Cellular immunology最新文献

{"title":"Lupeol mitigates spinal cord injury by modulating microglial M1/M2 polarization via Na+/K+-ATPase-mediated mitophagy","authors":"Ruyin Liu ,&nbsp;Zongjin Yue ,&nbsp;Jia'an Dong ,&nbsp;Cheng Zhang ,&nbsp;Chuanghao Guo ,&nbsp;Xinli Wang","doi":"10.1016/j.cellimm.2025.104955","DOIUrl":"10.1016/j.cellimm.2025.104955","url":null,"abstract":"<div><div>Spinal cord injury (SCI) often results in severe disability or even death, with inflammation playing a critical role in hindering recovery. Although Lupeol is known for its potent anti-inflammatory properties, its specific role in SCI-induced inflammation remains underexplored. In this study, an in vitro inflammation model was established using LPS-stimulated BV2 microglia. Lupeol treatment effectively counteracted LPS-induced reductions in Na⁺/K⁺-ATPase (NKA) activity, suppression of mitophagy, M1 polarization of microglia, release of inflammatory factors, and increased pyroptosis. Mechanistically, Lupeol alleviated microglial inflammation by enhancing mitophagy through the activation of NKA activity. Furthermore, Lupeol upregulated NKA activity and mitophagy by activating the AMPKα2-mTOR-TFEB pathway. In vivo, a mouse model of SCI was established, and Lupeol was administered daily via intraperitoneal injection. Lupeol treatment significantly reduced neuronal loss, promoted microglial polarization from the M1 to the M2 phenotype, attenuated inflammation, and improved motor function recovery in SCI mice. In conclusion, Lupeol promotes mitophagy by enhancing NKA activity via the AMPK–mTOR–TFEB pathway, thereby suppressing the pro-inflammatory phenotype of microglia and mitigating SCI progression.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104955"},"PeriodicalIF":3.7,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143869303","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":"Aged mice-derived bronchial epithelial cells regulate Th17 cell differentiation in asthma via the MBD2-sICOSL axis","authors":"Zhifeng Chen ,&nbsp;Yulin Shang ,&nbsp;Yu Yuan ,&nbsp;Xiaoying Ji ,&nbsp;Subo Gong ,&nbsp;Qingping Zeng ,&nbsp;Xudong Xiang","doi":"10.1016/j.cellimm.2025.104954","DOIUrl":"10.1016/j.cellimm.2025.104954","url":null,"abstract":"<div><div>Th17 cells are involved in the pathogenesis of elderly asthma. Bronchial epithelial cells (BECs) can act as antigen-presenting cells, and our previous studies have shown that methyl-CPG binding domain protein 2 (MBD2) in BECs can promote Th17 cell differentiation in asthma. However, the effect of BECs from different age groups (young and old) on Th17 cells remains unclear. In this study, BECs were co-cultured with CD4⁺ T cells, and it was found that BECs from young mice promoted the biased differentiation of Th2 cells, while BECs from older mice facilitated the biased differentiation of Th17 cells. Interestingly, MBD2 was highly expressed in BECs from older mice compared to BECs from young mice. MBD2 silencing induced inhibition of Th17 cell differentiation, while MBD2 overexpression reversed this change and promoted Th cell differentiation into Th17 cells. Soluble inducible T cell costimulator ligand (sICOSL) is mainly involved in the regulation of T cells after activation. In this study, we found that sICOSL levels were lower in BECs of old mice compared to BECs of young mice. Mechanistically, sICOSL levels increased with MBD2 silencing and decreased with MBD2 overexpression. As expected, the addition of anti-sICOSL antibodies significantly enhanced Th17 cell differentiation and suppressed Th2 cell differentiation, while exogenous sICOSL supplementation promoted Th2 cell differentiation and inhibited Th17 cell differentiation. However, neither anti-sICOSL nor exogenous sICOSL affected the expression of MBD2. Taken together, these results suggest that BECs from older mice regulate Th17 cell differentiation via the MBD2-sICOSL axis. These findings provide new insights into the pathogenesis of Th17-activated asthma in elderly patients.