Cellular immunology最新文献

{"title":"Corrigendum to “BCG and β-glucan primed monocytes yield dendritic cells that hamper the induction of pro-inflammatory T cell immunity” [Cell. Immunol. 419 (2026) 105060]","authors":"Jorge Cuenca-Escalona , Robbin Kramer , Clara Marjalizo-Jimenez , Jorge Domínguez-Andrés , Mihai G. Netea , Georgina Flórez-Grau , I. Jolanda M. de Vries , Sophie K. Horrevorts","doi":"10.1016/j.cellimm.2026.105087","DOIUrl":"10.1016/j.cellimm.2026.105087","url":null,"abstract":"","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"423 ","pages":"Article 105087"},"PeriodicalIF":2.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431138","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":"Clarifying diagnostic rigor and cohort characteristics in neurosyphilis nomogram development: a response to Kenyon","authors":"Yun Ling","doi":"10.1016/j.cellimm.2026.105073","DOIUrl":"10.1016/j.cellimm.2026.105073","url":null,"abstract":"","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"422 ","pages":"Article 105073"},"PeriodicalIF":2.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146147631","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":"Peiminine modulates T cell-associated gene expression and inflammatory activity in experimental autoimmune hepatitis","authors":"Amin Azizan ,&nbsp;Mohammad Ali Abyazi ,&nbsp;Seyed Kiarash Aghayan ,&nbsp;Majid Mirzaei Nodooshan ,&nbsp;Akbar Ghorbani Alvanegh ,&nbsp;Hadi Esmaeili Gouvarchin Ghaleh","doi":"10.1016/j.cellimm.2025.105055","DOIUrl":"10.1016/j.cellimm.2025.105055","url":null,"abstract":"<div><div>Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease characterized by immune-mediated hepatocellular injury and insufficient regulatory T cell (Treg) control. Despite the efficacy of corticosteroids and azathioprine, incomplete response, side effects, and relapse often limit treatment, underscoring the need for novel therapeutic strategies. To date, little is known about the potential of natural compounds in modulating T cell–related pathways in AIH.</div><div>This study aimed to evaluate the therapeutic effects of peiminine, an alkaloid with reported anti-inflammatory and immunomodulatory properties, in an experimental model of AIH. We investigated its impact on liver histopathology, inflammatory markers, and expression of T cell–associated genes (FOXP3, Tbx21, and RORc), comparing its efficacy with prednisolone.</div><div>Our results demonstrated that peiminine treatment significantly alleviated interface hepatitis, reduced inflammatory cell infiltration, and improved lobular architecture. Quantitative histological scoring confirmed that peiminine, particularly at higher doses, exerted protective effects comparable to prednisolone. At the molecular level, peiminine increased FOXP3 expression while suppressing Tbx21 and RORc, suggesting restoration of Treg/Th1/Th17 balance. These findings were consistent with reductions in pro-inflammatory cytokine expression and improved liver function indices.</div><div>Collectively, our findings provide promising preclinical evidence that peiminine can attenuate autoimmune-mediated liver injury by modulating T cell–associated immune pathways. While further validation in human studies is necessary, these results identify peiminine as a potential adjunct or alternative therapeutic candidate for AIH, with implications for broader autoimmune disease management.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"420 ","pages":"Article 105055"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145602702","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":"Vitiligo immunopathogenesis: Insight of immune components and prospects of emerging immunotherapies","authors":"Manoj Kumar Tembhre ,&nbsp;Wajihul Hasan Khan","doi":"10.1016/j.cellimm.2025.105058","DOIUrl":"10.1016/j.cellimm.2025.105058","url":null,"abstract":"<div><div>Vitiligo is an acquired depigmenting disease characterized by the loss of pigmentation from the skin due to selective killing of pigment forming cells (melanocytes) by cytotoxic T cells (CD8+ T cells). The pathogenesis of vitiligo has broad spectrum ranging from genetic, biochemical and immunological factors. Based on these multifactorial aetiologies several hypotheses have been suggested with substantial evidence. Recent advances in the understanding of immunopathogenesis of the disease have opened new avenues that may be translated into effective treatment strategies. There is requirement of new immunomolecular targets aiming to reinstate the skin homeostasis by maintaining the fine tuning with immune parameters and melanocyte microenvironment of the skin. The present review will address the recent advances in the pathogenesis of generalized vitiligo (GV) giving emphasis on memory T cells, regulatory T cells (Tregs), cytokines and chemokines with prospects of promising immunotherapies.