Journal of Interferon and Cytokine Research最新文献_第2页

Long-Term IFN-β Therapy Enhances and Prolongs IFN Responses in Multiple Sclerosis. 长期IFN-β治疗可增强和延长多发性硬化症患者的IFN应答

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-09-01 Epub Date: 2026-06-10 DOI: 10.1177/10799907261458149

Jeffrey Ke, Conrad Moss, Xuan Feng, Anthony T Reder

{"title":"Long-Term IFN-β Therapy Enhances and Prolongs IFN Responses in Multiple Sclerosis.","authors":"Jeffrey Ke, Conrad Moss, Xuan Feng, Anthony T Reder","doi":"10.1177/10799907261458149","DOIUrl":"10.1177/10799907261458149","url":null,"abstract":"Multiple sclerosis (MS) is a central nervous system (CNS) disease with autoimmune inflammation, demyelination, and neurodegeneration. Untreated MS patients exhibit subnormal activation of the p-Ser-STAT1 transcription factor in peripheral blood mononuclear cells (PBMCs), causing weak interferon (IFN) signaling and low expression of some IFN-stimulated genes (ISGs). IFN-β therapy reduces MS exacerbations, delays progression, and largely corrects abnormal gene expression in PBMC. We hypothesize that long-term IFN-β therapy improves weak IFN responses and regulates MS immunity through a priming effect and induction of a more IFN-responsive state. The duration and strength of IFN-stimulated gene expression during prolonged therapy and their diminution after discontinuation are unknown. Using paired comparisons of 1- and 7-month PEG-IFN-β-treated MS patients' PBMCs, we investigated short- and long-term responses to in vivo IFN-β. Prolonged therapy created a new IFN setpoint with elevated expression of antiviral, immune, anti-inflammatory, and neuroprotective ISG while decreasing inflammatory and metabolic gene expression, often doubling their half-life. Genes that inhibit IFN-β signaling also showed long-term induction, reflecting a regulatory state that prevents overactivation. Strong IFN responses during long-term therapy of MS reflect a shift from subnormal IFN signaling and dysregulated immune control to a more responsive state that persists for months.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"253-263"},"PeriodicalIF":1.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211226","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

Fish Cytokines at the Crossroads: From Ancient Immune Signals to Modern One Health and Aquaculture Vaccines. 十字路口的鱼类细胞因子：从古代免疫信号到现代健康和水产养殖疫苗。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-08-22 DOI: 10.1177/10799907261481824

Amiya K Sahoo, Bimal P Mohanty, Sam Martin, Ram Savan, Subhendu K Otta

引用次数: 0

Letter: Type I Interferon Treatment and Risk of Granuloma Annulare and Lichen Planus: A Global Cohort Study. I型干扰素治疗和肉芽肿、环形和扁平苔藓的风险：一项全球队列研究。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-08-11 DOI: 10.1177/10799907261475008

Brandon Block, Jaanvi Mehta, Alice Tang, Gabriella Soto-Canetti, Riley Spingler, Benjamin Ungar, Jordan Talia

引用次数: 0

Human Macrophages Secrete Both Interferon α and Interferon β Proteins During Infection with Mycobacterium tuberculosis. 结核分枝杆菌感染时人巨噬细胞分泌干扰素α和干扰素β蛋白

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-08-01 Epub Date: 2026-04-27 DOI: 10.1177/10799907261446997

Gina Leisching, Donal Cox, Vincent Bondet, Anjali S Yennemadi, Seán Donohue, Darragh Duffy, Joseph Keane

引用次数: 0

IL-6-JAK2-STAT3 Signaling Pathway and the Pathogenesis of Chronic Tonsillitis. IL-6-JAK2-STAT3信号通路与慢性扁桃体炎的发病机制

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-08-01 Epub Date: 2026-04-17 DOI: 10.1177/10799907261442845

