Cellular immunology最新文献

{"title":"METTL3 positively regulates the development and cytotoxicity of human embryonic stem cells-derived NK cells.","authors":"Xiaofeng Yin, Zhaohui Zhang, Jiaxing Qiu, Yuxing Gong, Qinghua Bi, Meng Meng, Qiangqiang Lai, Hongchen Wang, Shaochang Zhou, Yuan Gao, Lingling Zhang, Wei Wu, Liang Song, Junping Wang, Fangjie Wang, Zhaoyang Zhong, Youcai Deng","doi":"10.1016/j.cellimm.2025.105011","DOIUrl":"10.1016/j.cellimm.2025.105011","url":null,"abstract":"<p><p>Human embryonic stem cell-derived NK (hESC-NK) cells or induced pluripotent stem cell derived NK cells have demonstrated efficacy and safety in clinical trials for cancer therapy and serve as a valuable tool for studying the mechanisms of human NK cell development and effector functions. We previously demonstrated that the methylase METTL3 was essential for the development and effector functions of murine NK cells, but its role in human NK cells remained unknown. Herein, we constructed an H1 ESC strain with reduced METTL3 expression using lentivirus-delivered short hairpin (sh) RNA and generated hESC-NK cells via a two-stage differentiation system. Our findings demonstrated that METTL3 knockdown in hESCs reduced the proportion of hematopoietic stem and progenitor cells (HSPCs, CD34⁺ cells) during embryoid bodies (EBs) formation, and impaired subsequent differentiation into mature NK cells. Moreover, ESC-NK cells derived from shMETTL3-ESC (called shMETTL3-ESC-NK) showed impaired anti-tumor activity, evidenced by downregulation of mRNA and protein levels of critical effectors (perforin, granzyme B and IFN-γ) and reduced cytotoxicity against target cells. Furthermore, both mRNA and protein levels of T-BET and EOMES were significantly down-regulated in shMETTL3-ESC-NK cells. These transcription factors are critical for NK cell development and cytotoxicity, and their downregulation may underlie the maturation defects of shMETTL3-ESC-NK cells. Collectively, our study elucidates that METTL3 promotes the development, maturation and cytotoxicity of hESC-NK cells, recapitulating previous reports in murine NK cells.</p>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"415-416 ","pages":"105011"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144803699","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":"Identification of Epstein-Barr virus nuclear antigen 1 (EBNA1)-specific T-cell receptors: implications for immunotherapy targeting EBV-associated malignancies","authors":"Ying Liu ,&nbsp;Yaqi Pan ,&nbsp;Huirong Ding ,&nbsp;Wei He ,&nbsp;Huanyu Chen ,&nbsp;Zhe Hu ,&nbsp;Zheming Lu ,&nbsp;Yang Ke","doi":"10.1016/j.cellimm.2025.105002","DOIUrl":"10.1016/j.cellimm.2025.105002","url":null,"abstract":"<div><h3>Background</h3><div>Epstein-Barr virus nuclear antigen (EBNA1) is uniquely expressed across all three EBV latency types, making it an ideal target for TCR-engineered T-cell therapy against EBV-associated malignancies. However, preparation of EBNA1-specific TCR-T cells, particularly for EBV latency I type, remains exploratory.</div></div><div><h3>Methods</h3><div>EBNA1-specific T cells were stimulated using autologous dendritic cells (DCs) pulsed with peptides synthesized from the complete sequence (except the glycine-alanine repeat region) of the EBNA1 of EBV strain B95–8. For pre-stimulated and post-stimulated T cells, candidate EBNA1-specific TCRs with significantly increased frequencies were identified using high-throughput single-cell TCR V(D) J sequencing. The functionality of EBNA1-specific TCR-engineered T cells was assessed <em>in vitro</em> against lymphoblastoid cell lines (LCLs) and EBNA1 peptide-pulsed DCs.</div></div><div><h3>Results</h3><div>EBNA1-specific T cells were successfully expanded. Candidate EBNA1-specific TCRs were isolated, corresponding TCR gene sequences were constructed and introduced into peripheral blood T cells. Engineered T cells expressing EBNA1-specific TCR demonstrated specific recognition of EBNA1 presented by autologous LCLs and DCs <em>in vitro</em>.