Immunotherapy advances最新文献

{"title":"Correction to: Applying population mechanistic modelling to find determinants of chimeric antigen receptor T-cells dynamics in month-one lymphoma patients.","authors":"","doi":"10.1093/immadv/ltaf028","DOIUrl":"10.1093/immadv/ltaf028","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/immadv/ltaf001.].</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf028"},"PeriodicalIF":4.9,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12421572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042351","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":"CD40L and IL-4 suppress NK cell-mediated antibody-dependent cellular cytotoxicity through the HLA-E:NKG2A axis.","authors":"Lara V Graham, Ludmila Horehajova, Marco V Haselager, Jack G Fisher, Jamie Lee Roos, Russell B Foxall, Mel John, Kerry L Cox, Robert J Oldham, Martin C Taylor, Margaret Ashton-Key, Ben Sale, Laura G Bartlett, Ali Roghanian, Eric Eldering, Andres F Vallejo, Francesco Forconi, Salim I Khakoo, Mark S Cragg, Matthew D Blunt","doi":"10.1093/immadv/ltaf029","DOIUrl":"10.1093/immadv/ltaf029","url":null,"abstract":"<p><strong>Background: </strong>Anti-CD20 antibodies are first-line treatments for B cell malignancies. Natural killer (NK) cells are important mediators of anti-CD20 antibody efficacy in humans through antibody-dependent cellular cytotoxicity (ADCC). In B cell malignancies, the lymph nodes are a critical site of pathology and the T cell-derived signals CD40L and IL-4 within the lymph node microenvironment can mediate tumour proliferation, survival and resistance to pro-apoptotic therapy. CD40L and IL-4 have recently been shown to inhibit NK cell activation against chronic lymphocytic leukaemia (CLL) cells via the HLA-E:NKG2A immune checkpoint axis. However, the effect of these signals on NK cell-mediated ADCC of malignant B cells is unclear.</p><p><strong>Methods: </strong>Using a combination of clinical samples, murine models, flow cytometry, immunoblotting, immunohistochemistry, ELISA, bioinformatics and functional assays, we examined the impact of lymph node-mimicking conditions on NK cell-mediated ADCC against malignant B cells. Exogenous CD40L and IL-4 were used to mimic T-B cell interactions in 2D malignant B cell cultures, in addition to a 3D spheroid model of T cell-dependent CLL proliferation.</p><p><strong>Results: </strong>CD40L and IL-4 increased HLA-E expression on the surface of primary CLL cells and non-Hodgkin's lymphoma (NHL) cell lines, and this decreased NK cell-mediated ADCC via ligation of the inhibitory receptor NKG2A. High HLA-E surface expression was observed in lymph node FFPE sections of CLL and NHL patients and in a 3D <i>ex vivo</i> lymph node-mimicking model of CLL. NKG2A blockade potentiated NK cell-mediated ADCC against malignant B cells treated with CD40L and IL-4 and improved anti-CD20 antibody therapy in a murine model of B cell lymphoma.</p><p><strong>Conclusion: </strong>These results reveal a novel mechanism of resistance to anti-CD20 therapy in B cell malignancies and demonstrate that the combination of anti-NKG2A with anti-CD20 could improve the treatment of patients with CLL or NHL.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf029"},"PeriodicalIF":4.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115133","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":"Going viral: targeting glioblastoma using oncolytic viruses.","authors":"Katie Coates, Robert J Nibbs, Alasdair R Fraser","doi":"10.1093/immadv/ltaf024","DOIUrl":"10.1093/immadv/ltaf024","url":null,"abstract":"<p><p>Glioblastoma (GBM) is a devastating malignant disease with a remarkably low 5-year survival rate and invariably poor prognosis. Current conventional treatment options (surgery, targeted radiotherapy, and a limited number of chemotherapies) are rarely entirely effective, leading to the majority of GBM patients experiencing disease recurrence shortly after primary treatment. Thus far, immunotherapeutic approaches towards GBM treatment have been largely unsuccessful due to the tumour site and profoundly immunosuppressive tumour microenvironment (TME). However oncolytic virus therapy (OVT) has been recently developed and licenced for the treatment of cancers and has the potential to switch the TME to become immune-reactive. This has been shown to both directly reduce tumour burden while also enhancing responsiveness to other therapies. In this review, we review the challenges faced by standard immunotherapies in GBM and outline the various approaches to OV treatment of GBM. We highlight the promise of OVT for targeting GBM by critically assessing the outcomes from recent clinical trials.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf024"},"PeriodicalIF":4.9,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12290287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144735888","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":"Cytokine-induced memory-like NK cells combined with Tafasitamab demonstrate efficacy against B-cell acute lymphoblastic leukemia.","authors":"Dimitrios Filioglou, Geovana S F Leite, Helena Batatinha, Nina Santa-Cruz, Dan W Davini, Forrest L Baker, Richard J Simpson, Emmanuel Katsanis","doi":"10.1093/immadv/ltaf025","DOIUrl":"10.1093/immadv/ltaf025","url":null,"abstract":"<p><p>Cytokine-induced memory-like natural killer cells (CIMLNK) represent a novel form of adoptive cellular therapy that is easy to manufacture and readily available. These cells are generated after overnight stimulation of purified