Journal of Interferon and Cytokine Research最新文献

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Beyond Traditional Publishing: Social Media as a Catalyst for Biomedical Research Dissemination and Collaboration. 超越传统出版:社会媒体作为生物医学研究传播和合作的催化剂。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-07-01 Epub Date: 2025-05-07 DOI: 10.1089/jir.2025.0074
Jaleel Shujath
{"title":"Beyond Traditional Publishing: Social Media as a Catalyst for Biomedical Research Dissemination and Collaboration.","authors":"Jaleel Shujath","doi":"10.1089/jir.2025.0074","DOIUrl":"10.1089/jir.2025.0074","url":null,"abstract":"<p><p>The expansion of social media has fundamentally transformed biomedical research dissemination and collaboration, particularly within the interferon and cytokine research community. This paper explores recent trends (2024-2025) that have amplified the role of platforms such as Twitter (now \"X\"), LinkedIn, Mastodon, Threads, and Bluesky. These tools have facilitated rapid knowledge exchange, democratized access to scientific discourse, enabled diverse voices to participate meaningfully, and fostered cross-disciplinary and global collaborations. Additionally, the integration of preprint repositories like bioRxiv and medRxiv, along with the evolution of open access publishing, further accelerates the accessibility and immediacy of scientific communication. Despite evident benefits, the rapid dissemination facilitated by social media also poses ethical challenges, including concerns about misinformation, premature dissemination of preliminary data, and privacy considerations. Practical strategies for researchers and institutions to effectively navigate these platforms responsibly are presented, aiming to optimize the impact of social media on scientific discovery and public engagement.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"247-253"},"PeriodicalIF":1.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028148","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
Investigating Causal Associations Between Circulating Cytokines and Vestibular Disorders Using Mendelian Randomization: Insights from Large-Scale Genome-Wide Association Studies Data in European Populations. 使用孟德尔随机化研究循环细胞因子与前庭疾病之间的因果关系:来自欧洲人群大规模全基因组关联研究数据的见解。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-07-01 Epub Date: 2025-04-28 DOI: 10.1089/jir.2025.0030
Ke Shi, Hongwei Liu, Miaomiao Hou, Minheng Zhang
{"title":"Investigating Causal Associations Between Circulating Cytokines and Vestibular Disorders Using Mendelian Randomization: Insights from Large-Scale Genome-Wide Association Studies Data in European Populations.","authors":"Ke Shi, Hongwei Liu, Miaomiao Hou, Minheng Zhang","doi":"10.1089/jir.2025.0030","DOIUrl":"10.1089/jir.2025.0030","url":null,"abstract":"<p><p>The presence of circulating cytokines has a significant impact on the development and progression of vestibular disorders. However, further investigation is needed to determine the direction of causation and causal effects. By applying two-sample Mendelian randomization (MR), we analyzed the potential causal connection between 41 circulating cytokines and vestibular disorders using the integrated data from genome-wide association studies (GWAS). The major analysis utilized for MR was inverse variance weighted (IVW). To examine reverse causation, we conducted reverse MR analysis. In addition, we assessed the robustness of the findings by performing pleiotropy and heterogeneity tests. Our results demonstrated that two circulating cytokines were significantly correlated with vestibular disorders risk. More specifically, vascular endothelial growth factor [IVW, odds ratio (OR) = 0.999, 95% confidence interval (CI) = 0.999-1.000, <i>P</i> = 0.046] and interleukin-7 (IVW, OR = 0.999, 95% CI = 0.998-1.000, <i>P</i> = 0.033) were negatively correlated with vestibular disorders risks, respectively. No evidence was identified to support associations between the remaining 39 circulating cytokines and vestibular disorders. These findings reveal a distinct correlation between circulating cytokines and vestibular diseases, providing a novel perspective and potential biological target for future clinical interventions for vestibular disorders.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"263-273"},"PeriodicalIF":1.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144029523","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