Siyu Li, Xiuguo Li, Jing Lu, Haojun Yang, Haochen Yang, Hui Zhang

{"title":"IL-6-JAK2-STAT3 Signaling Pathway and the Pathogenesis of Chronic Tonsillitis.","authors":"Siyu Li, Xiuguo Li, Jing Lu, Haojun Yang, Haochen Yang, Hui Zhang","doi":"10.1177/10799907261442845","DOIUrl":"https://doi.org/10.1177/10799907261442845","url":null,"abstract":"Tonsils are among the largest lymphoid tissues within the Waldeyer's ring. They generate lymphocytes that facilitate immune responses and play essential protective roles in host defense. When tonsillar crypts are exposed to specific bacterial or viral infections, persistent allergic stimuli, or immune dysregulation, an inflammatory cascade may be triggered, increasing the risk of chronic tonsillitis (CT). CT is a common otolaryngological condition characterized by recurrent episodes of inflammation or a single prolonged episode (>3 months), and it typically presents with repeated acute pharyngalgia, fever, cough, tonsillar swelling and suppuration, itching of the throat, and dryness. The Janus kinase (JAK) and signal transducer and activator of transcription (STAT) signaling pathways, first described by Darnell and Stark in the early 1990s, are highly conserved transmembrane signal transduction mechanisms. They act as central hubs for cytokine-mediated signaling and enable communication between cells and their external environment. Many cytokines exert their biological effects through this pathway. This review elaborates on the activation mechanism of the IL-6-JAK2-STAT3 signaling pathway, summarizes the major drug classes targeting this pathway, highlights the clinical significance in CT, and addresses the current knowledge gaps in the field.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"46 8","pages":"217-225"},"PeriodicalIF":1.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352344","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

Biochemical Signature in Deciphering the Metastasis-Associated Lung Adenocarcinoma Transcript 1/microRNA-145 Axis and Its Molecular Correlation with Nuclear Factor Kappa Beta/Transforming Growth Factor-Beta and Apoptotic Proteins Expression in Colorectal Cancer. 结直肠癌转移相关肺腺癌转录物1/microRNA-145轴的生化特征及其与核因子Kappa β /转化生长因子β和凋亡蛋白表达的分子相关性

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-08-01 Epub Date: 2026-04-21 DOI: 10.1177/10799907261444320

Asmaa Atef, Basant Mahmoud, Basma Sayed, Saeed S Mohamed, Nabil A Hasona

{"title":"Biochemical Signature in Deciphering the Metastasis-Associated Lung Adenocarcinoma Transcript 1/microRNA-145 Axis and Its Molecular Correlation with Nuclear Factor Kappa Beta/Transforming Growth Factor-Beta and Apoptotic Proteins Expression in Colorectal Cancer.","authors":"Asmaa Atef, Basant Mahmoud, Basma Sayed, Saeed S Mohamed, Nabil A Hasona","doi":"10.1177/10799907261444320","DOIUrl":"https://doi.org/10.1177/10799907261444320","url":null,"abstract":"Colorectal cancer (CRC) is a multifactorial malignancy characterized by complex interactions between oncogenic signaling networks and noncoding RNA regulators. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and microRNA-145 (miR-145) have been recognized as reliable diagnostic biomarkers for cancer. This study evaluates their biochemical interaction, along with their connection to the nuclear factor kappa beta (NF-κβ)/transforming growth factor-beta (TGF-β) signaling pathway and crosstalk with vascular endothelial growth factor (VEGF) and apoptotic markers in CRC. Serum samples were collected from 120 participants, including 90 CRC patients exhibiting a range of tumor grades and anatomical sites, in addition to 30 healthy controls. The expression levels of NF-κB and apoptotic markers were quantified using standardized immunoassays, while the relative expression levels of MALAT1, miR-145, TGF-β, and VEGF were assessed using real-time polymerase chain reaction. Integrative analysis of CRC samples reveals that MALAT1 overexpression correlates with downregulation of miR-145, increased NF-κβ, elevated levels of TGF-β and VEGF, and alterations in apoptotic proteins. Moreover, receiver operating characteristic analysis revealed excellent discriminative power for MALAT1 and miR-145 in distinguishing patients with CRC from healthy controls. These findings suggest that the MALAT1/miR-145 axis serves as a central biochemical node linking inflammatory and fibrotic signaling pathways and apoptotic protein expression in colorectal carcinogenesis. Targeting this regulatory network may offer novel therapeutic opportunities to suppress NF-κβ/TGF-β-driven tumor progression and improve CRC outcomes.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"46 8","pages":"236-243"},"PeriodicalIF":1.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352229","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

