Central European Journal of Immunology最新文献

{"title":"KLF14 restrained NLRP3-mediated pyroptosis in sepsis-induced acute lung injury by activating DTX3L","authors":"Xiuying Fan, Libin Tang, Jiawei Xia, Le Zhang, Yunzhen Li, Zhongxu Ma","doi":"10.5114/ceji.2025.158218","DOIUrl":"https://doi.org/10.5114/ceji.2025.158218","url":null,"abstract":"Introduction Acute lung injury (ALI) is characterized by inflammation of the lungs, leading to impaired gas exchange and respiratory distress. This study aimed to investigate the mechanisms underlying the role of Krüppel-like factor 14 (KLF14) in ALI pathogenesis. Material and Methods Protein and gene expression levels were quantified using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot. Cell viability and pyroptosis were assessed by Cell Counting Kit-8 (CCK-8) and flow cytometry. Interleukin (IL)-18 and IL-1 levels were measured by enzyme-linked immunosorbent assay (ELISA), while lactate dehydrogenase (LDH) activity was evaluated with a commercial assay kit. The interaction between Deltex E3 ubiquitin ligase 3-like (DTX3L) and KLF14 or nucleotide-binding domain like receptor 3 (NLRP3) was analyzed using chromatin immunoprecipitation (ChIP), co-immunoprecipitation (Co-IP), and dual-luciferase reporter assay. Results BEAS-2B cells treated with lipopolysaccharide (LPS) exhibited reduced viability and elevated pyroptosis-related markers. Notably, KLF14 upregulation suppressed NLRP3-mediated pyroptosis in LPS-induced cells. Similarly, DTX3L overexpression attenuated pyroptosis in LPS-treated BEAS-2B cells. Mechanistically, KLF14 enhanced DTX3L transcription, and DTX3L promoted NLRP3 degradation via ubiquitination. Furthermore, KLF14 upregulation inhibited NLRP3-driven pyroptosis by inducing DTX3L expression. Conclusions Upregulation of KLF14 inhibited NLRP3-mediated pyroptosis through DTX3L activation, thereby improving sepsis-induced acute lung injury.","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ceji.termedia.pl/pdf-207399-134844?filename=KLF14-restrained-NLRP3-me.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147904349","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}

{"title":"LncSLED1 inhibits monosodium urate-induced macrophage inflammation by promoting Cosmc methylation to upregulate CA72-4.","authors":"Ning Ren, Xiaojie Qu, Zhenzhen Wang, Xiaoning Zhang, Honglei Hu, Xueshan Bai","doi":"10.5114/ceji/205599","DOIUrl":"10.5114/ceji/205599","url":null,"abstract":"<p><strong>Introduction: </strong>The core event of gout is intensified macrophage inflammation. Our preliminary research found that carbohydrate antigen 72-4 (CA72-4) secreted by monosodium urate (MSU)-induced human synovial cells (HFLS) could upregulate transforming growth factor <i>β</i>1 (TGF-<i>β</i>1) in macrophages. Herein, the mechanism of MSU-induced abnormal upregulation of CA72-4 in HFLS was investigated.</p><p><strong>Material and methods: </strong>Cell viability was assessed by CCK-8 assay. The secretion levels of cytokines and CA72-4 were measured by ELISA. Methylation-specific PCR (MSP) was employed to detect the methylation level of the Cosmc promoter. The molecular interactions were analyzed by RIP and ChIP assays.</p><p><strong>Results: </strong>Our results demonstrated that CA72-4 derived from MSU-treated HFLS markedly inhibited MSU-induced macrophage inflammation. Mechanistically, MSU-induced lncSLED1 upregulation in HFLS reduced MSU-induced macrophage inflammation by promoting CA72-4 secretion. In addition, lncSLED1 facilitated CA72-4 secretion in MSU-treated HFLS by promoting the methylation level of the Cosmc promoter through recruiting EZH2. As expected, Cosmc silencing in HFLS reversed the weakening effect of lncSLED1 downregulation on mCM (the conventional medium from MSU-treated HFLS)-induced inhibition of MSU-induced macrophage inflammation.</p><p><strong>Conclusions: </strong>MSU elevated lncSLED1 in HFLS, boosting CA72-4 secretion by increasing Cosmc promoter methylation via EZH2 recruitment, thus reducing MSU-induced macrophage inflammation.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"95-107"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161355","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}