GPNMB Suppresses Inflammation and Extracellular Matrix Degradation in Nucleus Pulposus Cells by Inhibiting Pro-Inflammatory Cytokine Production and Activation of the NF-κB Signaling Pathway. GPNMB通过抑制促炎细胞因子的产生和NF-κB信号通路的激活,抑制髓核细胞的炎症和细胞外基质降解。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-01 Epub Date: 2025-04-16 DOI: 10.1089/jir.2025.0022
Jun Zheng, Yaodong Song, Bing Yu
{"title":"GPNMB Suppresses Inflammation and Extracellular Matrix Degradation in Nucleus Pulposus Cells by Inhibiting Pro-Inflammatory Cytokine Production and Activation of the NF-κB Signaling Pathway.","authors":"Jun Zheng, Yaodong Song, Bing Yu","doi":"10.1089/jir.2025.0022","DOIUrl":"10.1089/jir.2025.0022","url":null,"abstract":"<p><p>Lumbar disc herniation is primarily caused by intervertebral disc degeneration (IVDD). Nucleus pulposus (NP) cell dysfunction leads to pro-inflammatory cytokines secretion increase, causing extracellular matrix (ECM) degradation. ECM is essential for maintaining normal disc function. Glycoprotein (Transmembrane) Nmb (GPNMB) is strongly associated with inflammation, and its expression and effects in IVDD are unclear. We categorized 40 clinically collected IVDD samples using the magnetic resonance imaging (MRI)-based Pfirrmann grading system. GPNMB mRNA expression was notably suppressed in patients with severe IVDD compared with patients with mild IVDD. Increased GPNMB mRNA expression correlated with decreased Interleukin-6 (IL-6) expression and increased collagen type II (COL2A1) expression levels. We utilized lentivirus to overexpress GPNMB in IL-1β-induced NP cells to explore its function in IVDD. GPNMB overexpression inhibited pro-inflammatory cytokines Tumor necrosis factor-alpha and IL-6 secretion in IL-1β-induced NP cells, while anti-inflammatory cytokine IL-10 content was increased. In addition, GPNMB overexpression inhibited NP ECM degradation by decreasing ECM-degrading enzymes matrix metalloproteinases-3/13 and a disintegrin and metalloproteinase with thrombospondin motifs-4/5 <i>in vitro</i>. Mechanism studies revealed that GPNMB was bound to CD44, a receptor expressed on the NP cell surface. GPNMB overexpression inhibited nuclear factor-κB (NF-κB) p65 phosphorylation and nuclear translocation <i>in vitro</i>, possibly through CD44. In conclusion, GPNMB suppressed the expression of pro-inflammatory cytokines and ECM degradation in NP cells by inhibiting activation of NF-κB.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"238-246"},"PeriodicalIF":1.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015098","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
Lienal Polypeptide Decreases Immune Thrombocytopenia in a Mouse Model by Upregulating Cytokine Production and Increasing the Levels of CD4+, CD8+, and T Regulatory Cells. 连纳尔多肽通过上调细胞因子的产生并提高 CD4+、CD8+ 和 T 调节细胞的水平,减少小鼠模型中的免疫性血小板减少症。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-01 Epub Date: 2025-03-21 DOI: 10.1089/jir.2024.0256
Zhaorong Yue, Fei Xie, Ruyue Wang, Xin Wang, Hongyu Li
{"title":"Lienal Polypeptide Decreases Immune Thrombocytopenia in a Mouse Model by Upregulating Cytokine Production and Increasing the Levels of CD4<sup>+</sup>, CD8<sup>+</sup>, and T Regulatory Cells.","authors":"Zhaorong Yue, Fei Xie, Ruyue Wang, Xin Wang, Hongyu Li","doi":"10.1089/jir.2024.0256","DOIUrl":"10.1089/jir.2024.0256","url":null,"abstract":"<p><p>Primary immune thrombocytopenia (ITP) is a condition marked by immune-mediated inadequate platelet production or excessive destruction. This study investigates the effects of Lienal polypeptide injection (LP) on T lymphocyte subgroups in the spleen and thymus, megakaryocyte counts in the bone marrow, and cytokine levels related to megakaryocyte development in mice with antibody-induced ITP, aiming to elucidate potential therapeutic