Immunobiology最新文献

{"title":"Specific human antibodies against SARS-CoV-2 and monkeypox virus generated via a rapid construction and screening system","authors":"Guanglei Gu ,&nbsp;Jinhai Wang ,&nbsp;Xiaoyun Hu ,&nbsp;Xiuling Gu ,&nbsp;Shirui Li ,&nbsp;Hanle Li ,&nbsp;Min Fang","doi":"10.1016/j.imbio.2025.153124","DOIUrl":"10.1016/j.imbio.2025.153124","url":null,"abstract":"<div><div>Monoclonal antibodies are playing an increasingly important role in modern medicine. Human monoclonal antibodies have become a key focus in the development of monoclonal antibody therapeutics due to their safety. We developed an integrated platform that rapidly constructs and screens human antibodies by combining recombinant antigen production, fluorescent antigen tetramers, memory B-cell sorting, single-cell gene amplification, and single-chain antibody expression for rapid screening of antibody specificity. Using peripheral blood mononuclear cells from healthy donors, we successfully generated human monoclonal antibodies targeting the N and S1 proteins of SARS-CoV-2. Furthermore, we applied the platform to produce protective human antibodies against the M1R protein of the monkeypox virus (MPXV). These results demonstrate that our system enables the rapid and efficient discovery of specific monoclonal antibodies, offering broad applicability for combating emerging infectious diseases and advancing cancer immunotherapies.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153124"},"PeriodicalIF":2.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145217335","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":"Corrigendum to \"UMI-77 targets MCL-1 to activate mitophagy and ameliorate periodontitis in mice\" [Immunobiology 230(5) (2025) 153108].","authors":"Dalei Sun, Shu Ouyang, Xiaoxuan Xu, Jingjing Yan, Heqian Wang, Chenkai Lan, Wubin Ouyang, Liangjun Zhong, Jun Lin","doi":"10.1016/j.imbio.2025.153120","DOIUrl":"10.1016/j.imbio.2025.153120","url":null,"abstract":"","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":" ","pages":"153120"},"PeriodicalIF":2.3,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137317","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":"sgp130Fc alleviates cartilage degeneration and knee osteoarthritis by inhibiting IL-6 trans-signaling pathway","authors":"Chunrong He ,&nbsp;Lingjie Tan ,&nbsp;Chi Liang ,&nbsp;Jiewen Luo ,&nbsp;Ke Xiao ,&nbsp;Song Wu ,&nbsp;Jinshen He","doi":"10.1016/j.imbio.2025.153122","DOIUrl":"10.1016/j.imbio.2025.153122","url":null,"abstract":"<div><h3>Background</h3><div>Interleukin-6 (IL-6) trans-signaling plays a pivotal role in the pathogenesis and progression of osteoarthritis (OA), contributing to chronic intra-articular inflammation and cartilage degradation. Soluble gp130-Fc (sgp130Fc) is a selective inhibitor of IL-6 trans-signaling that spares classical signaling. This study aimed to elucidate the role of IL-6 trans-signaling in knee OA and evaluate the therapeutic potential of sgp130Fc.</div></div><div><h3>Methods</h3><div>Synovial fluid from OA patients at different disease stages was analyzed for IL-6, soluble IL-6 receptor (sIL-6R), and sgp130 levels by ELISA. Primary rat chondrocytes were treated with Hyper-IL-6 to activate IL-6 trans-signaling and co-treated with sgp130Fc to assess cell viability, gene expression, and lipid metabolism alterations. A rat OA model was established via the Hulth method, followed by intra-articular administration of sgp130Fc. Histological, immunohistochemical, and lipidomic analyses were performed to evaluate cartilage integrity and inflammatory responses.</div></div><div><h3>Results</h3><div>Levels of IL-6, sIL-6R, and sgp130 in synovial fluid increased with OA progression. Hyper-IL-6 impaired chondrocyte viability, activated JAK1-STAT3 signaling, promoted inflammatory and catabolic gene expression, and disrupted lipid metabolism, all of which were reversed by sgp130Fc treatment. In vivo, sgp130Fc injections alleviated cartilage degradation, reduced synovitis, suppressed inflammatory mediators, and restored lipid homeostasis.