Cancer immunology, immunotherapy : CII最新文献

{"title":"Favorable impact of zanubrutinib combined with R-CHOP regimen in MYD88-mutated new-diagnosed diffuse large B-cell lymphoma: a retrospective study with propensity score-matched analysis.","authors":"Xiubin Xiao, Shunzong Yuan, Xilin Chen, Xia Liu, Ruiqing Zhao, Shihua Zhao, Yun Lu, Yi Ma, Junli Chen, Yueqi Wang, Nana Cheng, Hua Yin, Honghao Gao, Pan Feng, Wenrong Huang","doi":"10.1007/s00262-025-04090-4","DOIUrl":"10.1007/s00262-025-04090-4","url":null,"abstract":"<p><p>Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease, with MYD88 mutations associated with poor outcomes. Enhancing standard rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) therapy with targeted agents such as zanubrutinib, a selective Bruton tyrosine kinase inhibitor, may improve patient prognosis. This retrospective study evaluated patients with MYD88-mutated DLBCL treated with zanubrutinib plus R-CHOP (ZR-CHOP). The ZR-CHOP group (n = 20) was compared with a propensity score-matched control group (n = 40) of patients without MYD88 mutation who received standard R-CHOP. Key outcomes included complete response rate (CRR), overall response rate (ORR), progression-free survival (PFS), and overall survival (OS). Univariate logistic regression analyzed prognostic factors, and safety was assessed by comparing adverse events between groups. The ZR-CHOP group had a similar CRR of 75.0% compared to 67.5% in the control group and an ORR of 90.0% versus 97.5%. With a median follow-up of 26.5 months (range: 1-41), PFS and OS were analyzed. At 36 months, PFS was 61.9% in the ZR-CHOP group versus 63.8% in the control, while OS was 77.5% versus 76.7%. Among patients with MYD88/CD79B double mutations, the CRR was 90.0%. Elevated lactate dehydrogenase levels were linked to a lower likelihood of achieving a complete response. The most common treatment-related adverse events were infections (50%) and bleeding (15%) in the ZR-CHOP group. ZR-CHOP may improve outcomes in MYD88-mutated DLBCL, particularly in patients with MYD88/CD79B double mutations. Although further studies are needed, zanubrutinib shows promise as a targeted therapy in this population.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"259"},"PeriodicalIF":0.0,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12228930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Divergent therapeutic and prognostic impacts of immunogenic features in undifferentiated pleomorphic sarcoma and myxofibrosarcoma.","authors":"Siddh van Oost, Debora M Meijer, Zeynep B Erdem, Marieke E IJsselsteijn, Jessica Roelands, Suk Wai Lam, Melissa S Boejharat, Brendy E W M van den Akker, Ruud van der Breggen, Inge H Briare-de Bruijn, Lukas J A C Hawinkels, Anouk A Kruiswijk, Manon van der Ploeg, Pauline M Wijers-Koster, Rick L Haas, Michiel A J van den Sande, Noel F C C de Miranda, Judith V M G Bovee","doi":"10.1007/s00262-025-04123-y","DOIUrl":"10.1007/s00262-025-04123-y","url":null,"abstract":"<p><p>Undifferentiated pleomorphic sarcoma (UPS) and myxofibrosarcoma (MFS) are genetically complex soft tissue sarcomas with distinct morphological features. Treatment typically involves surgery, often combined with neoadjuvant chemo- or radiotherapy. To better understand the immunobiology of these sarcomas and its associations with treatment response and prognosis, we performed transcriptomic and immunophenotypic profiling. RNA sequencing was performed on 13 UPS and 10 MFS, and immunological profiles were compared with soft tissue sarcoma data from The Cancer Genome Atlas (n = 206 including 44 UPS and 17 MFS). Immune contextures were further evaluated in 14 UPS and 15 MFS using imaging mass cytometry. Characterization of T cell and macrophage infiltration in tumors was further assessed in 23 UPS and 22 MFS through multispectral immunofluorescence and immunohistochemical analysis. UPS and MFS demonstrated immunogenic features compared to other soft tissue sarcomas, with subsets of UPS and MFS demonstrating high T cell infiltration, while UPS demonstrated a higher infiltration by myeloid cells as compared to MFS. Prognostically, T cells and CD68⁺CD163⁺ macrophages were associated with metastasis-free survival in UPS but not in MFS. Notably, in UPS, neoadjuvant radiotherapy appeared to induce cytotoxic T cell infiltration and depletion of myeloid cells, whereas these effects were not observed in MFS. These findings highlight important differences in the immunobiology of UPS and MFS with therapeutic and prognostic implications. These differences should be taken into account given the growing availability of immunotherapeutic options for treating patients with soft tissue sarcomas.