mechanisms. We first assessed the effects of LP on Meg-01 megakaryocytic cells regarding proliferation, apoptosis, and differentiation using Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assays, Western blot analysis, and flow cytometry for apoptosis and CD41 expression as a differentiation marker. Following this, LP was administered intraperitoneally at 60 mg/(kg·d) for 11 days to ITP mice. We quantified peripheral blood platelets and bone marrow megakaryocytes, measured spleen and thymus indices, and assessed serum levels of stem cell factor (SCF), interleukin-3 (IL-3), interleukin-6 (IL-6), and platelet factor-4 (PF-4) via enzyme-linked immunosorbent assay (ELISA). Flow cytometry quantified T-helper cells (CD4<sup>+</sup>), cytotoxic T cells (CD8<sup>+</sup>), and regulatory T cells (Tregs). LP significantly induced apoptosis in Meg-01 cells while not markedly affecting differentiation. In ITP mice, LP effectively prevented platelet decline without affecting megakaryocyte counts or maturity. Increased SCF, IL-3, and IL-6 levels, alongside decreased PF-4 levels, correlated with enhanced platelet production. Moreover, CD4<sup>+</sup>/CD8<sup>+</sup> ratios and Treg populations increased, contributing to reduced platelet destruction. In conclusion, LP exerts a protective effect in ITP by modulating SCF, IL-3, IL-6, and PF-4 levels and restoring the balance of T cell subtypes, elucidating its therapeutic potential.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"214-226"},"PeriodicalIF":1.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670119","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
KLF13 Attenuates Lipopolysaccharide-Induced Alveolar Epithelial Cell Damage by Regulating Mitochondrial Quality Control via Binding PGC-1α. KLF13通过结合PGC-1α调节线粒体质量控制,减轻脂多糖诱导的肺泡上皮细胞损伤。
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-01 Epub Date: 2024-07-01 DOI: 10.1089/jir.2023.0234
Qiong Xi, Lin Liu, Qin Zhao, Shan Zhu
{"title":"KLF13 Attenuates Lipopolysaccharide-Induced Alveolar Epithelial Cell Damage by Regulating Mitochondrial Quality Control via Binding PGC-1α.","authors":"Qiong Xi, Lin Liu, Qin Zhao, Shan Zhu","doi":"10.1089/jir.2023.0234","DOIUrl":"10.1089/jir.2023.0234","url":null,"abstract":"<p><p>Sepsis is a clinically life-threatening syndrome, and acute lung injury is the earliest and most serious complication. We aimed to assess the role of kruppel-like factor 13 (KLF13) in lipopolysaccharide (LPS)-induced human alveolar type II epithelial cell damage and to reveal the possible mechanism related to peroxisome proliferator-activated receptor-γ co-activator 1-α (PGC-1α). In LPS-treated A549 cells with or without KLF13 overexpression or PGC-1α knockdown, cell viability was measured by a cell counting kit-8 assay. Enzyme-linked immunosorbent assay kits detected the levels of inflammatory factors, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining measured cell apoptosis. Besides, mitochondrial reactive oxygen species (MitoSOX) and mitochondrial membrane potential were detected using MitoSOX red- and JC-1 staining. Expression of proteins related to mitochondrial quality control (MQC) was evaluated by western blot. Co-immunoprecipitation (Co-IP) assay was used to analyze the interaction between KLF13 and PGC-1α. Results indicated that KLF13 was highly expressed in LPS-treated A549 cells. KLF13 upregulation elevated the viability and reduced the levels of inflammatory factors in A549 cells exposed to LPS. Moreover, KLF13 gain-of-function inhibited LPS-induced apoptosis of A549 cells, accompanied by upregulated BCL2 expression and downregulated Bax and cleaved caspase3 expression. Furthermore, MQC was improved by KLF13 overexpression, as evidenced by decreased MitoSOX, JC-1 monomers and increased JC-1 aggregates, coupled with the changes of proteins related to MQC. In addition, Co-IP assay confirmed the interaction between KLF13 and PGC-1α. PGC-1α deficiency restored the impacts of KLF13 upregulation on the inflammation, apoptosis, and MQC in LPS-treated A549 cells. In conclusion, KLF13 attenuated LPS-induced alveolar epithelial cell inflammation and apoptosis by regulating MQC via binding PGC-1α.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"227-237"},"PeriodicalIF":1.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141476790","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 Expression of Th17-Related Cytokines in Patients of Chronic Kidney Disease with and Without Systemic Lupus Erythematosus. 慢性肾病伴与不伴系统性红斑狼疮患者th17相关细胞因子的差异表达