{"title":"CircHMGA2 facilitates proliferation and invasion of laryngeal squamous cell carcinoma cells and M2 macrophage polarization <i>via</i> the miR-384/ROCK1 axis.","authors":"Zhenjun Wang, Ping Wu, Li Li, XianHua Zhu, Yueyong Xiao","doi":"10.5114/ceji/207758","DOIUrl":"10.5114/ceji/207758","url":null,"abstract":"<p><strong>Introduction: </strong>Laryngeal squamous cell carcinoma (LSCC) is a malignant tumor of the head and neck. CircRNA High Mobility Group AT-hook 2 (circHMGA2) has cancer-promoting functions. Nevertheless, the role of circHMGA2 in LSCC has not been reported yet. We attempted to illustrate the function and mechanism of circHMGA2 in LSCC.</p><p><strong>Material and methods: </strong>The clinicopathological association between circHMGA2 and LSCC was assessed via the chi-square test. The correlation between circHMGA2 and LSCC patient survival time was determined with Kaplan-Meier analysis. Quantitative real-time PCR was applied to determine circHMGA2 expression in LSCC. Cell Counting Kit-8 assay, Western blot, cell invasion, enzyme-linked immunosorbent assay, and co-culture assays were conducted to evaluate circHMGA2 function in LSCC. Dual-luciferase reporter assay and RNA pull-down were performed to explore the role of circHMGA2 in LSCC. Meanwhile, circHMGA2 function in vivo was evaluated using tumor xenograft experiments, hematoxylin-eosin staining, and immunohistochemical assays.</p><p><strong>Results: </strong>CircHMGA2 was raised in LSCC, and elevated circHMGA2 expression was associated with TNM stage of LSCC patients. Patients with elevated circHMGA2 levels had shorter overall survival. Functionally, circHMGA2 knockdown suppressed LSCC cell proliferation and invasion. Also, circHMGA2 knockdown inhibited M2 macrophage polarization. Mechanistically, circHMGA2 targeted miR-384, and miR-384 targeted ROCK1. Also, ROCK1 level was negatively associated with miR-384 in LSCC tissues, but positively associated with circHMGA2. Moreover, rescue experiments suggested that circHMGA2 knockdown ameliorated LSCC growth via miR-384/ROCK1 and suppressed M2 macrophage polarization through miR-384/ROCK1. Meanwhile, circHMGA2 knockdown inhibited LSCC growth in vivo.</p><p><strong>Conclusions: </strong>CircHMGA2 acts as a competing endogenous RNA, promoting LSCC progression through the miR-384/ROCK1 axis.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"167-183"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863571","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}

{"title":"The AGO2-ATOX1 axis exacerbates inflammation in a mouse sepsis model.","authors":"Peng Huang, Meiling He, Xiangyang Mo, Lipu Deng","doi":"10.5114/ceji/209136","DOIUrl":"10.5114/ceji/209136","url":null,"abstract":"<p><strong>Introduction: </strong>The study aimed to investigate the mechanism of the Argonaute RISC catalytic component 2 (AGO2)-antioxidant protein 1 (ATOX1) axis in the inflammatory response of sepsis.</p><p><strong>Material and methods: </strong>AGO2 was knocked down by tail vein injection of sh-Ago2 lentivirus, and a sepsis mouse model was established using the cecal ligation and puncture (CLP) method. RAW264.7 cells were transfected with AGO2 or ATOX1 knockdown or overexpression plasmids and treated with lipopolysaccharide (LPS) to construct a cellular sepsis model. Hematoxylin-eosin staining was used to evaluate lung and liver tissue damage in mice. Serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured using biochemical analysis. ELISA was performed to determine the levels of inflammatory cytokines: tumor necrosis factor <i>α</i> (TNF-<i>α</i>), interleukin (IL)-6, and IL-1 <i>β</i>. The expression of AGO2, ATOX1, inducible nitric oxide synthase (iNOS), and arginase 1 (Arg1) was analyzed using RT-qPCR and Western blotting. The effect of AGO2 on ATOX1 mRNA stability was assessed using an actinomycin D assay, and the interaction between AGO2 and ATOX1 was analyzed via RIP-qPCR.</p><p><strong>Results: </strong>AGO2 and ATOX1 were highly expressed in septic mice. In vitro experiments demonstrated that knockdown of AGO2 or ATOX1 suppressed LPS-induced inflammatory responses and macrophage polarization imbalance. AGO2 promoted M1 macrophage polarization and aggravated inflammatory damage by enhancing the stability of ATOX1 mRNA. In vivo experiments further confirmed that AGO2 knockdown significantly alleviated sepsis-induced lung and liver damage, reduced the inflammatory response, and inhibited ATOX1 expression.</p><p><strong>Conclusions: </strong>AGO2 binds to ATOX1 mRNA, promoting ATOX1 expression, inducing macrophage polarization imbalance, and exacerbating sepsis-induced inflammatory responses.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"133-147"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863661","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}

