Journal of Interferon and Cytokine Research最新文献_第4页

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

Embryonic Lethal Abnormal Visual-Like Protein 1 Aggravates Caerulein-Induced AR42J Cell Injury and Macrophage M1 Polarization to Accelerate Acute Pancreatitis by Upregulating TRAF6. 胚胎致命性异常视觉样蛋白 1 通过上调 TRAF6 加剧了 Caerulein 诱导的 AR42J 细胞损伤和巨噬细胞 M1 极化，从而加速了急性胰腺炎的发生。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-01-01 Epub Date: 2024-11-13 DOI: 10.1089/jir.2024.0149

Wenyong Zhou, Xin Wang, Bin Yan, Yue Sun

{"title":"Embryonic Lethal Abnormal Visual-Like Protein 1 Aggravates Caerulein-Induced AR42J Cell Injury and Macrophage M1 Polarization to Accelerate Acute Pancreatitis by Upregulating TRAF6.","authors":"Wenyong Zhou, Xin Wang, Bin Yan, Yue Sun","doi":"10.1089/jir.2024.0149","DOIUrl":"10.1089/jir.2024.0149","url":null,"abstract":"Tumor necrosis factor receptor-associated factor 6 (TRAF6) has been found to promote the progression of acute pancreatitis (AP). However, its underlying molecular mechanisms in AP need to be further revealed. Caerulein-induced AR42J cells were used to construct AP cell models. Cell viability and apoptosis were measured by Cell Counting Kit 8 assay and flow cytometry. Levels of inflammatory factors and oxidative stress-related markers were assessed. The medium of AR42J cells was collected for coculturing RAW264.7 cells. Macrophage marker CD86+ cell rates were checked with flow cytometry. The levels of TRAF6, embryonic lethal abnormal visual-like protein 1 (ELAVL1), and inducible nitric oxide synthase (iNOS) were examined by Western blot or quantitative real-time polymerase chain reaction. RNA immunoprecipitation assay was performed to evaluate the interaction between ELAVL1 and TRAF6. TRAF6 mRNA stability was tested using actinomycin D treatment. Caerulein treatment suppressed viability, induced AR42J cell apoptosis, inflammation, oxidative stress, and accelerated macrophage M1 polarization. TRAF6 downregulation could alleviate caerulein-induced AR42J cell injury and macrophage M1 polarization. ELAVL1 interacted with TRAF6 to stabilize its expression. Meanwhile, ELAVL1 knockdown relieved caerulein-induced AR42J cell injury and macrophage M1 polarization, while these effects were abolished by TRAF6 overexpression. TRAF6, stabilized by ELAVL1, promoted caerulein-induced AR42J cell injury and macrophage M1 polarization, suggesting that it might accelerate AP9 progression.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"20-28"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622229","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

Causal Relationship Between Inflammatory Cytokines and Pancreatitis Risk. 炎性细胞因子与胰腺炎风险的因果关系

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-01-01 Epub Date: 2024-12-24 DOI: 10.1089/jir.2024.0164

Haiping Yu, Weiwei Chu, Yunquan Zheng, Huihui Li

{"title":"Causal Relationship Between Inflammatory Cytokines and Pancreatitis Risk.","authors":"Haiping Yu, Weiwei Chu, Yunquan Zheng, Huihui Li","doi":"10.1089/jir.2024.0164","DOIUrl":"10.1089/jir.2024.0164","url":null,"abstract":"The causal relationship between inflammatory factors and acute pancreatitis (AP), chronic pancreatitis (CP), alcohol-induced acute pancreatitis (AAP), and alcohol-induced chronic pancreatitis (ACP) remains unclear. We aimed to examine the casual relationship between inflammatory factors and various forms of pancreatitis, namely, AP, CP, AAP, and ACP. We employed a two-sample Mendelian randomization (MR) analysis to investigate the causal relationship between 91 inflammatory factors and 41 inflammatory factors with respect to pancreatitis. The primary analysis involved the use of the inverse variance weighting (IVW). MR-Egger intercept test, Cochran's Q test, MR-PRESSO test, and Leave-One-Out analysis were used to assess the robustness of our findings. IVW analysis revealed evidence of association between 24 inflammatory cytokines and pancreatitis. Specifically, six cytokines were associated with AP, eight cytokines were associated with CP, three cytokines were associated with AAP, and seven cytokines were associated with ACP. The most significant associations were observed with β nerve growth factor (odds ratio [95% confidence interval]: 6.05 [1.59, 23.01]) and interleukin-4 [IL-4; 2.56 (0.91, 7.16)] in AAP, as well as interleukin-2 receiver subunit beta and IL-4 in ACP. Our findings suggest that certain inflammatory cytokines may have a significant role in the development of pancreatitis.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"12-19"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885649","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

