Cellular immunology最新文献_第8页

Lupeol mitigates spinal cord injury by modulating microglial M1/M2 polarization via Na+/K+-ATPase-mediated mitophagy lupel通过Na+/K+- atp酶介导的线粒体自噬调节小胶质细胞M1/M2极化，从而减轻脊髓损伤

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-04-19 DOI: 10.1016/j.cellimm.2025.104955

Ruyin Liu , Zongjin Yue , Jia'an Dong , Cheng Zhang , Chuanghao Guo , Xinli Wang

{"title":"Lupeol mitigates spinal cord injury by modulating microglial M1/M2 polarization via Na+/K+-ATPase-mediated mitophagy","authors":"Ruyin Liu , Zongjin Yue , Jia'an Dong , Cheng Zhang , Chuanghao Guo , 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<sup>+</sup>/K<sup>+</sup>-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":"2025-05-01","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}

引用次数: 0

Immunology of familial chorea-acanthocytosis with presenting generalized tonic-clonic seizure: Blood cell study for early diagnosis and management 出现全身强直-阵挛性发作的家族性舞蹈症-棘细胞增多症的免疫学：用于早期诊断和治疗的血细胞研究

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-04-01 DOI: 10.1016/j.cellimm.2025.104946

Amineh Salem, Narges Omidvar

引用次数: 0

Hyperoside suppresses NSCLC progression by inducing ATG13-mediated autophagy and apoptosis 金丝桃苷通过诱导atg13介导的自噬和凋亡来抑制NSCLC的进展

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-04-04 DOI: 10.1016/j.cellimm.2025.104947

Mingming Jin , Yuqing Lou , Xiaoshuo Wang , Jia Lv , Yue Wu , Gang Huang

{"title":"Hyperoside suppresses NSCLC progression by inducing ATG13-mediated autophagy and apoptosis","authors":"Mingming Jin , Yuqing Lou , Xiaoshuo Wang , Jia Lv , Yue Wu , 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":"2025-05-01","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}

引用次数: 0

Immunity in children: How does it begin? 儿童免疫：它是如何开始的？

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-03-24 DOI: 10.1016/j.cellimm.2025.104945

Simon Fillatreau

引用次数: 0

Aged mice-derived bronchial epithelial cells regulate Th17 cell differentiation in asthma via the MBD2-sICOSL axis 老年小鼠支气管上皮细胞通过MBD2-sICOSL轴调节哮喘Th17细胞分化

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-04-15 DOI: 10.1016/j.cellimm.2025.104954

Zhifeng Chen , Yulin Shang , Yu Yuan , Xiaoying Ji , Subo Gong , Qingping Zeng , Xudong Xiang

{"title":"Aged mice-derived bronchial epithelial cells regulate Th17 cell differentiation in asthma via the MBD2-sICOSL axis","authors":"Zhifeng Chen , Yulin Shang , Yu Yuan , Xiaoying Ji , Subo Gong , Qingping Zeng , 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<sup>+</sup> 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":"2025-05-01","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}

引用次数: 0

Novel and effective tandem CD38 and CD19 targeting CAR-T cells inhibit hematological tumor immune escape 新型有效的CD38和CD19串联靶向CAR-T细胞抑制血液学肿瘤免疫逃逸

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-04-15 DOI: 10.1016/j.cellimm.2025.104950

Xiuying Liu , Yaru Feng , Zhiru Song , Jingjing Liu , Zhiqiang Luo , Guohua Yu , Jianxun Wang

{"title":"Novel and effective tandem CD38 and CD19 targeting CAR-T cells inhibit hematological tumor immune escape","authors":"Xiuying Liu , Yaru Feng , Zhiru Song , Jingjing Liu , Zhiqiang Luo , Guohua Yu , 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":"2025-05-01","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}

引用次数: 0

USP14 inhibits sensitization-mediated degradation of KDM4D to epigenetically regulate dendritic cell tolerogenic capacity and mitigates airway allergy USP14抑制致敏介导的KDM4D降解，以表观遗传方式调节树突状细胞的耐受性，减轻气道过敏

