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

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

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 : 2025-02-10 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 IFNLR1.","authors":"Laura A Novotny, Christiana S Kappler, Eric G Meissner","doi":"10.1089/jir.2024.0262","DOIUrl":"https://doi.org/10.1089/jir.2024.0262","url":null,"abstract":"Distinct transcriptional isoforms of the interferon lambda receptor 1 (IFNLR1) are expressed in hepatocytes, but whether corresponding full-length and truncated IFNLR1 protein variants have discrete function is unclear. We quantitated IFNLR1 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 IFNLR1 to evaluate their function. IFNLR1 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 IFNLR1. A secreted IFNLR1 variant had no identified function in iHeps lacking endogenous IFNLR1. Although relative expression of individual IFNLR1 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.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-02-10","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

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 : 2025-02-06 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":"https://doi.org/10.1089/jir.2024.0259","url":null,"abstract":"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.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-02-06","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

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

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

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

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

Regulation of Ferroptosis in Intestinal Epithelial Cells by Formononetin via the RXRA/PPARG Pathway. 刺芒柄花素通过RXRA/PPARG通路调控肠上皮细胞铁凋亡

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-02-01 Epub Date: 2025-01-20 DOI: 10.1089/jir.2024.0148

Huijuan He, Xiaobo Xu, Zhengyao Yu, Fenfen Xu, Huazhen Chen

{"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":"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), Fe2+, 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, Fe2+, 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.","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}

引用次数: 0

Stimulator of Interferon Genes Signal in Lung Cancer Regulates Differentiation of Myeloid-Derived Suppressor Cells in the Tumor Microenvironment Via the Interferon Regulatory Factor 3/NF-κB Pathway. 肺癌干扰素基因信号刺激因子通过干扰素调节因子3/NF-κB通路调控肿瘤微环境中髓源性抑制细胞的分化

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-01-01 Epub Date: 2025-01-08 DOI: 10.1089/jir.2024.0150

Jiaojiao Ren, Jun Ying, Haijian Liu, Shanshan Hu, Jiangdong Li, Danfei Zhou

{"title":"Stimulator of Interferon Genes Signal in Lung Cancer Regulates Differentiation of Myeloid-Derived Suppressor Cells in the Tumor Microenvironment Via the Interferon Regulatory Factor 3/NF-κB Pathway.","authors":"Jiaojiao Ren, Jun Ying, Haijian Liu, Shanshan Hu, Jiangdong Li, Danfei Zhou","doi":"10.1089/jir.2024.0150","DOIUrl":"10.1089/jir.2024.0150","url":null,"abstract":"Background: This study was designed to explore the action mechanism of stimulator of interferon genes (STING) on the differentiation of myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment of lung cancer. Methods: Bioinformatics analysis yielded a potential pathway for STING to regulate MDSC differentiation, the interferon regulatory factor 3 (IRF3)/NF-κB axis. The transfection efficiency of STING overexpression plasmid and small interfering RNA against IRF3 (siIRF3) was examined by quantitative real-time polymerase chain reaction (qRT-PCR). After transfection, A9 cells were co-cultured with extracted bone marrow cells (BMCs). MDSC differentiation, protein expression of the IRF3/NF-κB pathway, and changes in nuclear translocation of NF-κB were analyzed by flow cytometry, Western blot, and immunofluorescence staining experiments. A transplanted tumor mouse model was used for in vivo experiments. After cyclic diadenyl monophosphate (CDA; STING agonist) treatment, changes in MDSC differentiation and protein expression of the IRF3/NF-κB axis in transplanted tumors were verified by immunohistochemical staining, qRT-PCR, and Western blot. Results: Coculture of A9 cells and BMCs promoted MDSC differentiation, inhibited activation of IRF3/NF-κB signal in A9 cells, and boosted nuclear translocation of NF-κB. However, after the upregulation of STING, IRF3/NF-κB signal was activated, while MDSC differentiation and nuclear translocation of NF-κB were inhibited. SiIRF3 reversed the effects of STING overexpression. In vivo, CDA dampened MDSC differentiation and promoted protein expression of the IRF3/NF-κB axis. Conclusion: STING signal in lung cancer cells inhibits MDSC differentiation through activation of the IRF3/NF-κB pathway.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"29-37"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142950212","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 Impact of Chemokine-Like Receptor 1 Gene Knockout on Lipopolysaccharide-Induced Epididymo-Orchitis in Mice. 类趋化因子受体 1 基因敲除对脂多糖诱导的小鼠附睾炎的影响

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-01-01 Epub Date: 2024-10-29 DOI: 10.1089/jir.2024.0152

Zhonglin Xiao, Jie Chen, Xiujun Fan, Wei Zhao, Chiawei Chu, Jian V Zhang

{"title":"The Impact of Chemokine-Like Receptor 1 Gene Knockout on Lipopolysaccharide-Induced Epididymo-Orchitis in Mice.","authors":"Zhonglin Xiao, Jie Chen, Xiujun Fan, Wei Zhao, Chiawei Chu, Jian V Zhang","doi":"10.1089/jir.2024.0152","DOIUrl":"10.1089/jir.2024.0152","url":null,"abstract":"This comprehensive study delved into the pivotal function of chemokine-like receptor 1 (CMKLR1) in lipopolysaccharide (LPS)-triggered epididymo-orchitis in mice. Upon LPS exposure, wild-type (WT) mice exhibited marked elevations in serum pro-inflammatory markers, including G-CSF, IL-6, and RANTES, along with heightened levels of TNF-α and IL-6 in testicular and epididymal tissues, which accompanied by pronounced structural damage within the testicular tissue and a concurrent decline in serum testosterone, estradiol (E2) levels, and testicular steroid synthetase expression. Remarkably, Cmklr1 gene ablation intensified the pro-inflammatory response in the serum (especially IFN-γ), testes, and epididymis of epididymo-orchitis models. Furthermore, Cmklr1 deficiency uniquely induced structural alterations within the epididymis, which is absent in the WT model. This genetic manipulation also exacerbated the decline in serum testosterone and E2 levels and testicular steroid synthase activity. While chemerin levels were significantly diminished in WT epididymo-orchitis models, Cmklr1 knockout had no discernible effect on chemerin expression in the model. In addition, a noteworthy observation was the elevation of the serum low density lipoprotein/high density lipoprotein (LDL/HDL) ratio in Cmklr1-deficient mice. Collectively, these findings underscore that the lack of chemerin/CMKLR1 signaling axis could potentially worsen the symptoms during LPS-induced epididymo-orchitis, highlighting its potential as a therapeutic target in related pathologies.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"1-11"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522124","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