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"258"},"PeriodicalIF":0.0,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12222583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TCR-based cellular immunotherapy for hepatocellular carcinoma: advances, challenges, and prospects.","authors":"Wanting Zeng, Wei Zhu, Guosheng Yuan, Jinzhang Chen, Zhanhui Wang, Jinlin Hou, De-Ke Jiang","doi":"10.1007/s00262-025-04122-z","DOIUrl":"10.1007/s00262-025-04122-z","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) ranks among the most prevalent malignant tumors globally. However, current frontline treatment modalities fail to achieve satisfactory therapeutic outcomes. In recent years, T-cell receptor (TCR)-T therapy has garnered increasing attention as a promising therapeutic approach. This review provides an overview of the epidemiology of HCC, evaluates the efficacy of current first-line treatment options, and introduces adoptive cellular therapies (ACTs), with a specific focus on TCR-T therapy. Notably, we categorize existing TCR-T research targeting different antigens for the treatment of HCC, covering both published literature and registered clinical trials. Furthermore, we discuss the limitations of current TCR-T research and applications, while offering insights into future research directions and development prospects. In summary, this review comprehensively examines the research progress on TCR-T therapy for HCC from the perspective of antigen targeting. Although several challenges remain to be addressed, we believe that TCR-T therapy represents a promising approach for the treatment of HCC.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"257"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12214192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Salvianic acid A enhances anti-PD-1 therapy by promoting HEV-mediated stem-like CD8 T cells infiltration in TNBC.","authors":"Xiaoming Ding, Gai Liang, Yan Luo, Xiaomei Zhou, Qu Zhang, Bo Luo","doi":"10.1007/s00262-025-04116-x","DOIUrl":"10.1007/s00262-025-04116-x","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to investigate the potential of Salvianic acid A (SAA) to enhance the efficacy of anti-PD-1 immunotherapy in triple-negative breast cancer (TNBC), with a focus on elucidating the mechanisms.</p><p><strong>Methods: </strong>To explore the effects of SAA on anti-PD-1 therapy efficacy, we established a mouse tumor model using 4T1 breast cancer cells and treated groups with SAA, anti-PD-1 (αPD-1), or their combination. Tumor growth, weight, and survival were monitored. A melanoma mouse model using B16 melanoma cells was also used to validate the efficacy of SAA enhanced immunotherapy. Tumor tissues were analyzed histologically and by flow cytometry to assess immune cell infiltration and function. The expression of immune markers and cytokines was evaluated using immunohistochemistry, Western blot, and quantitative RT-PCR. In vitro experiments were conducted on 4T1, MDA-MB-231, and MDA-MB-453 breast cancer cell lines, as well as CD8 T cells and endothelial cells, to investigate the direct effects of SAA on cell viability, activation, and phenotype maintenance. Additionally, the impact of SAA on high endothelial venules (HEVs) was assessed using immunofluorescence and flow cytometry.