A Stable Reporter Cell Line to Study Respiratory Syncytial Virus NS2-Mediated Inhibition of IFNB Promoter Activation. 研究呼吸道合胞病毒ns2介导的IFNB启动子激活抑制的稳定报告细胞系

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-08-01 Epub Date: 2026-04-24 DOI: 10.1177/10799907261443406

Marta Acchioni, Lydie Martin, Elina Gerber-Tichet, Chiara Acchioni, Dacquin M Kasumba, Marco Sgarbanti, Nathalie Grandvaux

{"title":"A Stable Reporter Cell Line to Study Respiratory Syncytial Virus NS2-Mediated Inhibition of IFNB Promoter Activation.","authors":"Marta Acchioni, Lydie Martin, Elina Gerber-Tichet, Chiara Acchioni, Dacquin M Kasumba, Marco Sgarbanti, Nathalie Grandvaux","doi":"10.1177/10799907261443406","DOIUrl":"https://doi.org/10.1177/10799907261443406","url":null,"abstract":"Human respiratory syncytial virus (RSV) is a major cause of severe lower respiratory tract disease in infants, older adults, and immunocompromised individuals. A hallmark of RSV pathogenesis is early innate immune evasion by the nonstructural proteins NS1 and NS2. NS2 is a multifunctional interferon (IFN) antagonist that dampens both IFNβ induction and type I IFN responsiveness by targeting multiple nodes of the RIG-I/IFN signaling axis. Because NS2-mediated inhibition is often partial and context dependent, quantifying its effects in conventional cell-based assays is challenging. Here, we report the generation and characterization of a stable, virus-free reporter system in human A549 cells to measure NS2-dependent inhibition of dsRNA-driven IFNB induction. The platform combines stable NS2 expression with genomic integration of a dual cassette encoding a non-targeting short hairpin RNA that constitutively activates IRF-3 to induce a luciferase reporter under IFNB promoter control. This configuration yields a sensitive, reproducible luminescence readout of IFNB promoter activity in controlled, infection-free conditions, enabling robust quantification of NS2 antagonism with reduced variability. The scalable luminescence-based format supports early-stage discovery and prioritization of inhibitors that counteract NS2 function, and the modular design is adaptable to other viral antagonists, pathways, and cell types for standardized comparative studies.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"46 8","pages":"226-235"},"PeriodicalIF":1.9,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352213","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

Syndecan-4 Acts as a Negative Regulator of the CXCL10-CXCR3 Axis to Attenuate Endothelial Inflammation in Sepsis-Associated ALI. Syndecan-4作为CXCL10-CXCR3轴的负调节因子，减轻脓毒症相关ALI中的内皮炎症

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-07-01 Epub Date: 2026-03-18 DOI: 10.1177/10799907261432941