</div></div><div><h3>Conclusions</h3><div>This study establishes the feasibility of expanding functional EBNA1-specific TCR-T cells, providing a foundation for adoptive cell therapy targeting all EBV-associated malignancies, including latency I.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"415 ","pages":"Article 105002"},"PeriodicalIF":2.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757208","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":"Establishing a clinical prediction model of neurosyphilis via a lumbar-puncture-free nomogram","authors":"Xuebi Wang ,&nbsp;Wei Wang ,&nbsp;Yabin Liu ,&nbsp;Peng Wang ,&nbsp;Qin Huang ,&nbsp;Di Tian ,&nbsp;Yixin Liao ,&nbsp;Zhigang Yi ,&nbsp;Feng Li ,&nbsp;Yuanjia Tang ,&nbsp;Chen Zhao ,&nbsp;Xiaohong Fan ,&nbsp;Yun Ling","doi":"10.1016/j.cellimm.2025.105012","DOIUrl":"10.1016/j.cellimm.2025.105012","url":null,"abstract":"<div><h3>Objectives</h3><div>Neurosyphilis (NS) can cause a range of central nervous system (CNS) damage, from asymptomatic states to severe mental disorders. While lumbar puncture is a reliable diagnostic method for NS, it is often poorly accepted due to its invasive nature, particularly by patients with mild symptoms. This study aims to develop a prediction model for the early diagnosis of NS that without requiring lumbar puncture.</div></div><div><h3>Methods</h3><div>Clinical data, including imaging, routine blood tests, immune markers, HIV status and cerebrospinal fluid (CSF) examination, were collected from the Shanghai Public Health Clinical Center from 2021 to 2023,. The dataset was randomly split into training and validation sets in an 8:2 ratio. Univariate analysis, the least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression were used to identify significant predictors.</div></div><div><h3>Results</h3><div>Out of 1078 suspected patients, 702 confirmed syphilis patients with positive <em>Treponema pallidum</em> specific antibody (anti-TP) and positive <em>Treponema Pallidum</em> Particle Agglutination (TRUST) in serum were selected. Among them, 246 patients were diagnosed as NS based on the positive anti-TP in CSF, while 456 patients were classified as non-neurosyphilis (NNS). In the NS group, cerebral ischemia/infarction, ataxia, decreased vision, mental/behavioral disorders, memory impairment, high levels of anti-TP and TRUST (&gt;1:16), elevated red blood cell (RBC) and platelet (PLT) counts, and shorter prothrombin time (PT) were identified. A nomogram was established based on independent prognostic factors. The receiver operating characteristic (ROC) curves and calibration curves showed high predictive accuracy, and clinical decision curve analysis (DCA) indicated good clinical applicability.</div></div><div><h3>Conclusions</h3><div>The developed nomogram offers a reliable and non-invasive method for early identification of NS in syphilis patients, regardless of their HIV or immune status.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"415 ","pages":"Article 105012"},"PeriodicalIF":2.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865995","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":"Chloroquine treatment ameliorates experimental autoimmune encephalomyelitis by inhibiting T cell differentiation and pDC accumulation","authors":"Yonghai Li ,&nbsp;Yue Shao ,&nbsp;Xianfen Ma ,&nbsp;Yaning Li ,&nbsp;Yijia Yang ,&nbsp;Fengyuan Wang ,&nbsp;Yushan Yan ,&nbsp;Xiaoxi Hu ,&nbsp;Yujie Dai ,&nbsp;Meng Li ,&nbsp;Max Löhning ,&nbsp;Ping Shen ,&nbsp;Juntang Lin","doi":"10.1016/j.cellimm.2025.105010","DOIUrl":"10.1016/j.cellimm.2025.105010","url":null,"abstract":"<div><h3>Objectives</h3><div>Chloroquine (CQ) has been used to treat rheumatoid arthritis and systemic lupus erythematosus, but its use in multiple sclerosis (MS) is limited by side effects and insufficient efficacy. To enhance treatment outcomes, understanding CQ's therapeutic mechanisms in MS is crucial. Thus, we administered CQ to mice with experimental autoimmune encephalomyelitis (EAE) and investigated its disease-ameliorating effects and underlying cellular mechanisms.