</div></div><div><h3>Conclusions</h3><div>Targeted inhibition of IL-6 trans-signaling with sgp130Fc effectively mitigates cartilage degeneration and inflammation in OA, highlighting its potential as a novel disease-modifying therapeutic strategy for knee osteoarthritis.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153122"},"PeriodicalIF":2.3,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148639","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":"Changpu Yujin Tang mitigates tourette syndrome by enhancing mitophagy and suppressing NLRP3 inflammasome-mediated pyroptosis","authors":"Shuang Huang ,&nbsp;Liwei Huang ,&nbsp;Mengxue Li ,&nbsp;Mingyang Sun ,&nbsp;Kexin Sun ,&nbsp;Xing Wei ,&nbsp;Bing Jiang ,&nbsp;Yuezhen He ,&nbsp;Fuchun Xue ,&nbsp;Lv Gao ,&nbsp;Manqi Lu ,&nbsp;Jing Shang ,&nbsp;Zhenggang Shi","doi":"10.1016/j.imbio.2025.153118","DOIUrl":"10.1016/j.imbio.2025.153118","url":null,"abstract":"<div><h3>Background</h3><div>Changpu Yujin Tang (CPYJT) is an effective Chinese herbal compound for treating Tourette syndrome (TS). However, its precise molecular mechanisms remain to be fully elucidated.</div></div><div><h3>Methods</h3><div>105 SD rats were randomly divided into the Control (<em>n</em> = 15) and the TS (<em>n</em> = 90) groups. The TS group was induced by intraperitoneal injection of 3,3′-iminodipropionitrile. After successful modeling, the TS group was further divided into 6 subgroups (<em>n</em> = 15 in each group): the Model group, the Tiapride group, the CPYJT group, the Rapamycin (RAPA) group, the 3-methyladenine (3-MA) group, and the CPYJT +3-MA group, and were treated with the corresponding drugs for 4 weeks.</div></div><div><h3>Results</h3><div>Compared with the Control group, rats in the Model group showed increased stereotyped and motor behaviors, damage to striatal neuronal cells and mitochondrial ultrastructure, decreased PINK1/Parkin-mediated mitophagy, and activation of NLRP3 inflammasome. CPYJT reduced stereotyped and motor behaviors, attenuated neuronal cell damage, and repaired mitochondrial pathology in the TS rats. Furthermore, both CPYJT and RAPA enhanced PINK1/Parkin-mediated mitophagy, eliminated ROS accumulation, and inhibited NLRP3 inflammasome activation. Notably, CPYJT counteracted 3-MA's inhibitory effect on PINK1/Parkin-mediated mitophagy, thereby suppressing NLRP3 inflammasome activation and pyroptosis.</div></div><div><h3>Conclusion</h3><div>CPYJT inhibits NLRP3 inflammasome activation and reduces pyroptosis by enhancing PINK1/Parkin-mediated mitophagy and attenuating ROS accumulation, which in turn ameliorates TS.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153118"},"PeriodicalIF":2.3,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145155629","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":"Serum exosome smallRNA array analysis identifies 5’tiRNA-PheGAA and tRF-1-IleAAT as potential biomarkers for diagnosis of rheumatoid arthritis","authors":"Yuanyuan Li ,&nbsp;Meiling Xu ,&nbsp;Nan Zhao ,&nbsp;Chong Qi ,&nbsp;Tingshuang Xu","doi":"10.1016/j.imbio.2025.153123","DOIUrl":"10.1016/j.imbio.2025.153123","url":null,"abstract":"<div><div>tRNA-derived small RNAs (tsRNAs) are a recently identified class of non-coding RNAs (ncRNAs) that exhibit aberrant expression in various diseases and are involved in multiple pathological processes. In this study, we isolated exosomes from the serum of patients with rheumatoid arthritis (RA) and healthy individuals, and extracted total RNA for analysis using small RNA microarrays and tsRNA sequencing. We identified 866 tsRNAs that were differentially