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-06-01 Epub Date: 2025-05-23 DOI: 10.1089/jir.2024.0265
Farhad Seif, Karrar Hadi Kadhim, Milad Ahmadaghdami, Paria Bayati, Somayeh Sadani, Homa Davoodi, Ali Memarian, Somayeh Ghorbani, Yasser Bagheri
{"title":"Differential Expression of Th17-Related Cytokines in Patients of Chronic Kidney Disease with and Without Systemic Lupus Erythematosus.","authors":"Farhad Seif, Karrar Hadi Kadhim, Milad Ahmadaghdami, Paria Bayati, Somayeh Sadani, Homa Davoodi, Ali Memarian, Somayeh Ghorbani, Yasser Bagheri","doi":"10.1089/jir.2024.0265","DOIUrl":"10.1089/jir.2024.0265","url":null,"abstract":"<p><p>Dysregulation of immune cells and cytokines, particularly T helper 17 (Th17) cells and their associated cytokines, is implicated in the pathogenesis of both systemic lupus erythematosus (SLE) and chronic kidney disease (CKD). This study aimed to investigate the serum levels of Th17-related cytokines (interleukin [IL]-17A, IL-21, IL-22, and IL-23) in CKD patients with and without SLE and explore their potential role in disease progression. A total of 118 participants were included, comprising 78 patients with CKD (stages 3-5) and 40 healthy controls. Cytokine levels were measured using enzyme-linked immunosorbent assay kits. Patients with CKD exhibited significantly lower IL-21 levels and higher IL-22 and IL-17A levels compared with controls, while patients with end-stage renal disease showed elevated IL-21 and IL-23 levels. Among SLE-negative nephrotic patients, IL-23 and IL-17A were significantly upregulated, whereas SLE-positive nephrotic patients had increased IL-22 and IL-17A levels. In addition, IL-21 and IL-17A were significantly correlated in patients with CKD, suggesting a potential immunoregulatory interplay. These findings indicate that Th17-related cytokines are differentially expressed depending on CKD stage and SLE status, potentially influencing immune responses, inflammation, and kidney fibrosis. Understanding alterations of these cytokines may aid in identifying targeted therapeutic, particularly for patients with CKD at risk of SLE-related complications.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"205-213"},"PeriodicalIF":1.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127873","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
Polymorphisms in IL-10- and IL-22-Binding Protein Genes as Genetic Predictors of the Direct-Acting Antivirals Treatment Response in Patients with Chronic Hepatitis C Virus. IL-10和il -22结合蛋白基因多态性作为慢性丙型肝炎病毒患者直接抗病毒治疗反应的遗传预测因子
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-05-01 Epub Date: 2025-03-19 DOI: 10.1089/jir.2025.0005
Komal Saleem, Hira Raheem Akbar, Zuzana Macek Jilkova, Ahmad Ali Shahid, Muhammad Idrees, Samia Afzal
{"title":"Polymorphisms in IL-10- and IL-22-Binding Protein Genes as Genetic Predictors of the Direct-Acting Antivirals Treatment Response in Patients with Chronic Hepatitis C Virus.","authors":"Komal Saleem, Hira Raheem Akbar, Zuzana Macek Jilkova, Ahmad Ali Shahid, Muhammad Idrees, Samia Afzal","doi":"10.1089/jir.2025.0005","DOIUrl":"10.1089/jir.2025.0005","url":null,"abstract":"<p><p>Cytokines are crucial in controlling inflammation during viral infection, particularly infection with the hepatitis C virus (HCV). Cytokine genetic polymorphisms can change how the immune system responds to this infection. We investigated how the HCV infection treatment was affected by single nucleotide polymorphisms in these genes. The goal of this study was to examine any connections between the cytokine gene polymorphisms for interleukins (IL)-22-binding protein rs6570136, as well as IL-10 rs1800872 and rs1878672 in the Pakistani population and responsiveness