Molecular immunology最新文献

{"title":"YY1/INSIG1 enhances atherosclerosis progression by regulating AMPK-mTOR signaling","authors":"Mengsi Yang ,&nbsp;Jing Zhang ,&nbsp;Zhichao Xu ,&nbsp;Li Yang ,&nbsp;Shengxing Tang","doi":"10.1016/j.molimm.2025.08.003","DOIUrl":"10.1016/j.molimm.2025.08.003","url":null,"abstract":"<div><h3>Objective</h3><div>The regulatory mechanisms of Insulin-Induced Gene 1 (INSIG1) in atherosclerosis (AS) remain largely unknown. This study aimed to investigate the role of the YY1/INSIG1 axis and its regulation of the AMPK-mTOR signaling pathway in AS pathogenesis.</div></div><div><h3>Methods</h3><div>Atherosclerosis mouse models were established. RNA sequencing was performed to determine differentially expressed genes. Human umbilical vein endothelial cells (HUVECs) and human vascular smooth muscle cells (HVSMCs) were treated with ox-LDL and/or transfected with plasmids for INSIG1. Cellular functions were evaluated by proliferation, migration, and inflammation assays. Key proteins in the AMPK/mTOR pathway were measured by western blotting. The regulation of INSIG1 by transcription factor YY1 was confirmed using a dual-luciferase reporter assay. Crucially, the functional role of the INSIG1-AMPK axis was validated in vivo using an AMPK inhibitor (Dorsomorphin, DM) in the AS mouse model.</div></div><div><h3>Results</h3><div>INSIG1 expression was significantly downregulated in atherosclerosis mouse models and patients. In HUVECs, INSIG1 promoted cell proliferation, migration, and invasion, while in HVSMCs, INSIG1 suppressed these functions. Higher INSIG1 levels reduced the proinflammatory mediators IL-6 and MCP-1. INSIG1 overexpression activated AMPK and inhibited mTOR phosphorylation. Crucially, in the mouse model, the protective anti-atherosclerotic effects of INSIG1 overexpression were significantly abolished by the administration of the AMPK inhibitor DM. Bioinformatics suggested a potential interaction between YY1 and INSIG1 in atherosclerosis, which was confirmed by a dual-luciferase reporter assay that demonstrated YY1 directly regulate the mRNA transcription of INSIG1.</div></div><div><h3>Conclusion</h3><div>These findings underscore the relevance of INSIG1 and YY1 in atherosclerosis and maybe in its treatment.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"186 ","pages":"Pages 26-38"},"PeriodicalIF":3.0,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144831205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Luteolin attenuates type 2 inflammation in asthmatic mice induced by OVA by regulating IL-33/ST2- GSK3β-M2 macrophage polarization","authors":"Xi Huang ,&nbsp;Hang Yu ,&nbsp;Yaolong Zhou,&nbsp;Cong Xie,&nbsp;Hanlin Shi,&nbsp;Mengmeng Chen,&nbsp;Weifeng Tang,&nbsp;Wenjing Chen,&nbsp;Jingrong Song,&nbsp;Zhen Gao,&nbsp;Jingcheng Dong,&nbsp;Qingli Luo","doi":"10.1016/j.molimm.2025.07.010","DOIUrl":"10.1016/j.molimm.2025.07.010","url":null,"abstract":"<div><div>Allergic asthma is a prevalent non-infectious inflammatory disease characterized by type 2 inflammation. Although multiple treatment options are available, their efficacy is often limited due to the heterogeneous nature of asthma. Luteolin (LUT), a naturally occurring flavonoid, has demonstrated therapeutic potential in various inflammatory conditions. The aim of this research is to investigate the underlying pathogenesis mechanisms of allergic asthma and to evaluate the therapeutic effects of LUT on allergic asthma via IL-33/ST2 signaling pathway. We established a murine model of allergic asthma by sensitizing and challenging BALB/c mice with ovalbumin (OVA), followed by treatment with LUT. The effects of LUT in allergic asthma mice were evaluated via the following techniques: pathological staining, Immunohistochemical staining (IHC), enzyme-linked immunosorbent assay (ELISA), real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB). Additionally, we also used IL-33 to stimulate RAW264.7 cells. Assays <em>in vitro</em> including cell counting Kit-8 (CCK-8), RT-qPCR and WB were performed to investigate potential