expressed between RA patients and healthy controls, with 146 upregulated and 720 downregulated. Among the upregulated tsRNAs, the five with the most significant increases were selected for further validation. qRT-PCR analysis confirmed that 5’tiRNA-PheGAA and tRF-1-IleAAT were significantly upregulated in RA patients. Pathway enrichment analysis suggested that these two tsRNAs are involved in tryptophan metabolism, autophagy, chemokine signaling, Rap1 signaling, and focal adhesion pathways. ROC curve analysis indicated that both tsRNAs exhibit strong diagnostic potential for RA. Collectively, our findings demonstrate that serum exosomal tsRNAs may serve as promising biomarkers for the effective diagnosis and prognosis of rheumatoid arthritis.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153123"},"PeriodicalIF":2.3,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145155630","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":"ATP–NLRP3 inflammasome axis enhances the immunosuppressive effect of myeloid-derived suppressor cells","authors":"Tatsuya Ando ,&nbsp;Kouhei Sakurai ,&nbsp;Masato Hoshi ,&nbsp;Hiroyuki Tezuka ,&nbsp;Yasuhiro Sakai ,&nbsp;Taku Kato ,&nbsp;Hiroyasu Ito","doi":"10.1016/j.imbio.2025.153119","DOIUrl":"10.1016/j.imbio.2025.153119","url":null,"abstract":"<div><div>The effectiveness of immune checkpoint inhibitors is diminished by the presence of myeloid-derived suppressor cells (MDSCs). Recent studies indicate that the NLR family pyrin domain-containing 3 (NLRP3) inflammasome regulates MDSC function, thereby reducing the efficacy of immune checkpoint inhibitors. However, the specific mechanism by which NLRP3 expression induces the immunosuppressive effects in MDSCs remains unclear. Here, we demonstrate that the adenosine triphosphate (ATP)–NLRP3 inflammasome axis enhances the immunosuppressive effects of MDSCs. We found that ATP increases the mRNA levels of immunosuppressive molecules in MDSCs, leading to the suppression of T cell proliferation. Additionally, we showed the efficacy of a novel immune checkpoint therapy that combines an ATP receptor inhibitor (P2X7 receptor inhibitor), an NLRP3 inhibitor, and an anti-PD-L1 antibody (Ab). This combination treatment significantly inhibited tumor growth compared to treatment with only the NLRP3 inhibitor and anti-PD-L1 Ab. These results suggest that the ATP–NLRP3 axis enhances the immunosuppressive effect of MDSCs. In conclusion, this study elucidates the mechanism through which MDSCs acquire immunosuppressive functions, potentially informing the development of novel cancer immunotherapies.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153119"},"PeriodicalIF":2.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145119337","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":"Role and mechanism of METTL3 in fibrosis-associated signaling in CVB3-infected H9c2 cardiomyocytes through the lncRNA MEG3/c-MYC/SMAD2 axis","authors":"Lu Huang ,&nbsp;Li Wang ,&nbsp;Jiaojiao Guo,&nbsp;Shiqian Lu,&nbsp;Qian Zhang,&nbsp;Taiming Liu","doi":"10.1016/j.imbio.2025.153117","DOIUrl":"10.1016/j.imbio.2025.153117","url":null,"abstract":"<div><div>Viral myocarditis (VMC) is an inflammatory disease of the heart muscle caused by viral infection and may lead to myocardial fibrosis. This study aims to investigate the role of METTL3 in myocardial fibrosis in VMC. METTL3 expression was intervened with in VMC cell models, followed by measurement of LDH, CK-MB, and TGF-β1. The expression of METTL3, lncRNA MEG3, c-MYC, SMAD2, Collagen I, Collagen III, and α-SMA was detected by RT-qPCR and Western blot. α-SMA expression was observed by immunofluorescence. MeRIP-qPCR was used to detect m6A levels of MEG3. RNA stability experiments were conducted to determine the residual level of MEG3. The bindings of lncRNA MEG3 to c-MYC and