to direct-acting antivirals (DAAs) treatment. This study evaluated 155 participants, which included 55 patients who achieved sustained virologic response (SVR), 40 relapse patients, and 60 healthy controls, to assess and compare the clinical parameters. The SVR and relapse groups were compared for their allelic and genotypic frequencies. We discovered that the SVR and the relapse groups had significantly different genotype frequencies for IL-10 rs1800872 and IL-22BP rs6570136 in the Pakistani population. The G/G genotype in rs6570136 and A/A genotype in rs1800872 were significantly associated with relapse following DAA therapy, with <i>P</i> values 0.002 and 0.0004, respectively. In contrast, rs1878672 showed no significant correlation with HCV relapse, <i>P</i> = 0.63.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"196-204"},"PeriodicalIF":1.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663655","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
IFN-γ Approaches in Tumor Suppression, Its Challenges, and Future Directions: A Review of Recent Advances. IFN-γ在肿瘤抑制中的应用、挑战和未来方向:近期进展综述
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-05-01 Epub Date: 2025-02-06 DOI: 10.1089/jir.2024.0259
Mohammad Reza Ataherian, Nasim Hafezi, Elaheh Ferdosi-Shahandashti, Fatemeh Sarina Abdinia
{"title":"IFN-γ Approaches in Tumor Suppression, Its Challenges, and Future Directions: A Review of Recent Advances.","authors":"Mohammad Reza Ataherian, Nasim Hafezi, Elaheh Ferdosi-Shahandashti, Fatemeh Sarina Abdinia","doi":"10.1089/jir.2024.0259","DOIUrl":"10.1089/jir.2024.0259","url":null,"abstract":"<p><p>IFN-γ is recognized as an immunoregulatory cytokine due to its dual role in both accelerating and dampening immunological responses. Accordingly, in the context of tumor immunotherapy, the therapeutic outcome of IFN-γ is contingent upon factors such as dosage and the expression status of downstream signaling molecules. Furthermore, the coadministration of IFN-γ with various immunestimulatory agents, including anticheckpoint inhibitors, chemotherapeutic agents, and herbal-based medicines, may potentially overcome the IFN-γ-related challenges and enhance the response rate. We decipher the mechanisms of tumor cell eradication facilitated by IFN-γ, the last achievements in IFN-γ-mediated tumor immunotherapy across various cancers, and the strategies to address the failure of IFN-γ-based tumor immunotherapy. Unraveling the molecular mechanisms that lead to failure in IFN-γ-based antitumor actions could assist in pinpointing therapeutic agents that target the immune-modulatory features of IFN-γ, thereby increasing the antitumor response rate.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"164-173"},"PeriodicalIF":1.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364819","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
Function of Interferon Lambda Receptor 1 Variants in Stem Cell-Derived Hepatocytes with Abrogated Endogenous IFNLR1. 干扰素受体1变异在内源性IFNLR1缺失的干细胞源性肝细胞中的功能
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-05-01 Epub Date: 2025-02-10 DOI: 10.1089/jir.2024.0262
Laura A Novotny, Christiana S Kappler, Eric G Meissner
{"title":"Function of Interferon Lambda Receptor 1 Variants in Stem Cell-Derived Hepatocytes with Abrogated Endogenous <i>IFNLR1</i>.","authors":"Laura A Novotny, Christiana S Kappler, Eric G Meissner","doi":"10.1089/jir.2024.0262","DOIUrl":"10.1089/jir.2024.0262","url":null,"abstract":"<p><p>Distinct transcriptional isoforms of the interferon lambda receptor 1 (<i>IFNLR1</i>) are expressed in hepatocytes, but whether corresponding full-length and truncated IFNLR1 protein variants have discrete function is unclear. We quantitated <i>IFNLR1</i> isoforms in liver and blood from individuals with chronic hepatitis C virus (HCV) infection before and after antiviral treatment, hypothesizing their relative expression may differentially change during resolution of virus-induced inflammation. We also expressed FLAG-tagged IFNLR1 variants in stem cell-derived hepatocytes (iHeps) with abrogated endogenous <i>IFNLR1</i> to evaluate their