mechanisms of LUT on IL-33/ST2 pathway activation and M2 macrophages polarization. LUT was verified to have crucial effects on ameliorating asthmatic mice lung function as evidenced by down-regulated airway resistance by 23 % and 48 % (p &lt; 0.05 vs. OVA/saline group); regulating airway type 2 inflammation via decrease the content of type 2 inflammatory cytokines (IL-4, IL-5, and IL-13) by 17 %-78 % (**p &lt; 0.01; ^***p &lt; 0.001 vs. OVA/saline group); decreasing airway inflammatory cells infiltration by 54 % and 65 % (^***p &lt; 0.001 vs. OVA/saline group); inhibiting mucus secretion by 75 % and 89 % (^***p &lt; 0.001 vs. OVA/saline group). Mechanistic research revealed that LUT can treat asthma via IL-33/ST2-GSK3β-M2 macrophages polarization pathway, thereby regulating airway inflammation, remodeling, and immune responses in allergic asthma. Collectively, these findings support LUT as a promising therapeutic agent for allergic asthma through targeted modulation of the IL-33/ST2–GSK3β–M2 macrophage polarization axis.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"186 ","pages":"Pages 1-12"},"PeriodicalIF":3.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144750491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of microglia in neurodegenerative diseases","authors":"Da-Ao Nie ,&nbsp;Jiangkun Yu ,&nbsp;Wenshan Huang ,&nbsp;Gui-Hua Li ,&nbsp;Xu-Ying He ,&nbsp;Jie-Hua Xu","doi":"10.1016/j.molimm.2025.07.014","DOIUrl":"10.1016/j.molimm.2025.07.014","url":null,"abstract":"<div><div>As resident immune surveillance cells within the central nervous system (CNS), microglia exert pivotal biological functions in maintaining CNS homeostasis through dynamic modulation of their proliferative capacity, chemotactic motility, efferocytosis activity, and biphasic secretory mechanisms involving both neuromodulatory factors and pro-inflammatory mediators. These specialized macrophages not only serve as the first line of defense in innate immunity but also orchestrate the regulation of adaptive immune responses; whose functional status directly governs both the physiological integrity of neural circuits and the progression of pathological outcomes. Notably, in neurodegenerative disease models, microglial functional states exhibit pronounced heterogeneity and are tightly regulated by microenvironmental cues. Upon encountering sustained hyperactivation or functional impairment, these cells precipitate a cascade of deleterious events within the neurovascular unit. Building upon these pathophysiological mechanisms, targeted modulation of microglial polarization equilibrium has emerged as a pivotal research focus in developing innovative neuroprotective therapeutic strategies. This review systematically integrates empirical evidence derived from cutting-edge methodologies—including molecular imaging, single-cell multi-omics profiling, and conditional genetic ablation—to mechanistically dissect the dual regulatory roles of microglia in orchestrating neural homeostatic maintenance and driving pathological progression in neurological disorders.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"185 ","pages":"Pages 127-135"},"PeriodicalIF":3.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144739688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Choline reduces inflammatory response and lipid accumulation in calf hepatocytes induced by NEFA via inhibiting ROS/ NF-κB/NLRP3 inflammasome axis","authors":"Rui Zhang ,&nbsp;Xueer Du ,&nbsp;Haitao Hu ,&nbsp;Juanfang Chen ,&nbsp;Junjian Yu ,&nbsp;Lamei Wang ,&nbsp;Junhu Yao ,&nbsp;Shimin Liu ,&nbsp;Jianguo Wang ,&nbsp;Yangchun Cao","doi":"10.1016/j.molimm.2025.07.013","DOIUrl":"10.1016/j.molimm.2025.07.013","url":null,"abstract":"<div><div>Perinatal dairy cows are highly susceptible to fatty liver syndrome, a prevalent metabolic disorder characterized by excessive hepatic lipid accumulation. Although inflammatory progression drives the transition from physiological lipid storage to pathological steatosis, the underlying mechanisms remain incompletely understood. This