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104954"},"PeriodicalIF":3.7,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843782","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":"Novel and effective tandem CD38 and CD19 targeting CAR-T cells inhibit hematological tumor immune escape","authors":"Xiuying Liu ,&nbsp;Yaru Feng ,&nbsp;Zhiru Song ,&nbsp;Jingjing Liu ,&nbsp;Zhiqiang Luo ,&nbsp;Guohua Yu ,&nbsp;Jianxun Wang","doi":"10.1016/j.cellimm.2025.104950","DOIUrl":"10.1016/j.cellimm.2025.104950","url":null,"abstract":"<div><div>Targeting CD19 with chimeric antigen receptor (CAR)-T cells is clinically effective, but tumor immune escape and tumor recurrence still occur. Designing CAR-T cells that target multiple antigens simultaneously is a viable approach for inhibiting tumor immune escape, and promising findings have been reported. In this study, we designed new CD19 and CD38 dual-target CAR-T cells that are strongly cytotoxic to target cells expressing CD19 or CD38. <em>In vitro</em> studies, compared with single-target CAR-T cells or CD19/CD38 tandem (Tan) CAR-T cells, CD38/CD19 Tan CAR-T cells presented similar CAR expression, superior cytotoxicity and antigen-stimulated T-cell proliferation. <em>In vivo</em> studies, CD38/CD19 Tan CAR-T cells demonstrated the same efficacy and safety as single-target CAR-T. These CD19/CD38 Tan CAR-T cells are fully compatible with existing clinical-grade T-cell manufacturing procedures and can be implemented using current clinical protocols. In summary, our findings provide an effective solution to the challenge of tumor immune escape in anti-CD19 CAR-T-cell therapy.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104950"},"PeriodicalIF":3.7,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834033","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 of CD44+CCR2+CD64−monocyte-derived macrophage in chronic rhinosinusitis with nasal polyps","authors":"Yuling Zhang ,&nbsp;Mengzhe Yang ,&nbsp;Yan Li ,&nbsp;Zaichuan Wang ,&nbsp;Shujian Zhang ,&nbsp;Limin Zhao ,&nbsp;Yingyue Liu ,&nbsp;Xinyi Li ,&nbsp;Xue Wang ,&nbsp;Feng Lan ,&nbsp;Luo Zhang","doi":"10.1016/j.cellimm.2025.104953","DOIUrl":"10.1016/j.cellimm.2025.104953","url":null,"abstract":"<div><div>Heterogeneity of monocyte-derived macrophages (MDMs) is gradually recognized in polyp tissue of chronic rhinosinusitis with nasal polyps (CRSwNP). However, the contributions of MDM subsets for sustaining inflammation remain unclear. This study therefore aimed to characterize MDM subsets in polyp tissues and estimate their functions. We identified MDM subsets in polyp tissues by flow cytometry, and analyzed the correlation between the expression of these subsets and disease severity. We also explored the similarities and differences between tissue MDMs and classical <em>ex vivo</em> polarized MDMs. By using appropriate substitutes for tissue MDMs, we investigated the function of MDMs. MDM1 (lin⁻CD44⁺CD64⁺) and MDM3 (lin⁻CD44⁺CCR2⁺CD64⁻) were identified in polyp tissues by flow cytometry. Recurrent CRSwNP patients exhibited higher levels of MDM3 compared to non-recurrent patients. This increase in MDM3 was positively correlated with the Lund-Mackay score, the number of infiltrated tissue eosinophils, and IL-5 expression levels. <em>Ex vivo</em> polarized alternatively activated (M2a) macrophage preferentially expressed MDM3 marker genes, which can be used as the substitute for MDM3 within the polyp tissues. M2a macrophages engulfed more <em>Staphylococcus aureus</em> than classically activated (M1) macrophages. However, interferon lambda 1 (IFN-λ1) did not alter the bacterial killing efficiency of M2a macrophages, nor did it affect the activation of reactive oxidase substrate (ROS) and signal transducer and activator of transcription 1 (STAT1) pathway and viability. The increase in MDM3 within polyp tissues, similar to classical M2a macrophages, acted as bacterial reservoirs and contributed to persistent inflammation, offering insights into the underlying mechanisms of CRSwNP.