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":"<p><p>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, <i>n</i> = 13), mild inflammation (1-2 points, <i>n</i> = 35), and severe inflammation (3-6 points, <i>n</i> = 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; <i>P</i> = 0.021) and decreased interferon-γ-induced protein-10 (IP-10) levels (73.4 vs. 68.8 vs. 112.2 pg/mL; <i>P</i> = 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.</p>","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}
{"title":"Acknowledgment of Reviewers 2024.","authors":"","doi":"10.1089/jir.2024.19874.revack","DOIUrl":"https://doi.org/10.1089/jir.2024.19874.revack","url":null,"abstract":"","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":"45 3","pages":"107"},"PeriodicalIF":1.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630368","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}
{"title":"Immunology Research in Latin America.","authors":"David L Woodland","doi":"10.1089/jir.2025.0024","DOIUrl":"10.1089/jir.2025.0024","url":null,"abstract":"","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"83-84"},"PeriodicalIF":1.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382691","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}
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":"<p><p>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.</p>","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}
{"title":"Cytokines 2024: 12th Annual Meeting of the International Cytokine and Interferon Society.","authors":"Grayson Rodriguez","doi":"10.1089/jir.2024.0241","DOIUrl":"10.1089/jir.2024.0241","url":null,"abstract":"","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"85-90"},"PeriodicalIF":1.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142978963","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}
{"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":"<p><p>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.</p>","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}
{"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":"<p><p>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: <i>SOCS1</i> through <i>SOCS7</i> and a highly related gene known as <i>CISH</i> (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 <i>JICR</i> 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.</p>","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}
{"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":"<p><p>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 (<i>P</i> < 0.05) than the healthy group. Salivary IL-10 levels did not differ significantly between the groups (<i>P</i> > 0.05). The salivary IL-1β levels of gingivitis (<i>P</i> < 0.001) and periodontitis groups (<i>P</i> < 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.</p>","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}
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":"<p><p>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 <i>Socs1</i> promoter. Homozygous Halo-SOCS1 mice (<i>Halo-Socs1<sup>KI/KI</sup></i>) 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 <i>Halo-Socs1<sup>KI/KI</sup></i> 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.</p>","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}
{"title":"Regulation of Ferroptosis in Intestinal Epithelial Cells by Formononetin via the RXRA/PPARG Pathway.","authors":"Huijuan He, Xiaobo Xu, Zhengyao Yu, Fenfen Xu, Huazhen Chen","doi":"10.1089/jir.2024.0148","DOIUrl":"10.1089/jir.2024.0148","url":null,"abstract":"<p><p>Recent studies have revealed that formononetin, a naturally occurring isoflavone found in kudzu root and licorice, has the potential to inhibit ferroptosis in intestinal epithelial cells. Inflammatory bowel disease (IBD) often involves oxidative stress-related pathways, making the modulation of ferroptosis a promising therapeutic avenue. We employed a combination of several techniques to explore how formononetin regulates the retinoid X receptor alpha/peroxisome proliferator activated receptor gamma (RXRA/PPARG) pathway to inhibit ferroptosis in Fetal Human Colonic Epithelial Cells (FHC) induced by RSL3. These techniques included propidium iodide staining, the levels of reactive oxygen species (ROS), Fe<sup>2+</sup>, malondialdehyde (MDA), and ferroptosis-inhibitory proteins glutathione peroxidase 4 (GPX4) and FTH analysis, Western blot analysis, and gene silencing. Our results demonstrate that formononetin significantly mitigated RSL3-induced ferroptosis as evidenced by reduced cellular levels of ROS, Fe<sup>2+</sup>, and MDA, alongside an increased expression of GPX4 and FTH. Silencing the RXRA gene reverses the protective effects of formononetin, highlighting that formononetin inhibits ferroptosis in FHC by upregulating the levels of RXRA. These findings provide new molecular targets for potential therapeutic intervention in IBD, suggesting that upregulating RXRA and PPARG expression via formononetin could be a viable strategy to mitigate ferroptosis-associated cellular damage. This could potentially lead to novel treatments for patients suffering from IBD.</p>","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"68-75"},"PeriodicalIF":1.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006768","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}