A Message from Editor-in-Chief David L. Woodland. 主编 David L. Woodland 的致辞。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-12-01 Epub Date: 2024-10-17 DOI: 10.1089/jir.2024.0193

David L Woodland

引用次数: 0

Nerve Growth Factor from Pancreatic Cancer Cells Promotes the Cancer Progression by Inducing Nerve Cell-Secreted Interleukin-6. 胰腺癌细胞的神经生长因子通过诱导神经细胞分泌白细胞介素-6促进癌症进展

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-12-01 Epub Date: 2024-11-08 DOI: 10.1089/jir.2024.0154

Jianbiao Xu, Yun Shang, Tongmin Wang, Jianlin Song, Wenchuan Zhu, Yunjun Zeng, Jianxun Wang, Xiaochun Yang

{"title":"Nerve Growth Factor from Pancreatic Cancer Cells Promotes the Cancer Progression by Inducing Nerve Cell-Secreted Interleukin-6.","authors":"Jianbiao Xu, Yun Shang, Tongmin Wang, Jianlin Song, Wenchuan Zhu, Yunjun Zeng, Jianxun Wang, Xiaochun Yang","doi":"10.1089/jir.2024.0154","DOIUrl":"10.1089/jir.2024.0154","url":null,"abstract":"Pancreatic cancer (PC) is a cancer with a poor prognosis, and nerve growth factor (NGF) is involved in the pathogenesis of PC within the unknown exact role. Herein, SW1990 cells and PC12 cells were co-cultured using transwell co-culture system and subsequently revealed that NGF was overexpressed in SW1990 cells and promoted PC12 cell proliferation. Knockdown of NGF expression in SW1990 cells using lentiviral shRNA effectively inhibited NGF expression in SW1990 cells and reduced its stimulatory effect on PC12 cell proliferation. Additionally, NGF in SW1990 cells increased the expression of IL-6, dopamine, and c-FOS, as well as decreased the level of lactate dehydrogenase, in PC12 cells, whereas the inhibition of NGF expression significantly reduced the levels of IL-6, dopamine and c-FOS, indicating the critical role of IL-6/STAT3 signaling in PC progression. Finally, cell proliferation, migration, and invasion were assessed using cell counting kit-8, scratch, and Transwell assays, which showed that activated neurons promoted the proliferation, migration, invasion, and NGF secretion of SW1990 cells through the IL-6/STAT3 pathway. The results revealed that NGF secreted by PC cells played a pivotal role in PC progression via regulating activated neural cells-secreted IL-6, providing new theoretical insights for the treatment of PC.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"541-549"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605157","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

Association of the Single Nucleotide Polymorphism 19216T/C in the TLR2 Gene (rs3804099) with Entamoeba histolytica/Entamoeba dispar/Entamoeba moshkovskii Infection Among Lebanese Children. TLR2基因中的单核苷酸多态性19216T/C（rs3804099）与黎巴嫩儿童中的组织溶解恩塔米巴/悬浮恩塔米巴/莫什科夫斯基恩塔米巴感染的关系。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-12-01 Epub Date: 2024-10-04 DOI: 10.1089/jir.2024.0183

Israa Dib, Hiba Noureddine, Mohamad Fakih, Alexandre Livet, Vanessa Alphonse, Abbas Illayk, Abdallah Ahmad Medlej, Mahdi Tarhini, Noureddine Bousserrhine