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104953"},"PeriodicalIF":3.7,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834034","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":"MAPK14 drives Ferroptosis and immune dysfunction in pediatric Sepsis-induced acute lung injury","authors":"Ning Zhang ,&nbsp;Yuanyuan Fan ,&nbsp;Juan Chen ,&nbsp;Juan Gu ,&nbsp;Xiangming Yan","doi":"10.1016/j.cellimm.2025.104948","DOIUrl":"10.1016/j.cellimm.2025.104948","url":null,"abstract":"<div><h3>Objective</h3><div>Sepsis-induced acute lung injury (ALI) is driven by inflammation, oxidative stress, and immune suppression. MAPK14 (p38α) plays a role in ferroptosis and immune regulation, but its specific function in pediatric sepsis remains unclear. Therefore, our study aimed to explore the role and underlying mechanism of MAPK14 in pediatric sepsis.</div></div><div><h3>Methods</h3><div>Bioinformatics analysis of GSE26440 and FerrDb identified ferroptosis-related genes in pediatric sepsis. STRING database was used to predict the proteins associated with MAPK14. MAPK14 expression in whole blood samples, LPS-treated MLE-12 cells, and a CLP mouse model was detected by qRT-PCR and western blot. Ferroptosis was assessed by measuring MDA, GSH, and Fe²⁺ levels, while ROS accumulation was analyzed using DCFH-DA staining and DHE staining. A cycloheximide (CHX) assay was performed to assess TTP53 protein stability. MPO immunohistochemistry and PD-L1 immunofluorescence assessed neutrophil infiltration, and flow cytometry evaluated neutrophil apoptosis.</div></div><div><h3>Results</h3><div>Bioinformatics analysis of GSE26440 and FerrDb identified MAPK14 as a ferroptosis-related gene in pediatric sepsis. MAPK14 expression was upregulated in sepsis patient samples, LPS-treated MLE-12 cells and CLP mouse lung tissues. Overexpression of MAPK14 led to increased MDA and Fe²⁺ levels, reduced GSH, and elevated ROS fluorescence intensity, confirming its role in promoting ferroptosis. Mechanistically, MAPK14 upregulated TTP53, which in turn suppressed SLC7A11 and GPX4, further driving ferroptosis. MAPK14 overexpression stabilized TTP53 and enhanced its activity. Additionally, MAPK14 enhanced MPO and PD-L1 expression to promote neutrophil infiltration and immune suppression. Additionally, MAPK14 overexpression inhibited neutrophil apoptosis, promoted neutrophil infiltration and enhanced immune suppression.</div></div><div><h3>Conclusion</h3><div>MAPK14 drives ferroptosis via the TTP53/SLC7A11/GPX4 pathway and exacerbates immune suppression by promoting neutrophil infiltration.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104948"},"PeriodicalIF":3.7,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807608","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":"A new chimeric protein composed by T-cell epitopes from peroxidoxin and pyridoxal kinase proteins is protective against visceral leishmaniasis","authors":"Daniela P. Lage ,&nbsp;Danniele L. Vale ,&nbsp;Marcela G.P. Silva ,&nbsp;Vívian T. Martins ,&nbsp;Ana A.M. Gonçalves ,&nbsp;Kamila A. Silva ,&nbsp;Gabriel J.L. Moreira ,&nbsp;Rafaela D. Olegário ,&nbsp;Flávia C. Rizzatti ,&nbsp;Camila S. Freitas ,&nbsp;Breno L. Pimenta ,&nbsp;Karolina O.M. Falcão ,&nbsp;Saulo S.G. Dias ,&nbsp;João A. Oliveira-da-Silva ,&nbsp;Raquel S.B. Câmara ,&nbsp;Isabela A.G. Pereira ,&nbsp;Miguel A. Chávez-Fumagalli ,&nbsp;Bruno M. Roatt ,&nbsp;Ricardo A. Machado-de-Ávila ,&nbsp;Alexsandro S. Galdino ,&nbsp;Eduardo A.F. Coelho","doi":"10.1016/j.cellimm.2025.104949","DOIUrl":"10.1016/j.cellimm.2025.104949","url":null,"abstract":"<div><div>Visceral leishmaniasis (VL) is a neglected tropical disease caused by intracellular protozoan parasites, and which present high