</div></div><div><h3>Methods</h3><div>CQ was applied intraperitoneally six days after EAE induction, immune responses, with a focus on inflammatory and regulatory T cells, as well as dendritic cells in blood, lymph nodes, spleen, and bone marrow were analyzed by flow cytometry.</div></div><div><h3>Results</h3><div>CQ treatment significantly reduced cumulative disease score and maximal disease score in CQ-treated group. Immunohistochemical analysis of the spinal cords confirmed the reduced demyelination after CQ treatment, which is accompanied by significantly decreased infiltration of T cells, B cells, and macrophages, and less activated microglia cells. Flow cytometry analysis of peripheral lymphoid organs revealed a significant decrease of inflammatory Th17 cells, which is associated with reduced pDC and their IFN-α expression, as well as Treg cells in CQ-treated mice. Indeed, depletion of pDC alone or simultaneously with CQ treatment significantly reduced EAE severity.</div></div><div><h3>Conclusion</h3><div>Our results demonstrated that CQ treatment inhibits the development of EAE disease on one hand by enhancing the expansion of Treg in dLN and spleen, and on the other hand by inhibiting the accumulation of pDC and their IFN-α expression in the spleen and bone marrow. This joint effort restricts the level of inflammation in peripheral and later in CNS. Furthermore, developing a pDC-targeted CQ treatment will not only increase the treatment efficiency, but also largely decrease side effects.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"415 ","pages":"Article 105010"},"PeriodicalIF":3.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144679089","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":"Sfrp2-deficient colonic fibroblasts drive mucosal inflammation and epithelial injury in ulcerative colitis","authors":"Mengyuan Zhu ,&nbsp;Zhanqiu Diao ,&nbsp;Lei Hu ,&nbsp;Zhipeng Fan","doi":"10.1016/j.cellimm.2025.105003","DOIUrl":"10.1016/j.cellimm.2025.105003","url":null,"abstract":"<div><div>Ulcerative colitis (UC) is a chronic inflammatory disorder targeting the colon, which remains clinically challenging due to limited targeted therapies. Although intestinal fibroblasts have emerged as critical regulators of mucosal immunity and tissue repair, their molecular mechanisms in UC pathogenesis are poorly defined. Here, we investigate the functional role of secreted frizzled-related protein 2 (SFRP2, a Wnt signaling modulator) knockdown fibroblasts in immune homeostasis and the severity of UC using <em>Sfrp2</em>^{<em>flox/flox</em>}; <em>Col1a2</em>-Cre mice (fibroblast-specific knockout). In the dextran sulfate sodium (DSS)-induced colitis model, we found SFRP2 in fibroblasts have negative correlation with the severity of UC. That <em>Sfrp2</em>^{<em>Col1a2</em>} CKO mice exhibited exacerbated colitis symptoms and accelerated inflammatory progression, and showed increased ratio of Th17 cells and decreased ratio of Treg cells. These findings revealed that <em>Sfrp2</em> in fibroblasts plays a crucial role in protecting against inflammatory responses and T-cell immune dysregulation. Therefore, <em>Sfrp2</em> may serve as a potential therapeutic target for UC treatment.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"415 ","pages":"Article 105003"},"PeriodicalIF":3.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144653934","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":"Enhancing the antitumor activity of CD19/BCMA CAR-T cells in vitro with a PD1IL7R chimeric switch receptor","authors":"Kai Yan,&nbsp;Zhongdang Xiao","doi":"10.1016/j.cellimm.2025.105001","DOIUrl":"10.1016/j.cellimm.2025.105001","url":null,"abstract":"<div><div>Chimeric antigen receptor (CAR)-T cell therapy has revolutionized the treatment of hematologic malignancies, but its long-term efficacy is hindered by antigen escape, T-cell exhaustion, and the immunosuppressive tumor microenvironment (TME). Programmed death ligand 1 (PD-L1) expression in the TME inhibits CAR-T cell