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-03-13 DOI: 10.1016/j.cellimm.2025.104943

Aizhi Zhang , Huanping Zhang , Le Liu , Hanqing Zhang , Lihua Mo , Wenkai Zhang , Hanis Hazeera Harith , Liying Cheng , Jieping Lv , Chau Ling Tham , Pingchang Yang

{"title":"USP14 inhibits sensitization-mediated degradation of KDM4D to epigenetically regulate dendritic cell tolerogenic capacity and mitigates airway allergy","authors":"Aizhi Zhang , Huanping Zhang , Le Liu , Hanqing Zhang , Lihua Mo , Wenkai Zhang , Hanis Hazeera Harith , Liying Cheng , Jieping Lv , Chau Ling Tham , Pingchang Yang","doi":"10.1016/j.cellimm.2025.104943","DOIUrl":"10.1016/j.cellimm.2025.104943","url":null,"abstract":"<div><div>Numerous immune disorders are caused by the dysfunction of dendritic cells (DC). The mechanism has not been fully comprehended yet. This research is designed to regulate the epigenetic status of lysine-specific demethylase 4D (KDM4D) to enhance DC's immune tolerogenic capacity. In this study, an airway allergy (AA) mouse model was established with dust mite extracts (DME) as the specific antigen. A mouse strain carrying <em>Kdm4d</em>-deficient DCs was employed in the experiments to assess the role of KDM4D in modulating DC's immune tolerogenic functions. The results showed that mice carrying <em>Kdm4d</em>-deficient DCs (KO mice) showed spontaneous Th2 polarization in the airways. Reduced quantities of KDM4D were detected in airway naive DCs (nDCs) of AA mice. The parameters of AA response had a negative correlation with the quantity of KDM4D. The immune tolerogenic capacity of airway nDCs was impaired in KO mice as well as in AA mice. The <em>Il10</em> promoter was found to be hypermethylated in airway nDCs of AA mice and KO mice. The low quantity of deubiquitinating enzyme 14 (USP14) was related to the high level of hyper ubiquitination observed in KDM4D in the <em>Il10</em> promoter locus of airway nDCs of AA mice. Exposure to recombinant USP14 increased the quantity of KDM4D in nDCs, restoring the immune tolerogenic capacity of nDCs in AA mice. In conclusion, dysfunctional tolerogenicity is caused by low levels of KDM4D in airway nDCs from AA mice. USP14 restores the tolerogenic capacity of nDCs in AA mice and mitigates experimental AA.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104943"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619580","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}

引用次数: 0

METTL3 promotes infantile pneumonia-induced lung injury by the m6A-TBL1XR1-ACSL1 axis METTL3通过m6A-TBL1XR1-ACSL1轴促进婴儿肺炎诱导的肺损伤。

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-03-16 DOI: 10.1016/j.cellimm.2025.104944

Fuxing Song, Fang Guo, Bo Su, Na Niu, Lina Sun, Min Yan, Min Liu

{"title":"METTL3 promotes infantile pneumonia-induced lung injury by the m6A-TBL1XR1-ACSL1 axis","authors":"Fuxing Song, Fang Guo, Bo Su, Na Niu, Lina Sun, Min Yan, 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":"2025-05-01","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}

引用次数: 0

The real-world impact of corticosteroid-associated adverse events in myasthenia gravis: A patient-reported survey analysis 在重症肌无力中，皮质类固醇相关不良事件的实际影响：一项患者报告的调查分析

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-04-29 DOI: 10.1016/j.cellimm.2025.104956

Jinyi Yan , Kalam Choi , Peicai Fu, Mengge Yang, Jing Lin, Mengcui Gui, Yue Li, Bitao Bu, Zhijun Li