{"title":"When protein stability drives tumor progression.","authors":"Jacek Tabarkiewicz, Paulina Niedźwiedzka-Rystwej, Marlena Tynecka, Andrzej Eljaszewicz","doi":"10.5114/ceji/221492","DOIUrl":"10.5114/ceji/221492","url":null,"abstract":"","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"1-2"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161810","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}

{"title":"Expanded dendritic cells loaded with placental gp96 to generate antigen-specific T cells for anti-tumor immunity: an <i>in vitro</i> study.","authors":"Chengshi Lin, Yu Lin, Pingqing Lin, Nengping Huang, Yongqing Ye","doi":"10.5114/ceji/204676","DOIUrl":"10.5114/ceji/204676","url":null,"abstract":"<p><p>The therapeutic potential of cancer immunotherapy has been increasingly recognized, particularly in strategies that exploit the body's own immune system to target and eliminate tumor cells. One promising approach involves the use of dendritic cells (DCs) as powerful antigen-presenting cells to generate antigen-specific T cells capable of targeting cancer cells. In this study, we explore the use of placental gp96, a stress-induced protein overexpressed in various tumors, to prime expanded dendritic cells for the generation of antigen-specific T cells. The expanded DCs, loaded with placental gp96, were shown to induce potent anti-tumor immunity in vitro, as evidenced by the strong T cell proliferation, activation, and cytotoxicity against cancer cell lines such as MCF-7, glioblastoma cell line U87MG and the neuroblastoma cell line SH-SY5Y. Notably, placental gp96-loaded DCs induced significantly higher cytotoxicity (67-71%) against tumor cell lines compared to recombinant gp96 (23-26%, p < 0.001), underscoring its clinical potential. This activity may be mediated by various tumor-associated peptides presented on the placental gp96. Moreover, this anti-tumor effect is MHC-restricted. These findings suggest that placental gp96-loaded expanded DCs hold significant promise as a novel immunotherapy strategy for cancers.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"148-157"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863584","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}

{"title":"Lymphocyte variant hypereosinophilic syndrome with severe eosinophilic pneumonia treated with mepolizumab: a case report.","authors":"Yubin Wang, Yuhan Tao, Hui Mao","doi":"10.5114/ceji/213650","DOIUrl":"10.5114/ceji/213650","url":null,"abstract":"<p><p>Lymphocyte variant hypereosinophilic syndrome (L-HES) is a rare disorder characterized by immunophenotypically abnormal T lymphocytes that produce excessive eosinophilopoietic cytokines, such as interleukin 5 (IL-5). Clinically, patients with L-HES can present with manifestations involving multiple organ systems, most commonly cutaneous lesions; however, isolated single-organ involvement excluding the skin is less common. The optimal treatment for L-HES remains poorly defined. Corticosteroids (CS) are often used as first-line therapy, while other agents - such as interferon <i>α</i> (IFN- <i>α</i>), anti-IL-5 monoclonal antibodies, cyclosporine, and mycophenolate - are also employed in steroid- refractory cases, although no standardized treatment consensus has been established. Here, we report a rare case of L-HES presenting severe eosinophilic pneumonia (EP) as the sole manifestation. After experiencing relapses during treatment with CS and IFN- <i>α</i>, the patient achieved a complete and favorable clinical response following initiation of low-dose mepolizumab - an anti-IL-5 monoclonal antibody - suggesting that mepolizumab may represent an effective therapeutic option for patients with L-HES complicated by EP.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"27-30"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161389","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}

{"title":"Glutaminolysis as a metabolic checkpoint of protective Th1/Th17 immunity against <i>Mycobacterium tuberculosis</i>.","authors":"Urszula Radzikowska, Sylwia Smolińska, Marlena Tynecka, Andrzej Eljaszewicz","doi":"10.5114/ceji/226300","DOIUrl":"10.5114/ceji/226300","url":null,"abstract":"","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"109-110"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863658","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}