</p><p><strong>Results: </strong>The combination of SAA and anti-PD-1 therapy significantly inhibited tumor growth and prolonged survival in the 4T1 mouse model and B16 mouse model respectively, compared to controls (P < 0.001). Tumor volumes and weights were consistently lower in the combination group, with no significant weight loss or toxicity observed. Histological analysis revealed increased stromal content and reduced tumor cell density in the SAA + αPD-1 group, indicating enhanced immune cell infiltration and tumor cell death. Flow cytometry showed that SAA significantly increased the infiltration of CD8 T cells and stem-like CD8 T cells (TCF1 and SLAMF6) into the tumor microenvironment when combined with αPD-1 (P < 0.001). The combination also enhanced the expression of IFN-γ and Ki-67 in CD8 T cells, indicating improved functional capacity. Additionally, SAA promoted the formation of HEVs in tumor tissues, as evidenced by increased CD31 and MECA-79 staining (P < 0.001). In vitro, SAA did not directly inhibit breast cancer cell viability or activate CD8 T cells but maintained the high endothelial phenotype in endothelial cells by upregulating key markers such as ACKR1 and CDH5. These findings demonstrate that SAA enhances anti-PD-1 efficacy by modulating the tumor immune microenvironment and promoting HEV formation, without direct cytotoxic effects on cancer cells or immune cells.</p><p><strong>Conclusion: </strong>SAA significantly enhances the efficacy of anti-PD-1 therapy by promoting HEV-mediated stem-like CD8 T cells infiltration in TNBC. The combination of SAA and αPD-1 represents a promising therapeutic strategy that warrants further exploration in preclinical and clinical settings.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"256"},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12209055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diversity of mast cell subpopulations in the tumor microenvironment of colorectal cancer and their prognostic implications.","authors":"Tianyu Qiao, Chao Ding, Songtao Yu, Wenyang Li, Yonghou Zhao, Guiyu Wang","doi":"10.1007/s00262-025-04119-8","DOIUrl":"10.1007/s00262-025-04119-8","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is one of the most common and deadly malignancies worldwide, with a particularly low 5-year survival rate in advanced patients. Immune cells in the tumor microenvironment, especially mast cells, play crucial roles in tumor initiation and progression. However, the dual role of mast cells in CRC remains poorly understood.</p><p><strong>Methods: </strong>In this study, we used single-cell RNA sequencing (scRNA-seq), bulk RNA sequencing, and bioinformatics analyses to explore the heterogeneity of mast cell subpopulations in the CRC tumor microenvironment and their relationship with prognosis. We analyzed gene expression signatures associated with mast cell subpopulations derived from single-cell data of 40 CRC tumor samples and combined bulk RNA-seq data from HMU, GEO, and TCGA cohorts for prognostic prediction. Non-negative matrix factorization was used for clustering of mast cell subpopulations, followed by analysis of their specific gene markers, transcription factor activity, and biological pathways. Survival analysis and ROC curves were performed to assess their prognostic significance.</p><p><strong>Results: </strong>Mast cells in the CRC tumor microenvironment were classified into three distinct subpopulations, each with unique gene markers and functional pathways. Mast cell subpopulations 1 and 3 were highly associated with pro-tumor pathways, while mast cell subpopulation 2 primarily exhibited anti-tumor immune regulatory characteristics. High expression of mast cell subpopulations 1 and 3 was associated with poor survival prognosis, while high expression of subpopulation 2 was linked to a better survival outcome. Key marker genes such as DNAJB1, SEMA7A, and XCR1 were identified as potential prognostic factors, with high expression of DNAJB1 and SEMA7A being significantly associated with poor prognosis, while high expression of XCR1 was linked to a favorable prognosis.</p><p><strong>Conclusion: </strong>This study reveals the functional heterogeneity of mast cell subpopulations in the CRC tumor microenvironment and their differential roles in tumor progression. Identification of mast cell subpopulation-specific marker genes provides new molecular targets for clinical diagnosis, prognostic prediction, and personalized immunotherapy in CRC.