Journal of Interferon and Cytokine Research最新文献_第3页

Suppression of miR-155 Attenuates Lung Cytokine Storm Induced by SARS-CoV-2 Infection. 抑制miR-155可减弱SARS-CoV-2感染诱导的肺细胞因子风暴

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-04-01 Epub Date: 2025-02-14 DOI: 10.1089/jir.2024.0253

Dharmendra Kumar Soni, Juan Cabrera-Luque, Swagata Kar, Anwar Ahmed, Chaitali Sen, Joseph Devaney, Roopa Biswas

{"title":"Suppression of miR-155 Attenuates Lung Cytokine Storm Induced by SARS-CoV-2 Infection.","authors":"Dharmendra Kumar Soni, Juan Cabrera-Luque, Swagata Kar, Anwar Ahmed, Chaitali Sen, Joseph Devaney, Roopa Biswas","doi":"10.1089/jir.2024.0253","DOIUrl":"10.1089/jir.2024.0253","url":null,"abstract":"Coronavirus disease 2019 (COVID-19) is a deadly human viral disease with a high rate of infection, morbidity, and mortality. Although vaccines and antiviral treatments are available, hospitalizations remain steady, and concerns about long-term consequences persist. Therefore, there is a great urgency to develop novel therapies. Here, we analyzed the role of miR-155, one of the most powerful drivers of host antiviral responses including immune and inflammatory responses, in the pathogenicity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Endogenous microRNAs (miRNAs, miRs) are key molecules in preventing viral entry and replication while building an antiviral cellular defense. Our study reveals that miR-155 expression is elevated in patients with COVID-19. Using a mouse model transgenic for human angiotensin-converting enzyme receptor 2, we evaluated the potential of anti-miR-155 therapy. Treating SARS-CoV-2-infected mice with anti-miR-155 significantly reduced miR-155 expression, improved survival, and slightly increased body weight. Notably, these mice showed altered expression of cytokines in the lungs. These findings suggest anti-miR-155 could be a promising therapy to mitigate the cytokine storm and long-lasting symptoms induced by SARS-CoV-2 infection, improving public health outcomes and enhancing global pandemic preparedness.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"150-161"},"PeriodicalIF":1.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414570","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

Cytokine-Based Validation of the Inflammation-Based Risk Score in Patients with ST-Segment Elevation Myocardial Infarction. 基于细胞因子的ST段抬高型心肌梗死患者炎症风险评分验证。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-03-01 Epub Date: 2024-10-02 DOI: 10.1089/jir.2024.0163

Brianda Amezcua-Guerra, Luis M Amezcua-Castillo, Jazmín A Guerra-López, Kietseé Díaz-Domínguez, Héctor González-Pacheco, Luis M Amezcua-Guerra

{"title":"Cytokine-Based Validation of the Inflammation-Based Risk Score in Patients with ST-Segment Elevation Myocardial Infarction.","authors":"Brianda Amezcua-Guerra, Luis M Amezcua-Castillo, Jazmín A Guerra-López, Kietseé Díaz-Domínguez, Héctor González-Pacheco, Luis M Amezcua-Guerra","doi":"10.1089/jir.2024.0163","DOIUrl":"10.1089/jir.2024.0163","url":null,"abstract":"This study aimed to validate an inflammation-based risk score in patients with ST-segment elevation myocardial infarction (STEMI) by examining their cytokine profiles. Upon admission, patients were evaluated for systemic inflammation using a risk score that assigned points based on specific biomarkers: 1 point for leukocyte count ≥9.3 × 10³ cells/μL, 2 points for high-sensitivity C-reactive protein (hsCRP) ≥13.0 mg/L, and 3 points for serum albumin ≤3.6 g/dL. Patients were categorized into three groups: no inflammation (0 points, n = 13), mild inflammation (1-2 points, n = 35), and severe inflammation (3-6 points, n = 26). Serum levels of 16 key cytokines were measured. Patients with higher risk scores showed elevated interleukin (IL)-6 levels (19.6 vs. 8.5 vs. 6.8 pg/mL; P = 0.021) and decreased interferon-γ-induced protein-10 (IP-10) levels (73.4 vs. 68.8 vs. 112.2 pg/mL; P = 0.011). IL-6 was positively correlated with hsCRP (ρ 0.307) and negatively correlated with albumin (ρ -0.298), while IP-10 was negatively correlated with leukocyte count (ρ -0.301). No other cytokines showed significant association with the risk score. Higher inflammation scores were also associated with an increased incidence of major adverse cardiovascular events, particularly acute heart failure. This study underscores the association between the inflammation-based risk score and cytokine levels, specifically IL-6 and IP-10, in patients with STEMI.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"91-98"},"PeriodicalIF":1.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361658","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