study investigates the therapeutic potential of choline in non-esterified fatty acid (NEFA)-induced hepatic inflammation and lipid metabolism dysregulation using an <em>in vitro</em> calf hepatocytes model. A hepatic steatosis model was established by treating primary calf hepatocytes with 1.2 mM NEFA for 24 h. Choline supplementation (75 μM) significantly enhanced hepatocyte viability and reduced intracellular triglyceride (TG) content (<em>P</em> &lt; 0.05). Transcriptomic analysis demonstrated that choline downregulated key components of the NLRP3 inflammasome (<em>P</em> &lt; 0.05) and interleukin-1β (IL-1β) expression (<em>P</em> &lt; 0.05). Mechanistically, choline attenuated NF-κB phosphorylation (<em>P</em> &lt; 0.05) and suppressed intracellular reactive oxygen species (ROS) generation (<em>P</em> &lt; 0.05), thereby inhibiting NLRP3 inflammasome assembly and subsequent IL-1β maturation (<em>P</em> &lt; 0.05). Notably, activation of NLRP3 inflammasome complete abolished choline's protective effects on lipid homeostasis and inflammatory responses (<em>P</em> &lt; 0.05). These findings demonstrate that choline ameliorates NEFA-induced hepatic steatosis by modulating the ROS/NF-κB-NLRP3-IL-1β/IL-18 signalling axis, providing novel therapeutic targets for intervention of steatohepatitis in periparturient dairy cows.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"185 ","pages":"Pages 116-126"},"PeriodicalIF":3.0,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144723095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-146a-5p targets IRAK1/TRAF6 to promote bacillus Calmette-Guérin survival by exosome-mediated autocrine actions","authors":"Hao-Rong Chen ,&nbsp;Huan-Shao Huang ,&nbsp;Si-Yi Zeng ,&nbsp;Yin-Fu Sun ,&nbsp;Lan Chen ,&nbsp;Shi-Ying Lai ,&nbsp;Jia-Jun Wang ,&nbsp;Fen Yang ,&nbsp;Jiang Pi ,&nbsp;Yan-guang Cong ,&nbsp;Jun-Fa Xu","doi":"10.1016/j.molimm.2025.07.012","DOIUrl":"10.1016/j.molimm.2025.07.012","url":null,"abstract":"<div><h3>Background</h3><div>Exosomes carry signaling molecules between cells and play important roles in the interaction between macrophages and <em>Mycobacterium tuberculosis</em> (Mtb). This study aimed to examine the function and content of exosomes secreted by macrophages infected with Bacillus Calmette-Guérin (BCG).</div></div><div><h3>Methods</h3><div>THP-1 monocytes and HEK293T cells were used. Macrophages were infected with BCG. A Transwell system was used to evaluate the effect of the exosomes secreted by macrophages. Cells were transfected with the miR-146a-5p plasmid or inhibitor to examine the effects of miR-146a-5p overexpression or inhibition. qRT-PCR was employed to investigate the expression levels of miR-320a-5p, miR-27a-5p, miR-26a-5p, miR-146a-5p, and miR-223–5p and the mRNA expression of IL-6, TNF-α, and IL-1β. Western blot was used to investigate the protein expression of IRAK1, TRAF6, CD63, CD81, GRP94, Alix, TSG101, P65, and p-P65. A dual luciferase assay was performed to investigate whether miR-146a-5p targets IRAK1 and TRAF6.</div></div><div><h3>Results</h3><div>The infected cells contained high miR-146a-5p levels that could be secreted into exosomes. Exosomal miR-146a-5p promoted Mtb survival and proliferation after uptake by host cells. Bioinformatics showed that high miR-146a-5p levels were found in exosomes from BCG-infected macrophages and blood samples from patients with tuberculosis. The phagocytosis of exosomes containing miR-146a-5p by BCG-infected macrophages suppressed the expression of inflammatory factors by regulating the IRAK1-TRAF6-NF-κB signaling pathway, ultimately leading to the inhibition of inflammatory factor expression in macrophages and a decrease in the macrophage BCG killing capacity.</div></div><div><h3>Conclusion</h3><div>The findings indicate a new immune evasion mechanism of Mtb. miR-146a-5p secreted in exosomes by BCG-infected macrophages can decrease the bactericidal potential of macrophages. The results offer a novel theoretical basis and potential biomarkers for diagnosing, treating, and managing tuberculosis.