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"255"},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12209079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simultaneous TGF-β and GITR pathway modulation promotes anti-tumor immunity in glioma.","authors":"Daniela Lorizio, Manuela Silginer, Julia Friesen, Alan L Epstein, Michael Weller, Patrick Roth","doi":"10.1007/s00262-025-04098-w","DOIUrl":"10.1007/s00262-025-04098-w","url":null,"abstract":"<p><p>The immunosuppressive tumor microenvironment of glioblastoma limits the effectiveness of most immunotherapies. Transforming growth factor (TGF)-β signaling drives tumor progression and prevents effective T cell activity. Notably, both regulatory T cells (Tregs) and effector T cells within glioblastoma and other tumors express high levels of the immune checkpoint receptor, glucocorticoid-induced tumor necrosis factor receptor (GITR), which modulates T cell activation and function. Combining GITR agonism with TGF-β inhibition may therefore offer a compelling approach to restore anti-tumor immunity. We evaluated the combined effects of TGF-β inhibition and GITR modulation using two different GITR agonists in syngeneic mouse glioma models. GITR modulation enhanced T cell activation, as shown by increased cytokine secretion and effector T cell proliferation in vitro. Combining GITR modulation with TGF-β inhibition amplified these effects, resulting in significantly stronger immune cell-mediated tumor cell killing compared to single-agent treatments. Combination therapy improved survival of glioma-bearing mice, with a higher fraction of long-term survivors compared to monotherapy. Surviving mice resisted tumor re-challenge, indicating durable adaptive immunity. In summary, dual targeting of TGF-β and GITR pathways synergistically enhances anti-tumor immunity in glioblastoma. This novel combination strategy demonstrates clinical potential by addressing the limitations of existing immunotherapies and offering a promising approach for durable and effective glioblastoma treatment.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"254"},"PeriodicalIF":0.0,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12206220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intratumoral IL12 mRNA administration activates innate and adaptive pathways in checkpoint inhibitor-resistant tumors resulting in complete responses.","authors":"Jayalakshmi Lakshmipathi, Sreevidya Santha, Man Li, Yuping Qian, Simon F Roy, Nadia Luheshi, Katerina Politi, Marcus Bosenberg, Jim Eyles, Viswanathan Muthusamy","doi":"10.1007/s00262-025-04105-0","DOIUrl":"10.1007/s00262-025-04105-0","url":null,"abstract":"<p><p>Despite the proven clinical activity of checkpoint inhibitors (ICIs) in several cancer indications, frequent occurrence of primary and secondary resistance reduces their overall effectiveness. Development of ICI resistance has been attributed mainly to genetic or epigenic alterations that affect the tumor antigen presentation machinery leading to diminished anti-tumor immune responses. There is an urgent need for new approaches which can either re-sensitize resistant tumors to the ICIs or engage alternate immune pathways to inhibit tumors. Intratumoral delivery of nanoparticle encapsulated murine IL12 (mIL12) mRNA induces powerful anti-tumor immune responses in murine tumor models, and the human version of this drug results in objective responses in patients with advanced disease. Here, we tested the efficacy of mIL12 mRNA as a single agent and in combination with anti-PD-L1 antibodies in ICI-sensitive Yummer 1.7 melanoma and MC38 colorectal murine tumors and in ICI resistant, β2-microglobulin (B2M) knockout versions of these models. mIL12 mRNA monotherapy was sufficient to cause complete responses (CRs) in ≥ 60% of both ICI-sensitive or -resistant Yummer 1.7 melanoma and MC38 colorectal carcinoma tumors. The mIL12 mRNA treatment resulted in potent upregulation of T_H1 type cytokines and chemokines. A reduction in number of Tregs, increase in numbers and activation state of both cytotoxic T cells (CTLs) as well as tumor-associated macrophages (TAMs) was observed indicating enhanced anti-tumor, cell-based immune responses in the tumor microenvironment. This mIL12-induced concerted immune activation was associated with a robust killing and phagocytosis of tumor cells resulting in durable CRs. These observations suggest that intratumoral IL12mRNA therapy may benefit patients with ICI-resistant cancers.