Acknowledgment of Reviewers 2024. 审稿人致谢

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-03-01 DOI: 10.1089/jir.2024.19874.revack

引用次数: 0

Immunology Research in Latin America. 拉丁美洲的免疫学研究。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-03-01 Epub Date: 2025-02-10 DOI: 10.1089/jir.2025.0024

David L Woodland

引用次数: 0

Distinctive Macrophage Migration Inhibitory Factor Receptor Patterns and Soluble Biomarkers in Rheumatoid Arthritis: Unveiling Key Associations with Disease Activity. 类风湿关节炎中独特的巨噬细胞迁移抑制因子受体模式和可溶性生物标志物：揭示与疾病活动的关键关联

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-03-01 Epub Date: 2025-02-06 DOI: 10.1089/jir.2024.0184

Gabriela Athziri Sánchez-Zuno, Richard Bucala, Jorge Hernández-Bello, Claudia Azucena Palafox-Sánchez, Alexis Missael Vizcaíno-Quirarte, José Francisco Muñoz-Valle

{"title":"Distinctive Macrophage Migration Inhibitory Factor Receptor Patterns and Soluble Biomarkers in Rheumatoid Arthritis: Unveiling Key Associations with Disease Activity.","authors":"Gabriela Athziri Sánchez-Zuno, Richard Bucala, Jorge Hernández-Bello, Claudia Azucena Palafox-Sánchez, Alexis Missael Vizcaíno-Quirarte, José Francisco Muñoz-Valle","doi":"10.1089/jir.2024.0184","DOIUrl":"10.1089/jir.2024.0184","url":null,"abstract":"We previously reported the peripheral blood cell patterns of expression for the migration inhibitory factor (MIF) canonical (CD74/CD44) and noncanonical receptors (CXCR2, CXCR4, and CXCR7) in rheumatoid arthritis (RA) patients and correlated this with clinical biomarkers and disease activity. This study aimed to evaluate the expression of these receptors alongside the serum levels of CXCL12 and CXCL8 (ligands for CXCR2, CXCR4, and CXCR7), which potentially regulate the action of these receptors and the influence the downstream effects of MIF. Additionally, we evaluated soluble levels of MIF, as well as its soluble cognate receptor (sCD74), in the serum of RA patients and control subjects (CS). Our findings revealed distinctive membrane expression patterns of MIF receptors in active (moderate and high disease activity) and non-active (low activity and remission) RA patients. Furthermore, RA patients exhibited elevated serum sCD74 levels, which correlated with disease activity, and elevated CXCL12 levels, which correlated with rheumatoid factor titers. Regarding serum CXCL8 and MIF levels, we observed higher CXCL8 levels in RA patients compared to CS, while MIF levels did not significantly differ between groups or by disease activity. The circulating sCD74/MIF ratio was elevated in RA patients, particularly in cases of moderate disease activity. Our study also indicated that treatment protocols did not significantly impact circulating MIF levels or the expression of its receptors. This study extends previous findings by supporting a role for sCD74 in downregulating MIF action and in the potential value of the sCD74/MIF ratio as a disease biomarker in RA.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"99-106"},"PeriodicalIF":1.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12021775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cytokines 2024: 12th Annual Meeting of the International Cytokine and Interferon Society. 细胞因子2024：国际细胞因子和干扰素学会第12届年会。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-03-01 Epub Date: 2025-01-13 DOI: 10.1089/jir.2024.0241