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"420 ","pages":"Article 105058"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145818219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pan-organ damage analysis in the R848-induced systemic lupus erythematosus mouse model","authors":"Xiaoliu Li ,&nbsp;Cheng Bao ,&nbsp;Min Xu ,&nbsp;Lingyun Sun ,&nbsp;Hongwei Chen","doi":"10.1016/j.cellimm.2025.105056","DOIUrl":"10.1016/j.cellimm.2025.105056","url":null,"abstract":"<div><h3>Background</h3><div>Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease that often leads to organ dysfunction. Resiquimod (R848) can induce the establishment of SLE models in mice within a relatively short period. However, there are few comprehensive systematic research reports on the degree and differences of organ involvement in this model. Therefore, the aim of this study was to clarify the systemic involvement of the SLE model induced by R848.</div></div><div><h3>Methods</h3><div>C57BL/6 mice were treated with 2 μg/μL R848 for 4 weeks. After the last administration, H&amp;E staining was used to examine pathological changes in multiple organs (bone, thymus, spleen, knee joints, kidney, etc.). Real-time quantitative PCR (RT-qPCR) and western blotting were used to detect the mRNA and protein levels of toll-like receptors (TLRs) and inflammatory factors. Flow cytometry analysis was performed to examine the changes in T- and B-cell subsets within the spleen. Immunofluorescence was used to analyse immune complex deposition in the kidneys.</div></div><div><h3>Results</h3><div>R848 successfully induced an SLE mouse model characterized by splenomegaly, elevated serum levels of anti-dsDNA antibodies, immune complex deposition in the kidneys, and imbalanced T-/B- cell populations, etc. Severe pathological changes were detected in specific organs, such as the bone, thymus, spleen, and knee joint, whereas no obvious lesions were observed in organs, such as the heart. Accordingly, the <em>Tlr7/8/9</em> pathway and its downstream inflammatory factor targets (<em>Tnf</em>, <em>Ifng</em>, <em>Il6</em>, and <em>Il10</em>) presented organ-specific expression profiles at the transcriptional level and the western blotting confirmed that the protein levels of TLR7/8 and TNF-α increased particularly in the spleen, but not in the kidney or submandibular gland.</div></div><div><h3>Conclusion</h3><div>R848-induced SLE mice exhibit systemic immune disorders, with differences in pan-organ damage, inflammatory cell infiltration, and TLR7/8-mediated inflammatory factor expression. This study provides a foundation for clarifying the multisystem mechanism of SLE.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"420 ","pages":"Article 105056"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145713207","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":"Actin cytoskeleton stabilization inhibits NLRP3 inflammasome activation and mitigates renal inflammation and fibrosis in obstructive nephropathy","authors":"Qiaoli Xu ,&nbsp;Jinxin Li ,&nbsp;Xing Wan ,&nbsp;Gaoling Wang ,&nbsp;Jiawei Wu ,&nbsp;Xinrui Chang ,&nbsp;Fang Yan ,&nbsp;Li Li ,&nbsp;Baosheng Han","doi":"10.1016/j.cellimm.2025.105053","DOIUrl":"10.1016/j.cellimm.2025.105053","url":null,"abstract":"<div><div>Obstructive nephropathy is characterized by progressive renal inflammation and tubular injury, in which the NLRP3 inflammasome plays a pivotal role. However, the contribution of cytoskeletal dynamics to inflammasome activation remains poorly understood. In this study, we investigated whether stabilizing the actin cytoskeleton using Bis-T-23, a filamentous actin (F-actin) stabilizer, could alleviate renal injury by suppressing NLRP3 signaling. In a unilateral ureteral obstruction (UUO) mouse model, Bis-T-23 treatment significantly reduced tubular dilation, interstitial fibrosis, and immune cell infiltration. Transcriptomic profiling revealed marked downregulation of inflammation-related pathways, including TNF, IL-17, and NOD-like receptor signaling. At the molecular level, Bis-T-23 inhibited