function. <i>IFNLR1</i> isoforms decreased in liver and blood during treatment of HCV, but no distinct pattern of decline was observed for any individual isoform. Expression of full-length IFNLR1 enabled lambda interferon (IFNL)-induced expression of antiviral and proinflammatory genes and augmented inhibition of hepatitis B virus (HBV) replication relative to wild-type (WT) iHeps. A noncanonical IFNLR1 variant missing part of the JAK1 binding domain enabled IFNLs to induce antiviral genes but could not support induction of proinflammatory genes or augmented HBV inhibition beyond that observed in WT iHeps with intact endogenous <i>IFNLR1</i>. A secreted IFNLR1 variant had no identified function in iHeps lacking endogenous <i>IFNLR1</i>. Although relative expression of individual <i>IFNLR1</i> isoforms did not distinctly change during HCV treatment, functional studies in iHeps suggest IFNLR1 variants could function to titrate antiviral versus proinflammatory responses in hepatocytes in the context of viral hepatitis.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"174-183"},"PeriodicalIF":1.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391051","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
Correlations of Levels of Peripheral Blood Inflammatory Cytokines and Serum Lipoprotein-Associated Phospholipase-A2 with Acute Ischemic Stroke and Their Early Prognostic Value. 外周血炎症因子和血清脂蛋白相关磷脂酶a2水平与急性缺血性卒中的相关性及其早期预后价值
IF 1.9 4区 医学
Journal of Interferon and Cytokine Research Pub Date : 2025-05-01 Epub Date: 2025-04-11 DOI: 10.1089/jir.2024.0176
Chengqing Zhong, Qin Han, Li Yang, Yidan Liu, Yun Zhang, Shucheng Li, Junmei Lv, Jianping Jiang
{"title":"Correlations of Levels of Peripheral Blood Inflammatory Cytokines and Serum Lipoprotein-Associated Phospholipase-A<sub>2</sub> with Acute Ischemic Stroke and Their Early Prognostic Value.","authors":"Chengqing Zhong, Qin Han, Li Yang, Yidan Liu, Yun Zhang, Shucheng Li, Junmei Lv, Jianping Jiang","doi":"10.1089/jir.2024.0176","DOIUrl":"https://doi.org/10.1089/jir.2024.0176","url":null,"abstract":"<p><p>Respecting the significant role of inflammation in acute ischemic stroke (AIS) development, we explored the correlations of inflammatory cytokines and lipoprotein-associated phospholipase-A<sub>2</sub> (Lp-PLA<sub>2</sub>) with AIS and their early prognostic value. The retrospectively enrolled subjects [Study (AIS patients) and Control (healthy volunteers) groups] were determined for serum index levels. Neurological impairment and early prognosis of AIS patients were assessed. The relationship of National Institutes of Health Stroke Scale (NIHSS) and the indexes and the risk factors and predictive value of peripheral blood inflammatory cytokines combined with Lp-PLA<sub>2</sub> for poor early prognosis were analyzed. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), and Lp-PLA<sub>2</sub> levels rose in AIS patients, while IL-10 dropped. The NIHSS score positively correlated with IL-1β, TNF-α, and Lp-PLA<sub>2</sub> and negatively correlated with IL-10. As AIS aggravated, IL-1β, IL-6, TNF-α, and Lp-PLA<sub>2</sub> rose dependently, but IL-10 dropped. Patients in the poor early prognosis group had higher diabetes proportions, NIHSS scores and serum IL-1β, IL-6, TNF-α, and Lp-PLA<sub>2</sub> levels at admission, as well as lower IL-10 levels than those in the good early prognosis group. IL-6, IL-1β, TNF-α, and Lp-PLA<sub>2</sub> were risk factors, but IL-10 was a protective factor against poor early prognosis in AIS patients, with their combined detection showing high predictive value. Collectively, highly expressed IL-6, TNF-α, IL-1β, and Lp-PLA<sub>2</sub> and lowly expressed IL-10 in patients with AIS closely related to AIS development and early prognosis, and their combination could increase the predictive value of NIHSS for AIS poor early prognosis.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"45 5","pages":"184-195"},"PeriodicalIF":1.9,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011160","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}
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