Grayson Rodriguez

引用次数: 0

Unraveling the Multifaceted Roles of Atypical Chemokine Receptors in Breast Cancer. 揭示非典型趋化因子受体在乳腺癌中的多重作用

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-02-01 Epub Date: 2024-11-11 DOI: 10.1089/jir.2024.0186

Qinan Yin, Yisha Yang, Zhifeng Qu, Mouna Ouchari, Li Zeng, Siya Tang, Jiayu Zheng, Shunshun Zhang, Haodi Ma, Youyou Chen, Jiayi Wang, Linlin Shi, Xuewei Zheng

{"title":"Unraveling the Multifaceted Roles of Atypical Chemokine Receptors in Breast Cancer.","authors":"Qinan Yin, Yisha Yang, Zhifeng Qu, Mouna Ouchari, Li Zeng, Siya Tang, Jiayu Zheng, Shunshun Zhang, Haodi Ma, Youyou Chen, Jiayi Wang, Linlin Shi, Xuewei Zheng","doi":"10.1089/jir.2024.0186","DOIUrl":"10.1089/jir.2024.0186","url":null,"abstract":"Breast cancer (BC) remains one of the most prevalent and deadly malignancies among women globally. A deeper understanding of the molecular mechanisms driving BC progression and metastasis is essential for the development of effective therapeutic strategies. While traditional chemokine receptors are well known for their roles in immune cell migration and positioning, atypical chemokine receptors (ACKRs) have recently gained attention as key modulators in cancer-related processes. Unlike conventional receptors, ACKRs-comprising ACKR1, ACKR2, ACKR3, and ACKR4-primarily function by scavenging chemokines, regulating their availability, and modulating receptor signaling in a ligand-independent manner. This review aims to elucidate the roles of ACKRs in BC, focusing on their influence on the tumor microenvironment (TME), cancer cell proliferation, survival, metastasis, and angiogenesis. Additionally, we will explore the potential of ACKRs as diagnostic and prognostic markers and assess their viability as therapeutic targets. By synthesizing recent research findings and highlighting future research directions, this review seeks to provide a comprehensive understanding of the significance of ACKRs in BC and underscore the need for continued investigation into their therapeutic potential.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"43-52"},"PeriodicalIF":1.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622232","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

Sorting Out the SOCS Genes and Their Role in Macrophage Activation. SOCS基因的筛选及其在巨噬细胞活化中的作用

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-02-01 Epub Date: 2025-01-27 DOI: 10.1089/jir.2025.0016

Raymond P Donnelly

{"title":"Sorting Out the SOCS Genes and Their Role in Macrophage Activation.","authors":"Raymond P Donnelly","doi":"10.1089/jir.2025.0016","DOIUrl":"10.1089/jir.2025.0016","url":null,"abstract":"The suppressors of cytokine signaling (SOCS) genes were first described in a group of articles published in 1997. Since that time, much has been learned about the functional activities mediated by the corresponding proteins encoded by the SOCS genes. The SOCS gene family contains eight members: SOCS1 through SOCS7 and a highly related gene known as CISH (cytokine-inducible SH2-containing protein). Although much is known about the ability of the SOCS proteins to autoregulate responses to individual cytokines, much less is known about the ability of the SOCS proteins to cross-regulate cytokine signaling. The studies described in a new report by Bidgood et al. in this issue of JICR demonstrate that SOCS1 expression induced by one cytokine, interferon (IFN)-γ, can cross-regulate signaling induced by another cytokine, granulocyte macrophage colony-stimulating factor (GM-CSF), in murine bone marrow-derived macrophages. The authors show that the ability of SOCS1 to inhibit cytokine signaling is dose- and time-dependent. SOCS1 must reach a critical threshold level before it can exert a marked inhibitory effect on autocrine signaling through the IFN-γ receptor or paracrine signaling through the GM-CSF receptor.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"39-42"},"PeriodicalIF":1.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047016","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