NLRP3 inflammasome activation, as evidenced by decreased levels of NLRP3, cleaved caspase-1, IL-1β, and IL-18 in both renal tissue and tubular epithelial cells. In vitro, TNFα/TGFβ1 co-stimulation induced a pro-fibrotic and pro-inflammatory phenotype in tubular cells, characterized by ZO-1 disruption, α-SMA upregulation, and enhanced NLRP3 expression, all of which were reversed by Bis-T-23. Furthermore, Bis-T-23 impaired ASC speck formation and disrupted NLRP3–ASC interactions, suggesting a direct blockade of inflammasome assembly. These findings identify cytoskeletal stabilization as a novel upstream mechanism for NLRP3 regulation and highlight Bis-T-23 as a potential therapeutic candidate for mitigating tubular inflammation in obstructive kidney disease.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"420 ","pages":"Article 105053"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145595766","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":"Chilean Phaseolus vulgaris landraces: A dietary source influencing NETs formation and phagocytic efficiency","authors":"Camila Ortiz-Salazar ,&nbsp;Camila Hernández-Barros ,&nbsp;Francisca Tellería ,&nbsp;Carlos Felipe Burgos ,&nbsp;Andrés Trostchansky ,&nbsp;Andrea Plaza ,&nbsp;Basilio Carrasco ,&nbsp;Carolina Espinoza-Robles ,&nbsp;Nicolas Blanco ,&nbsp;Sergio Wehinger ,&nbsp;Iván Palomo ,&nbsp;Eduardo Fuentes ,&nbsp;Marcelo Alarcón L.","doi":"10.1016/j.cellimm.2025.105057","DOIUrl":"10.1016/j.cellimm.2025.105057","url":null,"abstract":"<div><div>Neutrophil extracellular traps (NETs) are crucial for the antimicrobial defense; however, their dysregulated expression can lead to enhanced inflammation and tissue damage. NET formation requires reactive oxygen species (ROS), particularly those generated through the NADPH oxidase (NOX2) pathway. This study investigates the immunomodulatory effects of aqueous extracts of Chilean landraces of <em>Phaseolus vulgaris L.</em> (Hallado Alemán) with microwave-assisted extraction, on ROS-dependent NETosis and phagocytosis. Using an in vitro model of differentiated HL-60 neutrophil-like cells and human polymorphonuclear neutrophils (PMNs) stimulated with PMA, we evaluated ROS production, NETs release, myeloperoxidase (MPO) activity, and cf-DNA release, as well as phagocytic activity. All experiments were performed in triplicate (<em>n</em> = 3 independent biological replicates); data are presented as mean ± SEM. Both extracts have high polyphenol content and effectively inhibit superoxide production and NET release without cytotoxic effects and increase bacterial phagocytosis. The extract components, including gallic acid, quercetin, and kaempferol, were confirmed by HPLC-DAD. In silico docking analysis showed robust binding of the same polyphenols to key inflammatory-regulating proteins, including PKCb, NOX2, and TLR4/MD2. These findings suggest that aqueous extracts of <em>Phaseolus vulgaris</em> modulate neutrophil function by attenuating proinflammatory responses while preserving antimicrobial activity, indicating their value as natural innate immune modulators.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"420 ","pages":"Article 105057"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145713267","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":"Exosomes derived from ovarian cancer promote the progression of ovarian cancer through macrophage M2 polarization mediated by the THBS1/TGFBI signaling axis","authors":"Linlin Yang,&nbsp;Yue Jia,&nbsp;Ying Liu,&nbsp;Shaojia Wang,&nbsp;Shufen Tan,&nbsp;Youqin Ruan,&nbsp;Lingfeng Zhao,&nbsp;He Zhao,&nbsp;Ruolan Xu,&nbsp;Chunyan Ding,&nbsp;Hui Liu,&nbsp;Yan Qin,&nbsp;Haijuan Zhao,&nbsp;Xinyue Feng,&nbsp;Changyi Zeng,&nbsp;Yuye Li,&nbsp;Xiang Meng,&nbsp;Hongying Yang","doi":"10.1016/j.cellimm.2025.105054","DOIUrl":"10.1016/j.cellimm.2025.105054","url":null,"abstract":"<div><h3>Background</h3><div>Tumor-derived exosomes play a critical role in facilitating intercellular communication between cancer cells and tumor-associated macrophages (TAMs). Nevertheless, the precise molecular mechanisms underlying exosome-mediated interactions specifically in ovarian cancer remain incompletely elucidated.</div></div><div><h3>Methods</h3><div>TAMs were treated with exosomes isolated from clinical ovarian cancer specimens. Macrophage polarization was assessed using qRT-PCR, and western blot analysis. RNA sequencing was employed to identify key genes within the exosomes. The malignant phenotype of ovarian cancer cells was evaluated through cell counting kit-8 (CCK-8), Transwell assay, and wound-healing assays.