c-MYC to the SMAD2 promoter were analyzed. Results showed that METTL3, c-MYC, and SMAD2 were highly expressed in VMC cell models. METTL3 inhibition increased cell viability and reduced LDH, CK-MB, TGF-β1, Collagen I, Collagen III, and α-SMA. METTL3-mediated m6A modification promoted MEG3 expression, and MEG3 bound to c-MYC and enhanced SMAD2 expression. Overexpression of MEG3 or SMAD2 partially reversed the inhibitory effect of METTL3 on fibrotic-like changes of myocardial cells. In conclusion, METTL3 promotes fibrotic-like changes of myocardial cells in VMC cell models through the lncRNA MEG3/c-MYC/SMAD2 axis via m6A modification.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153117"},"PeriodicalIF":2.3,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145119338","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":"TRIM59 alleviates acute respiratory distress syndrome by regulating inflammatory cytokines through RING domain","authors":"Zheng Jin ,&nbsp;Xiaopeng Jing ,&nbsp;Ji Zeng ,&nbsp;Zhenhua Zhu","doi":"10.1016/j.imbio.2025.153116","DOIUrl":"10.1016/j.imbio.2025.153116","url":null,"abstract":"<div><div>Acute respiratory distress syndrome (ARDS) is characterized by significant morbidity and mortality. Particularly since the outbreak of COVID-19, the incidence and complexity of ARDS have been further highlighted. The etiology and pathogenesis of ARDS are multifactorial, involving complex interactions among genetic, environmental, and host factors. Further exploration of these factors is essential to enhance our understanding of ARDS and to develop more effective therapeutic strategies. Alveolar macrophages (AMs) are the first line of defense of innate immunity and are key to regulate the immune system, and are closely related to cytokine storm in ARDS. Therefore, macrophages are an important part to alleviate ARDS. TRIM59 is a molecule expressed on macrophages. Our previous studies have shown that TRIM59 was capable of modulating macrophage function. However, the role of TRIM59 in the pathogenesis and progression of ARDS remains to be elucidated. In this study, we established an animal model of ARDS using mice in which TRIM59 was specifically knocked out in bone marrow-derived macrophages (BMDMs). Our results confirmed that TRIM59 exerted a protective effect against ARDS in vivo via its regulation on macrophages. Mechanistic investigations revealed that TRIM59 inhibited the activation of the nuclear factor-κB (NF-κB) signaling pathway through its RING domain. In summary, the present findings indicate that TRIM59 may serve as a crucial regulatory molecule in the ARDS, potentially offering a novel therapeutic target for its alleviation.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153116"},"PeriodicalIF":2.3,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145119336","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":"Pan-cancer analysis of GINS1 identifies its prognostic and immunotherapy predictive value with in vitro experimental validation in nasopharyngeal carcinoma","authors":"Yang Xu ,&nbsp;Qingqing Zhang ,&nbsp;Wanting Qin ,&nbsp;Zhiyu Yan ,&nbsp;Shuhan Ma ,&nbsp;Yuanyuan Chang ,&nbsp;Kaihua Chen ,&nbsp;Ling Li ,&nbsp;Xiaodong Zhu","doi":"10.1016/j.imbio.2025.153114","DOIUrl":"10.1016/j.imbio.2025.153114","url":null,"abstract":"<div><h3>Background</h3><div>GINS complex subunit 1 (GINS1) is part of the tetrameric GINS complex involved in DNA replication, playing a vital role in controlling the start and continuation of DNA replication. Its role in cancer, however, is not well understood. Still, its relevance to cancer is uncertain. This study focused on exploring the role of GINS1 in different forms of cancer.