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"185 ","pages":"Pages 105-115"},"PeriodicalIF":3.0,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144722244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of macrophage pyroptosis by SIRT1 during Pseudomonas aeruginosa-induced pneumonia","authors":"Haibo Ding ,&nbsp;Xinzhu Xiao ,&nbsp;Yuping Zhan ,&nbsp;Yanqing Lin ,&nbsp;Changsheng Xu ,&nbsp;Yiming Zeng","doi":"10.1016/j.molimm.2025.07.005","DOIUrl":"10.1016/j.molimm.2025.07.005","url":null,"abstract":"<div><div><em>Pseudomonas aeruginosa</em> (PA), an opportunistic gram-negative bacterial pathogen, is the main cause of lung infections. Pulmonary infection induced by PA results in inflammatory lung injury characterized by macrophage pyroptosis. In our study, a mouse model of pulmonary infection was established by tracheal intubation with PA in vivo, and the MH-S macrophage line was stimulated with PA in vitro. HE staining was performed to observe changes in the lung tissue. The mechanism was further explored through various methods, including flow cytometry, LDH release assays, ELISA, real-time PCR, Western blotting (WB), and CCK8 assays. Additionally, the effect of MH-S cells on the proliferation of alveolar endothelial cells was observed by coculturing these two cell types. The results showed that PA-induced inflammatory injury in murine lung tissues increased the levels of inflammatory factors (IL-1β/6/12) and pyroptosis-related proteins (NLRP3, Caspase 1/11, and GSDMD-N) and promoted pulmonary macrophage pyroptosis. PA downregulated Sirt1 expression and increased p-NF-κB-p65 levels both in vitro and in vivo. Sirt1 activation or overexpression alleviated PA-induced lung tissue injury, inhibited macrophage pyroptosis, and decreased the expression of inflammatory factors and pyroptosis-related proteins. Sirt1 inhibition or knockdown critically strengthened the effect of PA on pulmonary macrophage pyroptosis. NF-κB inhibition suppressed the PA-induced increase in Sirt1-regulated pyroptosis in MH-S macrophages, decreased the levels of inflammatory factors and pyroptosis-related proteins, and weakened the inhibitory effect of MLE-12 cell proliferation on PA-infected MH-S cells. In conclusion, the Sirt1/NF-κB axis negatively regulates PA-induced inflammatory factor release and macrophage pyroptosis, promotes lung epithelial cell proliferation, and reduces inflammatory injury to the lung tissue.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"185 ","pages":"Pages 92-104"},"PeriodicalIF":3.2,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144703270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leven PRO-CR mediates 5-HT and gut microbiota via TPH1 to improve slow-transit constipation","authors":"Fei Xia,&nbsp;Qibin He,&nbsp;Shenglin Wang,&nbsp;Mengchao He,&nbsp;Ping Fang,&nbsp;Yanqiu Yu","doi":"10.1016/j.molimm.2025.07.007","DOIUrl":"10.1016/j.molimm.2025.07.007","url":null,"abstract":"<div><div>Slow-transit constipation (STC) is a chronic disorder causing prolonged colonic transit and discomfort; this study explores the therapeutic potential of probiotics mixture (Leven PRO-CR) in modulating gut microbiota and enhancing intestinal motility. A loperamide-induced STC mouse model was established, and the effects of Leven PRO-CR treatment were evaluated by measuring defecation frequency, stool water content, and intestinal transit rate. Histopathological analyses, including Hematoxylin &amp; Eosin (H&amp;E) staining, immunohistochemistry (IHC), and TUNEL assay, were performed to assess colonic tissue integrity, interstitial cells of Cajal (ICCs) density, and apoptosis. The expression levels of serotonin (5-HT)-related markers (TPH1, 5-HT receptors, SERT) and enteric neural markers (NOS1, BDNF, TRPV1, GDNF) were analyzed using quantitative PCR (qPCR), Western blotting, and immunofluorescence staining. The gut microbiota composition was examined through 16S rDNA sequencing. Statistical analyses were conducted using GraphPad Prism, with significance set at P &lt; 0.05. Leven PRO-CR significantly improved STC symptoms by reducing first defecation time, increasing stool frequency, fecal water content, and intestinal transit rate. We found that Leven PRO-CR restored colonic tissue integrity, enhanced ICC survival by upregulating c-Kit/SCF signaling, and reduced apoptosis. Leven PRO-CR upregulated TPH1 expression, increased 5-HT levels, and inhibited its degradation, thereby promoting intestinal motility. Leven PRO-CR also modulated NOS1, BDNF, TRPV1, and GDNF mRNA and protein expression, suggesting enhanced enteric nervous system function. 