{"title":"Interleukin 33 regulates the autophagy of oxygen-glucose-deprivation/reoxygenation microglia <i>via</i> macrophage polarization.","authors":"Fan Yong, Lin Lili, Huang Kailiang, Lin Jinying, Xu Junping, Zhou Xiaohui, Yang Yongkai","doi":"10.5114/ceji.2025.156132","DOIUrl":"10.5114/ceji.2025.156132","url":null,"abstract":"<p><strong>Introduction: </strong>Interleukin (IL)-33 is a pleiotropic cytokine in the immune system and inflammatory responses, which is involved in cerebral ischemia/reperfusion (I/R) injury. Evidence indicates that IL-33 plays an essential role in macrophage polarization activation, yet the potential molecular mechanisms remain elusive. This study explored the role of IL-33 in the activation of microglia/macrophage-mediated autophagy for cerebral I/R injury via in vitro experiments.</p><p><strong>Material and methods: </strong>Primary macrophages were harvested from mouse bone marrow, and microglia were isolated from mouse brains. Lipopolysaccharide (LPS) and interferon <i>γ</i> (IFN-<i>γ</i>) induced polarization toward the M1 phenotype macrophage, and IL-4 induced polarization toward the M2 phenotype macrophage. Oxygen glucose deprivation/reoxygenation (OGD/R) models of primary microglia were established and co-cultured with M1 and M2 macrophages, respectively. The IL-33 knockout microglia OGD/R model and M1/M2 macrophages were co-cultured to explore the effects of IL-33 in the transformation from pro-inflammatory (M1) phenotype to anti-inflammatory (M2) phenotype against inflammation and autophagy. Microglial activation/polarization, autophagy, and inflammation were detected using western blot, immunofluorescence, and ELISA.</p><p><strong>Results: </strong>Compared with microglia co-cultured with M1 macrophages, microglia co-cultured with M2 macrophages showed significantly higher expression of M2 intracellular markers (STAT6, PPAR-<i>γ</i>, IRF4, CEBP-<i>β</i>, and CD206 (p < 0.05). In contrast, the expression of STAT1 and IRF8 was significantly lower. IL-33 deficiency enhanced the anti-inflammatory phenotype of microglia/M2 macrophages. Furthermore, the expression of IL-10 and transforming growth factor <i>β</i> (TGF-<i>β</i>) was upregulated (p < 0.05), and the expression of IFN-<i>γ</i> was downregulated (p < 0.05) in microglia/M2 macrophages in comparison with microglia/M1 macrophages. Compared with the OGD/R model group, M1 macrophage co-culture increased Beclin-1 and ULK1 expression and reduced P62 expression, and M2 co-culture as well as IL-33 deletion reduced Beclin-1 and ULK1 expression and increased P62 expression levels.</p><p><strong>Conclusions: </strong>IL-33 deficiency inhibited hypoxia-induced microglia autophagy and promoted macrophage polarization toward the anti-inflammatory phenotype.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"84-94"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162113","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}

{"title":"N6-methyladenosine modification of CBLB affects LPS-induced endoplasmic reticulum stress in alveolar epithelial cells.","authors":"Bing Huang, Fangwei Chen, Guochao He, Yanchao Liang, Cancan Xie","doi":"10.5114/ceji.2025.157955","DOIUrl":"10.5114/ceji.2025.157955","url":null,"abstract":"<p><strong>Introduction: </strong>Acute lung injury (ALI) is defined as an acute hypoxic respiratory insufficiency that arises from injury to alveolar epithelial cells. The suppression of endoplasmic reticulum stress (ERS) was reported to protect against ALI. This study investigated the mechanism of N6-methyladenosine (m6A)-modified Casitas B lymphoma-b (CBLB) on ERS in lipopolysaccharide (LPS)-induced type II alveolar epithelial cells (AECIIs).</p><p><strong>Material and methods: </strong>AECII viability was evaluated via Cell Counting Kit-8 (CCK-8). The reactive oxygen species (ROS) level was examined via an ROS kit. TUNEL staining was applied to assay apoptosis. The levels of CBLB, LIM domain kinase 1 (LIMK1), methyltransferase-like 14 (METTL14), and ERS-related proteins were assessed by western blot and immunofluorescence. The ubiquitination level of LIMK1 was analyzed using immunoprecipitation. The interrelationship between CBLB and LIMK1 was identified via Co-IP. The m6A modification of CBLB was analyzed through MeRIP. The binding of METTL14 to the CBLB mRNA was verified by RIP.</p><p><strong>Results: </strong>CBLB facilitated the ubiquitination and degradation of LIMK1. The suppressive action of upregulated CBLB on apoptosis and ERS in LPS-induced AECIIs was reversed by LIMK1 overexpression. METTL14 reduced the stability of CBLB mRNA in a manner dependent on m6A methylation. CBLB knockdown reversed the inhibitory effects of METTL14 silencing on apoptosis and ERS in LPS-stimulated AECIIs.</p><p><strong>Conclusions: </strong>METTL14-mediated m6A modification of CBLB impaired the mRNA stability of CBLB to block the degradation of LIMK1, which promoted ERS in LPS-induced AECIIs.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"3-15"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161383","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}