function, limiting persistence and cytotoxic capacity. To address this, we engineered CD19/BCMA-targeted CAR-T cells co-expressing a PD1IL7R chimeric switch receptor (CSR). This novel receptor converts PD-L1-mediated inhibitory signals into IL7R-driven pro-survival and proliferative pathways, enhancing CAR-T cell expansion, persistence, and cytotoxicity in a PD-L1–dependent but antigen-specific manner. In vitro, CD19/BCMA-PD1IL7R CAR-T cells exhibit improved central memory T-cell formation, increased cytokine secretion, and superior antitumor activity compared to conventional CAR-T cells. Notably, these functional enhancements were evident even at low levels of PD-L1 expression on target cells, and no off-target effects were observed. Our findings suggest that incorporating the PD1-IL7R switch receptor into CAR-T cells effectively overcomes PD-L1–mediated immunosuppression, enhancing both their persistence and antitumor efficacy. This approach offers a versatile strategy for improving CAR-T therapy in the treatment of both hematologic and solid tumors.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"415 ","pages":"Article 105001"},"PeriodicalIF":3.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144614817","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":"Acetyl-CoA subcellular compartmentalization regulates T cell adaptation","authors":"Annefien Tiggeler ,&nbsp;Paul J. Coffer","doi":"10.1016/j.cellimm.2025.105000","DOIUrl":"10.1016/j.cellimm.2025.105000","url":null,"abstract":"<div><div>Upon activation, naïve T cells undergo rapid proliferation and differentiation, giving rise to clonally expanded populations specifically tailored for an effective immune response. To meet the heightened bioenergetic and biosynthetic demands associated with activation, T cells adapt and reprogram both their metabolism and transcriptome. Beyond this, T cells are also able to dynamically adapt to fluctuations in the microenvironmental nutrient levels. While the adaptability of T cells is a well-established hallmark of their functionality, the molecular mechanisms by which metabolic responses underpin this flexibility remain incompletely defined. Acetyl-CoA, with its role as a central metabolite in mitochondrial ATP production, and a substrate for nuclear histone acetylation reactions, emerges as a key player in a metabolic-epigenetic axis. Recent evidence indicates that enzymes responsible for generating acetyl-CoA can translocate to the nucleus, supporting sub-cellular local acetyl-CoA production. Here, we explore the impact of acetyl-CoA metabolism on T cell functionality within different subcellular compartments and highlight the potential for intervention in acetyl-CoA metabolic pathways in T cell-driven autoimmune diseases and cancers.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 105000"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144563117","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":"Polymorphonuclear myeloid-derived suppressor cells protect against hyperoxia-induced bronchopulmonary dysplasia in neonatal mice through suppression of excessive inflammatory response","authors":"Boshi Yu,&nbsp;Guixuan Hong,&nbsp;Yubai Li,&nbsp;Xudong Yan,&nbsp;Zhangbin Yu","doi":"10.1016/j.cellimm.2025.104995","DOIUrl":"10.1016/j.cellimm.2025.104995","url":null,"abstract":"<div><h3>Background</h3><div>Bronchopulmonary dysplasia (BPD), which primarily affects premature infants, is characterized by impaired lung development, reduced alveolarization, and chronic inflammation, leading to long-term respiratory complications. However, clinical prevention treatment of BPD remains challenging. Because immune cells may have a role in BPD pathogenesis and prevention, we investigated whether polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) protect against hyperoxia-induced BPD in a neonatal mouse model.