Evaluation of Salivary Il-38 Levels in Periodontitis: A Cross-Sectional Study. 牙周炎患者唾液 Il-38 水平的评估：一项横断面研究

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-02-01 Epub Date: 2024-03-18 DOI: 10.1089/jir.2023.0233

Ayşe Toraman, Ebru Sağlam, Levent Savran, Serhat Köseoğlu

{"title":"Evaluation of Salivary Il-38 Levels in Periodontitis: A Cross-Sectional Study.","authors":"Ayşe Toraman, Ebru Sağlam, Levent Savran, Serhat Köseoğlu","doi":"10.1089/jir.2023.0233","DOIUrl":"10.1089/jir.2023.0233","url":null,"abstract":"The goal of the current study was to assess levels of salivary interleukin (IL)-38, IL-1β, and IL-10 in various periodontal clinical conditions. In total, 60 (20 healthy, 20 gingivitis, and 20 stage II-III, grade A-B periodontitis) subjects were included in the study. Demographic and clinical periodontal parameters were recorded. Samples were examined for IL-38, IL-1β, and IL-10 levels by means of enzyme-linked immunosorbent assay. Results demonstrated that the periodontitis group had significantly lower salivary IL-38 levels (P < 0.05) than the healthy group. Salivary IL-10 levels did not differ significantly between the groups (P > 0.05). The salivary IL-1β levels of gingivitis (P < 0.001) and periodontitis groups (P < 0.01) were significantly higher than those of the healthy group. The present study indicated that IL-38 level is decreased in periodontal disease. The results suggested a possible role of IL-38 in the periodontal inflammation process. Clarifying the mechanisms of IL-38 in the inflammatory process may contribute to the development of novel treatment strategies in periodontal diseases.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"76-82"},"PeriodicalIF":1.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140143679","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

The Ability of SOCS1 to Cross-Regulate GM-CSF Signaling is Dose Dependent. SOCS1交叉调节GM-CSF信号的能力是剂量依赖性的。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-02-01 Epub Date: 2025-01-09 DOI: 10.1089/jir.2024.0140

Grace M Bidgood, Narelle Keating, Lizeth Meza Guzman, Kunlun Li, Evelyn Leong, Andrew Kueh, Jeffrey J Babon, Colin Hockings, Karen Doggett, Sandra E Nicholson

{"title":"The Ability of SOCS1 to Cross-Regulate GM-CSF Signaling is Dose Dependent.","authors":"Grace M Bidgood, Narelle Keating, Lizeth Meza Guzman, Kunlun Li, Evelyn Leong, Andrew Kueh, Jeffrey J Babon, Colin Hockings, Karen Doggett, Sandra E Nicholson","doi":"10.1089/jir.2024.0140","DOIUrl":"10.1089/jir.2024.0140","url":null,"abstract":"Suppressor of cytokine signaling (SOCS) 1 is a key negative regulator of interferon (IFN), interleukin (IL)12, and IL-2 family cytokine signaling through inhibition of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. To investigate the temporal induction of SOCS1 in response to cytokine in live cells and its selective regulation of signaling pathways, we generated a mouse expressing a Halo-tag-SOCS1 fusion protein (Halo-SOCS1) under control of the endogenous Socs1 promoter. Homozygous Halo-SOCS1 mice (Halo-Socs1KI/KI) were viable with minor T cell abnormalities, most likely due to enhanced Halo-SOCS1 expression in thymocytes compared with the untagged protein. IFNγ and IL-4 induced Halo-SOCS1 expression in macrophages derived from Halo-Socs1KI/KI mice, and a critical level of SOCS1 expression was required for inhibition of both IFNγ and granulocyte macrophage-colony stimulating factor (GM-CSF)-driven JAK-STAT signaling. In contrast, IFNγ priming to induce SOCS1 did not cross-regulate IL-4 signaling. This study indicates that while SOCS1 expression needs to exceed a critical threshold to inhibit IFNγ signaling, its selective regulation of cytokine signaling results from an as yet undetermined, level of regulatory control.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"53-67"},"PeriodicalIF":1.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142950214","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