incidence in populations in the world. The diagnosis is difficult to be performed, and treatment is toxic and/or presents high cost. In this context, prophylactic vaccination could help as an effective control measure against the disease. In this study, a new chimeric protein (LAV) was constructed with immunogenic T-cell epitopes from two immunogenic <em>Leishmania</em> proteins, and it was evaluated to protects BALB/c mice against <em>Leishmania infantum</em> infection. For this, animals were vaccinated with rLAV associated with micelles (Mic) or monophosphoryl lipid A (MPLA) as adjuvants; while the others received saline, rLAV, Mic or MPLA as controls. Results showed that the rLAV/Mic and rLAV/MPLA combinations induced higher cell proliferation indexes in stimulated cell cultures after infection, as well as the development of a polarized Th1-type cellular and humoral response before and after infection, which was based on the production of IFN-γ, IL-12, TNF-α, nitrite, and IgG2a isotype antibodies. In addition, both CD4⁺ and CD8⁺ T-cell subtypes were important for the IFN- secretion in both groups, as compared to the others. Control groups mice produced significantly higher levels of IL-4, IL-10 and anti-parasite IgG1 antibodies, suggesting the occurrence of a Th2-type immune profile in these unprotected animals. The parasite load was found to be significantly lower in mice vaccinated with rLAV/MPLA or rLAV/Mic, as compared to the others, by using a limiting dilution assay and qPCR. In conclusion, data suggest that rLAV plus adjuvant could be considered as a vaccine candidate in future studies to protect against VL.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104949"},"PeriodicalIF":3.7,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791384","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":"Hyperoside suppresses NSCLC progression by inducing ATG13-mediated autophagy and apoptosis","authors":"Mingming Jin ,&nbsp;Yuqing Lou ,&nbsp;Xiaoshuo Wang ,&nbsp;Jia Lv ,&nbsp;Yue Wu ,&nbsp;Gang Huang","doi":"10.1016/j.cellimm.2025.104947","DOIUrl":"10.1016/j.cellimm.2025.104947","url":null,"abstract":"<div><h3>Background</h3><div>Lung cancer is a leading cause for cancer–related mortality across the globe. In the last decade, significant advancements have been made in the research of non-small cell lung cancer (NSCLC). However, new biotherapeutic drugs urgently need to be developed. This study investigated the regulating effect of hyperoside on NSCLC progression.</div></div><div><h3>Methods</h3><div>The colony formation assay and Cell Counting Kit-8 were used to detect cell proliferation. The Transwell assay was used to monitor cell migration. NSCLC growth in vivo was examined using a subcutaneous xenograft model. Proteomics, immunohistochemistry, and immunofluorescence analyses were used to detect anticancer regulatory mechanisms.</div></div><div><h3>Results</h3><div>The results showed that hyperoside treatment inhibited cell migration, proliferation, and tumor growth in NSCLC in vivo and in vitro. Also, hyperoside treatment promoted apoptosis and cell cycle S-phase arrest. Proteomics, immunohistochemistry, and immunofluorescence detection also showed that hyperoside treatment promoted autophagy-related protein 13 (ATG13)-mediated autophagy, which further increased NSCLC apoptosis.</div></div><div><h3>Conclusion</h3><div>In summary, the findings illustrated that hyperoside treatment suppressed NSCLC progression by promotingATG13 expression and enhancing autophagy activation, finally promoting autophagy and apoptosis.