</div></div><div><h3>Results</h3><div>Our findings showed that exosomes derived from both early and late-stage malignant ovarian cancer tissues induced the upregulation of all M2 macrophage markers and the downregulation of M1 markers. RNA sequencing analysis identified thrombospondin-1 (THBS1) as a potential pivotal gene influencing exosome-regulated TAM polarization. THBS1 knockdown within exosomes inhibited the polarization of TAMs toward the M2 phenotype and concurrently decreased transforming growth factor beta induced (TGFBI) expression in macrophages. Notably, TGFBI knockdown in TAM reversed the M2 polarization induced by ovarian cancer cells-derived exosomes. In vivo, ovarian cancer cell-derived exosomes facilitate cancer progression, concomitantly increasing the polarization of M2 macrophages and upregulating THBS1 and TGFBI expression within tumor tissues.</div></div><div><h3>Conclusion</h3><div>THBS1, carried by ovarian cancer-derived exosomes, promotes M2 polarization of TAMs by modulating TGFBI expression. The subsequent M2 polarization of TAMs contributes to the establishment of an immunosuppressive tumor microenvironment, thereby facilitating disease progression. Consequently, targeting the exosome-mediated signaling axis between cancer cells and macrophages represents a promising avenue for developing novel therapeutic interventions.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"420 ","pages":"Article 105054"},"PeriodicalIF":2.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145571208","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":"Functional and structural analysis of KK-LC-1-specific T cell receptors from patients with lung Cancer for immunotherapy","authors":"Yasunori Fukushima ,&nbsp;Yizheng Wang ,&nbsp;Yuki Yada-Makino ,&nbsp;Hiroyasu Komuro ,&nbsp;Ayako Demachi-Okamura ,&nbsp;Yusuke Sugita ,&nbsp;Takanari Okamoto ,&nbsp;Hiromasa Ishihara ,&nbsp;Ryo Mizuta ,&nbsp;Yujia Sun ,&nbsp;Takuya Matsui ,&nbsp;Mitsugu Araki ,&nbsp;Ma Biao ,&nbsp;Yasushi Okuno ,&nbsp;Katsuhiro Masago ,&nbsp;Rui Yamaguchi ,&nbsp;Zhongliang Guo ,&nbsp;Kazuhide Onoguchi ,&nbsp;Yoshiko Yamashita ,&nbsp;Takashi Fukuyama ,&nbsp;Daisuke Muraoka","doi":"10.1016/j.cellimm.2025.105059","DOIUrl":"10.1016/j.cellimm.2025.105059","url":null,"abstract":"<div><div>Adoptive T-cell receptor (TCR)-engineered T cell therapy is a promising approach for cancer immunotherapy, particularly for cancer/testis antigens such as KK-LC-1. We evaluated four KK-LC-1 epitope-specific TCRs restricted by Human Leukocyte Antigen (HLA)-B*15:01, including three identified by our group and one previously reported. Their properties were characterised using TCRαβ-transduced γδT and Jurkat cells through functional analyses, including IFN-γ production, activation marker expression, cytotoxicity, TCR signalling, and T cell-target cell interactions, complemented by molecular dynamics simulations. One TCR exhibited superior performance, with the highest IFN-γ production, activation marker expression, and cytotoxicity, sustaining robust TCR signalling at low antigen levels and enhancing T cell-target interactions. Molecular dynamics simulations revealed that it exhibited a high binding affinity and stable interface, characterised by hydrogen bonds evenly distributed across the peptide and HLA α1/α2 helices, likely contributing to the conformational stability of the TCR–pMHC complex. These findings suggest that the functional superiority of this TCR is attributable to its structurally balanced and stable engagement with the pMHC complex. This study highlights the structural basis of TCR efficacy and provides a practical framework for optimising TCR selection for adoptive immunotherapy.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"419 ","pages":"Article 105059"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145904127","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":"An accurate predictive neurosyphilis scoring system depends on an accurate diagnosis of neurosyphilis","authors":"Kenyon Chris","doi":"10.1016/j.cellimm.2026.105061","DOIUrl":"10.1016/j.cellimm.2026.105061","url":null,"abstract":"","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"419 ","pages":"Article 105061"},"PeriodicalIF":2.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145974721","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}