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"250"},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor-promoting function of paternally expressed gene 10 and its immunogenicity in inducing anti-tumor helper T cells in head and neck squamous cell carcinoma.","authors":"Hiroki Komatsuda, Toshihiro Nagato, Akemi Kosaka, Takayuki Ohkuri, Takaaki Sasaki, Takumi Kumai, Michihisa Kono, Hidekiyo Yamaki, Risa Wakisaka, Shunsuke Yasuda, Takahiro Inoue, Ryusuke Hayashi, Nanami Ujiie, Ryosuke Sato, Kenzo Ohara, Kan Kishibe, Tatsuya Hayashi, Miki Takahara, Hiroya Kobayashi","doi":"10.1007/s00262-025-04110-3","DOIUrl":"10.1007/s00262-025-04110-3","url":null,"abstract":"<p><p>Paternally expressed gene 10 (PEG10) is expressed primarily in the placenta; its expression is extremely low or absent in normal tissues but up-regulated in various cancers, indicating that PEG10 is a potential target for cancer immunotherapy. However, the expression and role of PEG10 in head and neck squamous cell carcinoma (HNSCC) and the immunogenicity of possible PEG10-derived T-cell epitopes remain unclear. In the present study, we show that PEG10 is expressed in HNSCC, and its high expression is associated with poor patient survival. Suppression of PEG10 expression attenuated the proliferation, migration, and invasion of HNSCC cells and altered their gene expression profiles. We also identified a PEG10-derived peptide epitope (PEG10_216-232) capable of eliciting antigen-specific and promiscuous human leukocyte antigen (HLA)-DR-restricted helper T lymphocyte (HTL) responses. Notably, PEG10-specific HTLs exerted direct cytotoxicity against PEG10-positive HNSCC cells in an HLA-DR-restricted manner. Moreover, precursor T cells that react to PEG10_216-232 peptide were detected in HNSCC patients. These results indicate that PEG10 plays an important role in HNSCC tumorigenesis and qualifies as an immunotherapeutic target against HNSCC. The helper epitope peptide of PEG10 could effectively stimulate antigen-specific HTLs and induce anti-tumor responses against PEG10-positive cancers, including HNSCC.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"251"},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: KLF12 as a potential biomarker for lateral pelvic lymph node metastases in advanced rectal cancer.","authors":"Tixian Xiao, Fangze Wei, Sicheng Zhou, Fuqiang Zhao, Fei Huang, Liu Qian","doi":"10.1007/s00262-025-04114-z","DOIUrl":"10.1007/s00262-025-04114-z","url":null,"abstract":"","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"249"},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"T cell-derived small extracellular vesicles in cancer-immune interactions.","authors":"Ma Janelle Chichoco Garcia, Su Su Thae Hnit, Elena Shklovskaya, Yuling Wang","doi":"10.1007/s00262-025-04109-w","DOIUrl":"10.1007/s00262-025-04109-w","url":null,"abstract":"<p><p>Small extracellular vesicles (sEVs) are lipid-encapsulated nanoparticles released following the endocytic fusion of multivesicular bodies with the plasma membrane. sEVs are secreted by most eukaryotic cells, and they contain proteins, RNAs and DNA. They act primarily as mediators of intercellular communication through the transport of their contents from donor to recipient cells. Immune cells, including T cells, secrete sEVs following activation. T cell-derived sEVs (T-sEVs) have gained attention in cell-to-cell signalling and as promising immunotherapeutic agents. Growing evidence suggests that T-sEVs are key players in cancer immunotherapy responses. A better understanding of T-sEVs production and properties is key for grasping their biological functions. Extensive current literature on tumour-derived sEVs and their applications in diagnostics or therapeutics is in disconnect with fewer reports on T-sEVs. In this review, we discuss T-sEV biogenesis, their roles in cell-to-cell communication and potential applications in immunotherapy for cancer.</p>","PeriodicalId":520581,"journal":{"name":"Cancer immunology, immunotherapy : CII","volume":"74 8","pages":"252"},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}