16S rDNA sequencing revealed increased microbial diversity and a restored balance of beneficial bacteria after Leven PRO-CR treatment, indicating the beneficial effects of Leven PRO-CR on balancing gut microbiota in STC. Overall, Leven PRO-CR alleviated slow-transit constipation potentially by enhancing 5-HT secretion, upregulating TPH1 channels, and restoring microbiota balance.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"185 ","pages":"Pages 81-91"},"PeriodicalIF":3.2,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144695435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin mitigates testicular ischemia-reperfusion injury by suppressing NLRP3-mediated pyroptosis","authors":"Zhi Hu ,&nbsp;Jinrun Wang ,&nbsp;Jinzhuo Ning ,&nbsp;Fan Cheng","doi":"10.1016/j.molimm.2025.07.011","DOIUrl":"10.1016/j.molimm.2025.07.011","url":null,"abstract":"<div><h3>Background</h3><div>Testicular torsion results in damage by interrupting the blood supply. Nevertheless, the reestablishment of blood flow following testicular detorsion, a process known as testicular ischemia-reperfusion injury (IRI), often leads to further injury. Curcumin is a naturally occurring phenolic compound that has anti-inflammatory and antioxidant implications. It has been demonstrated to confer preventive implications in IRI between different organs. We propose ascertaining curcumin function in testicular IRI.</div></div><div><h3>Methods</h3><div>We created a mouse model to study testicular torsion/detorsion (T/D) and a germ cell model to study oxygen-glucose deprivation/reperfusion (OGD/R). The evaluation of testicular ischemia damage was conducted using histological staining. Testicular tissues were examined for the presence of reactive oxygen species (ROS) and pyroptosis-linked proteins employing western blot (WB), RT-qPCR, MDA, SOD assay kits, and immunohistochemistry analysis. Cell viability and cytotoxicity were measured via the Cell Counting Kit-8 (CCK-8) and LDH test kits. The amounts of inflammatory proteins were quantified employing ELISA, immunofluorescence, and immunoblotting methods.</div></div><div><h3>Results</h3><div>We observed that testicular IRI is involved in oxidative stress damage in cells, with an associated elevation in pyroptosis-linked proteins NLRP3 and caspase-1 (CASP-1) levels. Additionally, there is a rise in the inflammatory cytokines IL-1β and −18 levels. After treating with curcumin, we noted a significant inhibition of pyroptosis, particularly when the concentration was 20 μmol/L, where the inhibitory effect was most pronounced. Further investigation into the underlying mechanisms revealed that curcumin exerts its preventative implications against testicular IRI by targeting the NLRP3 pathway to suppress IRI-mediated pyroptosis.</div></div><div><h3>Conclusions</h3><div>Curcumin mitigates testicular IRI-induced pyroptosis by modulating the NLRP3 signaling pathway, thereby alleviating cellular and tissue damage.