{"title":"Association of the Single Nucleotide Polymorphism 19216T/C in the TLR2 Gene (rs3804099) with Entamoeba histolytica/Entamoeba dispar/Entamoeba moshkovskii Infection Among Lebanese Children.","authors":"Israa Dib, Hiba Noureddine, Mohamad Fakih, Alexandre Livet, Vanessa Alphonse, Abbas Illayk, Abdallah Ahmad Medlej, Mahdi Tarhini, Noureddine Bousserrhine","doi":"10.1089/jir.2024.0183","DOIUrl":"10.1089/jir.2024.0183","url":null,"abstract":"Toll-like receptors (TLRs), particularly the TLR2, take part in the elicitation of immune responses against Entamoeba histolytica. This study aimed to investigate the relationship between a specific polymorphism called rs3804099 in the TLR2 gene and E. histolytica/E. dispar/E. moshkovskii infection among Lebanese children. A case-control study encompassed 180 participants including 68 children with amebiasis and 112 matched controls. Blood samples were collected, and genomic DNA was extracted using the classical proteinase K digestion and phenol-chloroform extraction method. The variant rs3804099 was examined using the Amplification Refractory Mutation System Polymerase Chain Reaction. The accuracy of the genotyping was supported by sequencing 5% of samples. The TLR2 rs3804099 polymorphism was identified in the studied population, and the observed genotypic distributions were consistent with Hardy-Weinberg equilibrium (P > 0.05). The frequency of the rare CC genotype was significantly higher in patients compared to the noninfected group (P < 0.01). In controls, the homozygous TT genotype was less frequent than the heterozygous CT genotype. The rare CC genotype was associated with a higher risk of amebiasis among children (odds ratios = 3.27, P = 0.002). These findings provide evidence supporting the association between the rs3804099 SNP in the TLR2 gene and E. histolytica/E. dispar/E. moshkovskii infection among Lebanese children.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"550-556"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142467661","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

Adenohypophysis-Inducible Sex Hormones Correlate with Interleukin-6, -8, and Tumor Necrosis Factor-α in Patients with Systemic Lupus Erythematosus. 系统性红斑狼疮患者体内的腺皮质激素诱导性性激素与白细胞介素-6、-8 和肿瘤坏死因子-α相关。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-12-01 Epub Date: 2024-09-26 DOI: 10.1089/jir.2024.0160

Fengqi Liu, Yaning Tian, Ziqing Qu, Qilu Liu, Yumin Xia, Xiaoqian Hu

{"title":"Adenohypophysis-Inducible Sex Hormones Correlate with Interleukin-6, -8, and Tumor Necrosis Factor-α in Patients with Systemic Lupus Erythematosus.","authors":"Fengqi Liu, Yaning Tian, Ziqing Qu, Qilu Liu, Yumin Xia, Xiaoqian Hu","doi":"10.1089/jir.2024.0160","DOIUrl":"10.1089/jir.2024.0160","url":null,"abstract":"Adenohypophysis-inducible sex hormones include prolactin (PRL), follicle-stimulating hormone (FSH), and luteinizing hormone (LH). These hormones influence the occurrence of lupus erythematosus by affecting the endocrine and immune systems. The present study analyzed the relationship between serum sex hormones and several cytokines in patients with systemic lupus erythematosus (SLE). Compared with the healthy controls, early-onset SLE female patients with menopause had higher PRL levels than the healthy controls and cutaneous lupus erythematosus (CLE) group. FSH levels were higher in male patients with SLE than in the healthy controls or CLE group. In SLE patients, the estradiol levels correlated negatively with interleukin (IL)-8. The levels of FSH versus IL-8, PRL versus IL-6, PRL versus tumor necrosis factor (TNF)-α, and LH versus IL-8 levels were moderately positively correlated. In conclusion, PRL, FSH, and LH are positively associated with IL-6, IL-8, and TNF-α in the sera from SLE patients, which indicates that sex hormone levels can serve as an indicator of disease activity during SLE diagnosis.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"534-540"},"PeriodicalIF":1.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142348356","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

Overview of Immunological Response in Urological Membranous Nephropathy: Focus on Cytokine and Treatment Options. 泌尿系统膜性肾病的免疫反应概述：关注细胞因子和治疗方案。

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2024-12-01 Epub Date: 2024-10-25 DOI: 10.1089/jir.2024.0165

Chao Luo, Chengcheng Wei, Zhaoxian He, Renlei Feng

引用次数: 0