{"title":"The real-world impact of corticosteroid-associated adverse events in myasthenia gravis: A patient-reported survey analysis","authors":"Jinyi Yan , Kalam Choi , Peicai Fu, Mengge Yang, Jing Lin, Mengcui Gui, Yue Li, Bitao Bu, Zhijun Li","doi":"10.1016/j.cellimm.2025.104956","DOIUrl":"10.1016/j.cellimm.2025.104956","url":null,"abstract":"<div><h3>Background</h3><div>Corticosteroids are crucial for managing acute exacerbation symptoms and preventing relapses in myasthenia gravis (MG) patients.</div></div><div><h3>Methods</h3><div>Between April 15–30, 2024, 2368 online self - report questionnaires were distributed. Eventually, 444 MG patients who had received corticosteroid therapy completed the survey.</div></div><div><h3>Results</h3><div>Self-reported adverse events (AEs) were observed in 97.5 % of the respondents. Among them, 72.5 % (322 patients) reported experiencing more than four AEs. The quality of life (QOL) of patients with MG was significantly impacted, with average MG-QOL scores of 18.07 ± 12.03. Patients with a cumulative dosage exceeding 20 g experienced the highest incidence of various AEs compared to those with lower cumulative dosages (5–20 g and less than 5 g). Additionally, a longer duration of corticosteroid exposure was associated with a higher reported incidence of AEs. Cox risk regression modeling revealed that a longer disease course, a history of myasthenic crisis, and the average daily dose of steroids (exceeding 5 mg/d), were independent predictors of corticosteroid-associated AEs. The study revealed in a single MG center, the awareness of these AEs was low among Chinese patients.</div></div><div><h3>Conclusion</h3><div>This study systematically assessed the incidence and risk factors of corticosteroid-related AEs in Chinese MG patients. The study found that the occurrence of AEs was associated with the cumulative dosage and duration of corticosteroid use. Additionally, long disease duration, a history of myasthenic crises, and an average daily dosage exceeding 5 mg/d are identified as risk factors for corticosteroid-related AEs in patients with MG.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104956"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886816","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}

引用次数: 0

The NLRP3 Inflammasome in inflammatory diseases: Cellular dynamics and role in granuloma formation 炎性疾病中的NLRP3炎性小体：细胞动力学及其在肉芽肿形成中的作用

IF 3.7 4区医学

Cellular immunology Pub Date : 2025-05-01 Epub Date: 2025-05-03 DOI: 10.1016/j.cellimm.2025.104961

Isadora M. de Oliveira , Mariana M. Chaves

{"title":"The NLRP3 Inflammasome in inflammatory diseases: Cellular dynamics and role in granuloma formation","authors":"Isadora M. de Oliveira , Mariana M. Chaves","doi":"10.1016/j.cellimm.2025.104961","DOIUrl":"10.1016/j.cellimm.2025.104961","url":null,"abstract":"<div><div>The innate immune system recognizes pathogen-associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs) through pattern recognition receptors (PRRs). Inflammasomes, cytoplasmic protein complexes, are activated in response to PAMPs and DAMPs, leading to the release of inflammatory cytokines such as IL-1β and IL-18. NLRP3 inflammasome is one of the best characterized inflammasomes and recently its activation has been associated with granuloma formation, structures that aggregate immune cells in response to infections, such as those caused by bacteria, fungi and parasites, and autoinflammatory diseases, such as sarcoidosis. Activation of NLRP3 inflammasomes in macrophages induces the release of cytokines that recruit immune cells, such as monocytes and lymphocytes, to the site of infection. Neutrophils, monocytes, T and B lymphocytes are important in the formation and maintenance of granulomas. Although NLRP3 plays a key role in the immune response, cell recruitment and granuloma formation, many aspects of its function in different cell types remain to be elucidated. In this review, we aim to outline the NLRP3 inflammasome not only as a protein complex that aids innate immune cells in combating intracellular pathogens but also as a platform with broader implications in orchestrating immune responses. This underexplored aspect of the NLRP3 inflammasome presents a novel perspective on its involvement in immunity. Thus, we review the current understanding of the role of the NLRP3 inflammasome in immune cell infiltration and its significance in the organization and formation of granulomas in inflammatory diseases.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"411 ","pages":"Article 104961"},"PeriodicalIF":3.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143917556","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}

引用次数: 0