</div></div><div><h3>Methods</h3><div>Using a range of publicly available databases, we conducted a comprehensive study on the oncogenic function of GINS1 in pan-cancer through analyses of differential expression, survival, enrichment, gene mutations and tumor immune cell infiltration. Additionally, the expression and effects of GINS1 in nasopharyngeal carcinoma (NPC) were analyzed through a series of in vitro experiments.</div></div><div><h3>Results</h3><div>GINS1 was found to be overexpressed in nearly all tumors, demonstrating notable diagnostic and prognostic potential. Moreover, the relationship between GINS1 and specific immune characteristics (such as immune cell infiltration, immune checkpoint genes, tumor mutational burden, and microsatellite instability) suggests its potential role in guiding immunotherapy approaches. In vitro studies show that GINS1 notably enhances proliferation, migration, and invasion of NPC cells, with elevated expression levels correlating with a poorer prognosis.</div></div><div><h3>Conclusions</h3><div>GINS1 might serve as a prognostic and immunotherapy marker for different types of cancers, such as nasopharyngeal carcinoma.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153114"},"PeriodicalIF":2.3,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145059940","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":"Mechanism of astragaloside IV enhancing the sensitivity of non-small cell lung cancer to bevacizumab via the lncRNA-PVT1/miR-361-3p/HMGB1 axis","authors":"Mingfang Huang,&nbsp;Dewei Wang,&nbsp;Fengxia Chen,&nbsp;Liang Li","doi":"10.1016/j.imbio.2025.153115","DOIUrl":"10.1016/j.imbio.2025.153115","url":null,"abstract":"<div><h3>Objective</h3><div>This study investigated how astragaloside IV (AST-IV) enhances the responsiveness of non-small cell lung cancer (NSCLC) to bevacizumab (BV) via the lncRNA-PVT1/miR-361-3p/HMBG1 axis.</div></div><div><h3>Methods</h3><div>Human NSCLC A549 cells were cultured in vitro. oe-NC, A549 cells were transfected with oe-PVT1, oe-HMGB1, mimics NC, and mimics miR for 24 h using transfection reagents and then treated with 50 ng/mL AST-IV and 25 μmol/L BV for 24 h. Expression levels of PVT1, miR-361-3p, and HMGB1 were quantified by RT-qPCR, while protein levels of HMGB1, Ki67, Bax, and Cleaved-caspase-3 were examined through western blot analysis. Proliferation was measured using the CCK-8 assay, and apoptosis was assessed via flow cytometry. The targeting interactions between PVT1 and miR-361-3p, as well as miR-361-3p and HMGB1 were predicted by the BiBiServ2 database and verified by the luciferase reporter assay.</div></div><div><h3>Results</h3><div>AST-IV and BV-treated A549 cells exhibited significantly inhibited cell proliferation and Ki67/lncRNA-PVT1 expression levels while enhancing apoptosis and upregulating miR-361-3p and Bax and Cleaved-caspase-3. Co-treatment of AST-IV and BV enhanced the sensitivity of A549 cells to BV, further promoted apoptosis, and inhibited cell proliferation. Overexpression of lncRNA-PVT1 down-regulated miR-361-3p levels and partially reversed the promotional effect of AST-IV and BV on the sensitivity of A549 cells to BV. On the basis of overexpression of lncRNA-PVT1, upregulation of miR-361-3p expression significantly increased the sensitivity of A549 cells to BV. Binding interactions between lncRNA-PVT1 and miR-361-3p, as well as miR-361-3p and HMGB1, were confirmed through luciferase assays. Additionally, HMGB1 overexpression counteracted the suppressive effects of AST-IV and BV on A549 cell proliferation and resistance.</div></div><div><h3>Conclusions</h3><div>AST-IV increased miR-361-3p expression while suppressing HMGB1 via downregulation of lncRNA-PVT1, thereby enhancing BV sensitivity in NSCLC.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"230 6","pages":"Article 153115"},"PeriodicalIF":2.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085976","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}