li","doi":"10.1016/j.cyto.2025.157058","DOIUrl":"10.1016/j.cyto.2025.157058","url":null,"abstract":"<div><div><em>Background:</em> Polymyositis (PM) and dermatomyositis (DM) are two common subtypes of idiopathic inflammatory myopathies (IIM). The concentration of serum interleukin (IL)-41 in patients with PM/DM has not been reported. This study aims to investigate the levels of IL-41 in the serum of individuals diagnosed with PM/DM.</div><div><em>Methods:</em> A total of 118 participants were enrolled in the study, comprising 80 patients with PM/DM and 38 healthy controls (HC). Comprehensive clinical data for each participant were collected through physical examinations and detailed clinical histories. The levels of IL-41 were quantified using the enzyme-linked immunosorbent assay (ELISA). Spearman's correlation analysis was employed to examine the relationship between IL-41 levels and various clinical parameters. The diagnostic potential of IL-41 was assessed using the receiver operating characteristic (ROC) curve.</div><div><em>Results:</em> Serum IL-41 levels were significantly elevated in PM/DM patients with interstitial lung disease (ILD) compared to HC [1001.03 (572.95, 1604.83) pg/mL vs 361.03 (302.24, 541.06) pg/mL, <em>P</em> &lt; 0.0001]. Furthermore, a significant difference was also observed in serum IL-41 levels between PM/DM patients without ILD and HC [561.81 (407.94, 827.34) pg/mL vs 361.03 (302.24, 541.06) pg/mL, <em>P</em> = 0.0139]. IL-41 exhibits substantial diagnostic potential for PM/DM, and its combination with lactate dehydrogenase enhances diagnostic efficacy. Moreover, IL-41 acts as an independent risk factor for the onset of PM/DM.</div><div><em>Conclusions:</em> This study revealed that serum IL-41 levels are elevated in patients with PM/DM, suggesting that IL-41 could serve as a novel biomarker for the identification of these conditions.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157058"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145317987","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":"Anakinra ameliorates insulin resistance and inflammation in a murine model of gestational diabetes through downregulation of Th17 responses Anakinra for the treatment of GDM in mice","authors":"Lingyan Zhang ,&nbsp;Fudan Huang ,&nbsp;Shaik Althaf Hussain ,&nbsp;Yi Tian","doi":"10.1016/j.cyto.2025.157039","DOIUrl":"10.1016/j.cyto.2025.157039","url":null,"abstract":"<div><div>Gestational diabetes mellitus (GDM) is associated with low-grade inflammation which can contribute to insulin resistance and dysregulated glucose metabolism. Anakinra is a recombinant form of IL-1 receptor antagonist (IL-1Ra) that has shown promise in the control of several inflammatory diseases. The present study aimed to evaluate the potential of Anakinra in the control of inflammation and glucose metabolism in a genetic model of GDM.</div><div>Pregnant C57BL/KsJdb/+ (db/+) mice were used as the murine model of GDM and the glucose metabolism, insulin resistance as well as levels of inflammatory mediators were evaluated. The populations of Th17 and Treg cells were also analyzed in spleens of mice. Some GDM-associated parameters were studied in offspring along with an evaluation of oxidative stress in the liver and placenta.</div><div>Anakinra improved the glucose tolerance and insulin sensitivity of GDM mice and controlled the weight gain of the pregnant mice. The population of Th17 cells as key mediators of inflammatory processes declined in the Anakinra-received mice and the serum levels of pro-inflammatory cytokines as well as the activation of the NF-κB pathway declined accordingly. Besides, the infiltration of T-cells into the placenta was diminished in Anakinra-treated mice.</div><div>Anakinra demonstrated a potential for control of GDM by targeting low-grade inflammation and improving glucose metabolism. Regarding the fair properties of small molecules that render them suitable therapeutic tools, Anakinra might be a candidate therapeutic for the control of GDM more efficiently.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157039"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145263708","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":"T1-mapping quantitative assessment of renal function and changes in serum cytokine levels after renal transplantation in children","authors":"XueyingWang ,&nbsp;Jun Hu","doi":"10.1016/j.cyto.2025.157027","DOIUrl":"10.1016/j.cyto.2025.157027","url":null,"abstract":"<div><div>Background: Postoperative renal function assessment in pediatric kidney transplant recipients faces the challenge of insufficient sensitivity of traditional indicators. T1-mapping, a non-invasive imaging technique, can quantify changes in the microscopic structure of renal tissue. However, its application in the pediatric population and its relationship with serum cytokines remain unclear. This study hypothesized that T1-mapping can quantitatively assess early renal microstructural damage in pediatric kidney transplant recipients and that T1 values correlate with the activation of immune-inflammatory responses (reflected by serum cytokine levels). It aimed to explore the value of T1-mapping in evaluating renal function and its mechanistic association with inflammatory responses.</div><div>Materials and Methods: A total of 31 pediatric kidney transplant recipients (observation group, Obs group) and 31 healthy children (control group, Ctrl group) were enrolled. In the Obs group, T1-mapping was performed at 1, 3, and 6 months post-transplantation to measure T1 values in the renal cortex, medulla, and whole kidney. Serum creatinine (SCr), glomerular filtration rate (GFR), and other renal function indicators were assessed, along with CD4+, CD8+ lymphocyte counts, and levels of cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). Based on the 6-month postoperative prognosis, participants were divided into the good prognosis group (GPG, <em>n</em> = 20) and poor prognosis group (PPG, <em>n</em> = 11).</div><div>Results: The T1 values of the renal cortex, medulla, and whole kidney in the Obs group were significantly higher than those in the Ctrl group (<em>P</em> &lt; 0.05). Specifically, the cortical T1 value in the PPG was (1820 ± 110) ms, significantly higher than that in the GPG (1650 ± 80) ms (<em>P</em> &lt; 0.05). The SCr in the PPG was (220 ± 35) μmol/L, and the GFR was (22 ± 5) mL/min/1.73m², both significantly worse than the GPG (85 ± 12 μmol/L, 78 ± 10 mL/min/1.73m², <em>P</em> &lt; 0.05). The CD4+/CD8+ ratio in the GPG (1.49 ± 0.21) was higher than that in the PPG (0.87 ± 0.15), while the CD8+ cell count (550 ± 60 × 10⁶/L) in the GPG was lower than that in the PPG (780 ± 75 × 10⁶/L, <em>P</em> &lt; 0.05). Levels of IL-6 (28.8 ± 6.5 pg/mL) and TNF-α (45.5 ± 8.3 pg/mL) in the PPG were significantly higher than those in the GPG (12.5 ± 3.0 pg/mL, 18.2 ± 4.1 pg/mL, <em>P</em> &lt; 0.05).</div><div>Conclusion: T1-mapping technology can quantitatively assess changes in renal function following pediatric kidney transplantation, with increased T1 values closely associated with immune-inflammatory activation and renal function damage. Serum cytokine levels reflect the intensity of the inflammatory response, providing new evidence for postoperative monitoring and intervention.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"196 ","pages":"Article 157027"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145107834","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}