Jiayue Qin, Liuyi Song, Hongmei Zhou, Qian Hao, Zhipeng Zhu

{"title":"Syndecan-4 Acts as a Negative Regulator of the CXCL10-CXCR3 Axis to Attenuate Endothelial Inflammation in Sepsis-Associated ALI.","authors":"Jiayue Qin, Liuyi Song, Hongmei Zhou, Qian Hao, Zhipeng Zhu","doi":"10.1177/10799907261432941","DOIUrl":"10.1177/10799907261432941","url":null,"abstract":"Endothelial cell injury and dysfunction are among the main causes of sepsis-associated acute lung injury (ALI); however, the underlying mechanism through which endothelial activation coordinates the adhesion and migration of immune cells remains elusive. Bioinformatics analysis revealed that the hub gene (C-X-C motif chemokine ligand 10 [CXCL10]) was predicted to be involved in both endothelial activation and syndecan 4 (SDC4) binding capacity. In both the LPS- and tumor necrosis factor-alpha -induced sepsis models, the expression level and biological function of the hub gene were confirmed by means of quantitative PCR and immunofluorescence staining. With the knockdown of SDC4 and the HS mutation technique, loss-of-function experiments and downstream pathway experiments following modulation of the hub gene's expression were conducted to elucidate the underlying molecular mechanism. Through the overlap of GSE5883 and the glycosaminoglycan-binding DB, seven genes were discovered to be involved in the biological processes of SDC binding and cytokine-cytokine receptor interactions, including those involving CXCL10. Compared with that in the normal state, the expression of CXCL10 in the ALI state markedly increased during the acute phase of inflammation, and the SDC4 mRNA level greatly increased. Mechanistically, CXCL10 induces a proinflammatory response with the help of SDC4 as a coreceptor, leading to CXCR3/NF-κB pathway activation and VCAM1 overexpression. This proinflammatory phenotype was further enhanced by knockdown of SDC4. By mutating the heparan sulfate (HS) chain of SDC4, the severity of inflammation was exacerbated, and the recruitment of immune cells was also enhanced. In summary, endothelial-derived SDC4 acts as a negative mediator to ameliorate ALI through modulation of the CXCR3 pathway with the help of HS chains.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"46 7","pages":"189-203"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148143577","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

Cytokines 2025: 13th Annual Meeting of the International Cytokine & Interferon Society. 细胞因子2025：第十三届国际细胞因子与干扰素学会年会。

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-07-01 Epub Date: 2026-03-23 DOI: 10.1177/10799907261435098

Yang Zhao

引用次数: 0

Serum Level of Interleukin-11 Is Associated with the Severity of Hepatic Fibrosis in Adults with Metabolic Dysfunction-Associated Steatotic Liver Disease. 成人代谢功能障碍相关脂肪变性肝病患者血清白介素-11水平与肝纤维化严重程度相关

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-07-01 Epub Date: 2026-03-14 DOI: 10.1177/10799907261432064

Yingying Xue, Hsiuying Fu, Hongyan Wu, Ziwei Wang, Lixuan Shen, Jingyu Zhu, Ziwei Zhu, Yue Cao, Yingying Xiang, Xizhong Yu, Wenbin Shang, Ruonan Zhou

{"title":"Serum Level of Interleukin-11 Is Associated with the Severity of Hepatic Fibrosis in Adults with Metabolic Dysfunction-Associated Steatotic Liver Disease.","authors":"Yingying Xue, Hsiuying Fu, Hongyan Wu, Ziwei Wang, Lixuan Shen, Jingyu Zhu, Ziwei Zhu, Yue Cao, Yingying Xiang, Xizhong Yu, Wenbin Shang, Ruonan Zhou","doi":"10.1177/10799907261432064","DOIUrl":"10.1177/10799907261432064","url":null,"abstract":"The rising prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) poses a critical public health challenge, yet current diagnostic and therapeutic approaches remain limited. Interleukin-11 (IL-11) is a pro-inflammatory cytokine expressed by various cell types in the liver. Although preclinical studies have revealed the pro-fibrotic role of IL-11 in mouse models, the clinical relevance between serum IL-11 and human MASLD remains unclear. This cross-sectional study enrolled 375 patients with MASLD from the outpatient department to explore the relationship between the serum level of IL-11 and the indicators of MASLD in adults with MASLD. Demographic characteristics, clinical parameters, laboratory biomarkers, FibroScan results, and serum IL-11 concentrations were prospectively collected in patients with MASLD for further analysis. As a result, the liver stiffness measurement values were significantly elevated in patients with detectable serum IL-11 compared to the IL-11-undetectable group, while the controlled attenuation parameter values between the groups showed no significant difference. It was also illustrated by logistic regression models that serum IL-11 is an independent predictor of advanced hepatic fibrosis. Our findings provide the references for further developing IL-11 as a potential evaluative biomarker and therapeutic target of MASLD.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"46 7","pages":"204-211"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148143626","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