</div></div><div><h3>Methods</h3><div>Neonatal C57BL/6 mice were exposed to either normoxia (21 % oxygen) or hyperoxia (85 % oxygen) since birth. Lung development was analyzed on postnatal days 3, 7, and 14 by using histological techniques [hematoxylin and eosin (H&amp;E) staining and radial alveolar count (RAC) measurement]. Moreover, we used flow cytometry to identify lung myeloid-derived suppressor cell (MDSC) subsets. PMN-MDSCs' therapeutic potential at key developmental stages was evaluated through adoptive transfer experiments. PMN-MDSC transplantation outcomes in the lung tissues were assessed through histological analysis, immunofluorescence staining for alveolar and vascular markers, and proinflammatory cytokine measurement.</div></div><div><h3>Results</h3><div>Hyperoxia-exposed mice exhibited considerable lung damage, including enlarged and irregular alveoli, low RACs, and decreased body weights compared with normoxic controls. Hyperoxia reduced PMN-MDSC numbers but increased monocytic MDSC numbers. PMN-MDSC transplantation preserved alveolar structure and increased alveolar and pulmonary vessel numbers. Immunofluorescence staining confirmed enhanced alveolar and vascular development. Finally, PMN-MDSCs reduced proinflammatory cytokine levels in lung tissues.</div></div><div><h3>Conclusion</h3><div>PMN-MDSCs may protect against hyperoxia-induced lung injury by promoting alveolar and vascular development and reducing inflammation in neonatal mice. Further research elucidating precise mechanisms underlying the protective effects of PMN-MDSCs and their potential for clinical translation is warranted.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104995"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280815","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 “Modular activation of macrophage-like cells by beta-2-microglobulin via mitochondria and the cGAS-STING pathway” [Cell. Immunol. 413 (2025) 104962]","authors":"Josefine Kofoed Corneliussen ,&nbsp;Helena Borland Madsen ,&nbsp;Nadia Thaulov Zelander ,&nbsp;Mogens Holst Nissen ,&nbsp;Claus Desler","doi":"10.1016/j.cellimm.2025.104984","DOIUrl":"10.1016/j.cellimm.2025.104984","url":null,"abstract":"","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104984"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246663","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":"Aerobic exercise activates let-7e-5p through TP73-AS1 to inhibit the HMGB1/RAGE axis and alleviate asthma airway inflammation and remodeling","authors":"Dan Wang ,&nbsp;Jing Zhao ,&nbsp;Chunyan Yang ,&nbsp;Daogang Qin ,&nbsp;Dengna Zhu","doi":"10.1016/j.cellimm.2025.104990","DOIUrl":"10.1016/j.cellimm.2025.104990","url":null,"abstract":"<div><div>The rising incidence of asthma, a chronic respiratory condition, has been associated with the involvement of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in its pathogenesis. Nevertheless, there is a shortage of data pertaining to the impact of lncRNA TP73-AS1 and let-7e-5p on this disease. Therefore, we aimed to explore the possible effects of aerobic exercise (AE) on lncRNA TP73-AS1, let-7e-5p, inflammation, and high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) in asthma mouse models. HMGB1/RAGE was significantly upregulated in asthma mouse models using ovalbumin (OVA) stimulation. The overexpression of let-7e-5p, which was found to be significantly downregulated in asthma mouse models, appeared to inhibit EMT and might alleviate airway inflammation in asthmatic mice through the suppression of the HMGB1/RAGE pathway. Aerobic exercise was associated with reduced airway inflammation and remodeling in asthmatic mice, and appeared to suppress TP73-AS1 expression in asthma OVA-mouse models. Furthermore, TP73-AS1 may exacerbate airway inflammation and remodeling in OVA-induced asthmatic mice by downregulating let-7e-5p expression, which could activate the HMGB1/RAGE-NF-κB pathway. These findings suggest potential innovative approaches for asthma management, which warrant further validation.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"414 ","pages":"Article 104990"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240096","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}