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104947"},"PeriodicalIF":3.7,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843781","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":"Immunology of familial chorea-acanthocytosis with presenting generalized tonic-clonic seizure: Blood cell study for early diagnosis and management","authors":"Amineh Salem,&nbsp;Narges Omidvar","doi":"10.1016/j.cellimm.2025.104946","DOIUrl":"10.1016/j.cellimm.2025.104946","url":null,"abstract":"<div><div>A male, who involved familial chorea-acanthocytosis (ChAc), was introduced to provide direction for early diagnosis and management. The admitted patient was found to have the significant episode with generalized tonic-clonic seizure, gradually progressive abnormal movements, and generalized weakness. According to the peripheral blood smears, the acanthocytosis was diagnosed primarily. The neuroimaging observation revealed atrophied head of caudate nuclei and dilation of anterior horn in the lateral ventricles. For the early diagnosis and prevention of syndrome complications, neuroacanthocytosis should be considered in the differential diagnosis of patients presenting with generalized tonic-clonic seizure, peripheral neuropathy, and behavioral disorder associated with movement complications.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104946"},"PeriodicalIF":3.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143759088","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":"Immunity in children: How does it begin?","authors":"Simon Fillatreau","doi":"10.1016/j.cellimm.2025.104945","DOIUrl":"https://doi.org/10.1016/j.cellimm.2025.104945","url":null,"abstract":"","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":" ","pages":"104945"},"PeriodicalIF":3.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742362","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":"METTL3 promotes infantile pneumonia-induced lung injury by the m6A-TBL1XR1-ACSL1 axis","authors":"Fuxing Song,&nbsp;Fang Guo,&nbsp;Bo Su,&nbsp;Na Niu,&nbsp;Lina Sun,&nbsp;Min Yan,&nbsp;Min Liu","doi":"10.1016/j.cellimm.2025.104944","DOIUrl":"10.1016/j.cellimm.2025.104944","url":null,"abstract":"<div><h3>Background</h3><div>Methyltransferase-like 3 (METTL3) is the catalytic subunit of methyltransferase complex that catalyzes mRNA methylation and has been identified to be involved in lipopolysaccharide (LPS)-induced lung cell injury. In this study, we investigated whether METTL3 is involved in the progression of infantile pneumonia (IP)-induced lung injury and its underlying mechanism.</div></div><div><h3>Methods</h3><div>WI-38 cells were exposed to LPS to induce in vitro proliferation, inflammation, apoptosis, and ferroptosis. The mRNA and protein levels of METTL3, TBL1XR1, IGF2BP1/2/3, and ACSL1 were measured by qRT-PCR and western blotting, respectively. The N6-methyladenosine (m6A) modification was analyzed using a methylated RNA immunoprecipitation assay. Protein interactions were determined using a Co-IP assay. LPS-induced pneumonia in mice was used for the in vivo analysis.</div></div><div><h3>Results</h3><div>METTL3 was highly expressed in IP and LPS-induced WI-38 cells. Knockdown of METTL3 reversed LPS-induced apoptosis, inflammation, and ferroptosis in vitro and in vivo and improved LPS-induced lung injury and collagen deposition in lung tissues of IP mice. Mechanistically, METTL3 induces TBL1XR1 m6A modifications and stabilizes its expression in an m6A-IGF2BP1-dependent manner. Functionally, the protective effects mediated by METTL3 silencing in LPS-treated WI-38 cells were reversed by TBL1XR1 overexpression. In addition, TBL1XR1 interacts with ACSL1, and METTL3 regulates ACSL1 expression via TBL1XR1. Further functional analysis showed that TBL1XR1 deficiency suppressed LPS-induced apoptosis, inflammation, and ferroptosis, which were abolished by ACSL1 up-regulation.</div></div><div><h3>Conclusion</h3><div>METTL3 stabilized TBL1XR1 expression through IGF2BP1-m6A methylation, promoting LPS-induced IP lung injury by upregulating ACSL1 expression.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104944"},"PeriodicalIF":3.7,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673312","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}