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"185 ","pages":"Pages 71-80"},"PeriodicalIF":3.2,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144695393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of the role of cytokines on HIV infection in people living with HIV with and without comorbidities","authors":"Nayana de Oliveira Souza ,&nbsp;Natalia Alves Cortelette ,&nbsp;Mayara Paes Santos ,&nbsp;Marcelo Dias-Baruffi ,&nbsp;Daniela Amorim Melgaço Guimarães ,&nbsp;Lorena Rocha Ayres ,&nbsp;João Alexandre Trés Pancoto","doi":"10.1016/j.molimm.2025.07.008","DOIUrl":"10.1016/j.molimm.2025.07.008","url":null,"abstract":"<div><div>Infection with the human immunodeficiency virus (HIV) causes a deterioration of the immune system. Changes in cytokine levels are seen in HIV infection and contribute to the pathogenesis of the disease. This study evaluated cytokine levels and single nucleotide polymorphisms (SNP) of genes associated with HIV infection and the development of comorbidities. The dosage of cytokines [(tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ) and interleukins (IL) 1, 6, 10 and 17)] were subjected to immunoenzymatic assays, and genotypes for TNF-α SNP −308 G/A, IFN-γ + 874 T/A, IL-1β −511 C/T, IL-6 −174 G/C and IL-10 −592 C/A by the polymerase chain reaction technique of the 200 enzymes used (CONT) and 200 people living with HIV (PLHIV). Relevant results were observed in the dosage of all as cytokines. There was an increase in the levels of TNF-α, IL-1β and IL-10 and a reduction in the levels of INF-γ, IL-6 and IL-17 in PLHIV compared to CONT. As the SNP demonstrated a predominance of the genotype of high TNF-α producer and low IFN-γ and IL-10 producers in the PLHIV group. Changes in the TNF-α, IFN-γ tests observed in the PLHIV group may be associated with the studied SNP, while the SNP IL-10 −592 C/A seems to indicate an association of this polymorphism with risk of HIV infection. Thus, investigations of the immunoregulatory mechanisms of HIV infection may be important in the establishment of new biomarkers for prognosis, in the discovery of new therapeutic targets, in the development of immunotherapies and in the results for curing the infection.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"185 ","pages":"Pages 63-70"},"PeriodicalIF":3.2,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144679001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship between Interleukin 1 beta single nucleotide polymorphisms and systemic lupus erythematosus among the Chinese Han population","authors":"Mao Liu ,&nbsp;Xiru Ling ,&nbsp;Zhenboyang Tang ,&nbsp;Chunyan Huang ,&nbsp;Ping Wang ,&nbsp;Jiqiang Wu ,&nbsp;Yue He ,&nbsp;Jie Chen","doi":"10.1016/j.molimm.2025.07.003","DOIUrl":"10.1016/j.molimm.2025.07.003","url":null,"abstract":"<div><h3>Objective</h3><div>Systemic lupus erythematosus (SLE) is a typical autoimmune disease whose etiology is related to genetic factors. This study is designed to evaluate the association between Single Nucleotide Polymorphisms (SNPs) of the Interleukin 1 beta (IL-1β) gene (rs16944, rs1143627, rs1143634) and SLE susceptibility and clinical characteristics in the Chinese Han population.</div></div><div><h3>Methods</h3><div>This case-control study recruited 155 SLE patients and 140 controls. DNA was extracted from the venous blood of all subjects and genotyped using PCR and mass spectrometry.</div></div><div><h3>Results</h3><div>Individuals with at least one mutant gene G (AG+GG genotype) at rs16944, at least one mutant gene A (AG+AA genotype) at rs1143627 and the AG Genotype at rs1143634 were associated with a lower risk of SLE compared to healthy controls(<em>P</em> = 0.009; <em>P</em> = 0.005; <em>P</em> = 0.016). The AG genotype at rs16944 increased the risk of anti-SSA(Ro) antibody positivity and thrombocytopenia (<em>P</em> = 0.033; <em>P</em> = 0.018), while the G allele decreased the risk of lupus nephritis (<em>P</em> = 0.040). For rs1143627, the A allele was linked with an increased risk of LA2 positivity for lupus anticoagulant (<em>P</em> = 0.041) and a lower risk of lupus nephritis (<em>P</em> = 0.044), and the AG genotype was associated with an increased risk of thrombocytopenia (<em>P</em> = 0.009). There was no correlation between rs1143634 and clinical features of SLE.</div></div><div><h3>Conclusion</h3><div>In conclusion, IL-1β gene polymorphisms are related to SLE susceptibility and clinical features in the Chinese population.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"185 ","pages":"Pages 53-62"},"PeriodicalIF":3.2,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}