natural killer (NK) cells with interleukin-12 (IL-12), interleukin-15 (IL-15), and interleukin-18 (IL-18). While CIMLNK has demonstrated efficacy in patients with relapsed or refractory acute myeloid leukemia (AML), its potential application in B-cell acute lymphoblastic leukemia (B-ALL) remains unclear. Tafasitamab (TAFA), a monoclonal antibody (mAb) directed against CD19, a surface antigen expressed on B-ALL cells, has been developed to augment anti-tumor efficacy through antibody-dependent cellular cytotoxicity (ADCC), a mechanism predominantly mediated by NK cells. Consequently, we sought to assess the susceptibility of B-ALL to the combination of CIMLNK and TAFA using three B-ALL cell lines: NALM6, SUP-B15, and RS4;11. The addition of TAFA significantly augmented the cytotoxic activity, degranulation capacity, and IFN-γ production of CIMLNK. TAFA-induced ADCC was found to be dose-dependent and was abolished after CD16 blockade. Furthermore, TAFA-mediated effects against NALM6 and SUP-B15 were more pronounced in CIMLNK compared to unstimulated NK cells. In vivo, the combination of CIMLNK and TAFA led to a more pronounced survival benefit in leukemia-bearing mice. In summary, our findings suggest that this combination holds promise as a potential alternative treatment option for patients with relapsed refractory B-ALL.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf025"},"PeriodicalIF":4.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12264592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144651326","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":"SMAC mimetics induce human macrophages to phagocytose live cancer cells.","authors":"Samantha Y Liu, Max P M Hulsman, Philipp Leyendecker, Eugena Chang, Katherine A Donovan, Fabian Strobel, James Dougan, Eric S Fischer, Michael Dougan, Stephanie K Dougan, Li Qiang","doi":"10.1093/immadv/ltaf026","DOIUrl":"10.1093/immadv/ltaf026","url":null,"abstract":"<p><p>Macrophages engulf apoptotic bodies and cellular debris as part of homeostasis, but they can also phagocytose live cells, such as aged red blood cells. Pharmacologic reprogramming with the SMAC mimetic LCL161 in combination with T-cell-derived cytokines can induce macrophages to phagocytose live cancer cells in mouse models. Here we extend these findings to encompass a wide range of monovalent and bivalent SMAC mimetic compounds, demonstrating that live cell phagocytosis is a class effect of these agents. We demonstrate robust phagocytosis of live pancreatic and breast cancer cells by primary human macrophages across a range of healthy donors. Unlike mouse macrophages, where a combination of SMAC mimetics with lymphotoxin enhanced phagocytosis, human macrophages were more efficiently polarized to phagocytose live cells by the combination of SMAC mimetics and IFNg. We profiled phagocytic macrophages by transcriptional and proteomic methodologies, uncovering a positive feedback loop of autocrine TNFa production.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf026"},"PeriodicalIF":4.9,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12314603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144777079","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":"Targeting of acute myeloid leukemia by five-gene engineered T cells expressing transgenic T-cell receptor specific to WT1, chimeric antigenic receptor specific to GM-CSF receptor, bispecific T-cell engager specific to CD33, and tEGFR suicide gene system.","authors":"Kristýna Šmilauerová, Martin Štach, Martin Mucha, Šárka Vaníková, Jana Rychlá, Pavel Otáhal","doi":"10.1093/immadv/ltaf022","DOIUrl":"10.1093/immadv/ltaf022","url":null,"abstract":"<p><strong>Background: </strong>Cancer immunotherapy with transgenic T-cell receptor-engineered T cells (TCR-T) enables the targeting of intracellular tumor-specific antigens; in contrast, chimeric antigen receptor-modified T cells (CAR-T) mediate tumor cell killing via the recognition of surface antigens. In the case of acute myeloid leukemia, the lack of leukemia-specific surface antigens limits the efficacy of CAR-T cells; therefore, TCR-T cells may represent a more targeted immunotherapy approach. However, the tumor immunosuppressive environment eliminates the best-functioning, high-avidity TCR-T cells, thus creating a need for novel, enhanced TCR-T cells.</p><p><strong>Methods: </strong>The piggyBac transposon vector used for gene modification of T cells expresses a T-cell receptor specific to the WT1 tumour antigen, an NFAT promoter-regulated CAR specific to GM-CSF receptor, a CD3xCD33 bispecific T-cell engager, and a truncated EGFR suicide gene system. The transgenic T cells were generated by electroporation using a single expression vector, and the efficiency of these engineered TCR-T cells was evaluated using models that utilized AML cell lines and primary AML cells.</p><p><strong>Results: </strong>The NFAT-driven GM-CSF CAR significantly enhances the antileukemic activity of WT1-specific TCR-T cells, which importantly maintain specificity for their HLA/peptide antigenic complex. Next, by inserting the CD3xCD33 bispecific T-cell engager into the transposon vector, both TCR-T cells and recruited non-transfected bystander T cells can efficiently target the CD33 antigen, providing more robust antileukemic effects.</p><p><strong>Conclusion: </strong>The presented strategy, utilizing a single piggyBac transposon vector, enables the complex redirection of T-cell specificity against acute myeloid leukemia by inserting TCR, CAR, BiTE constructs, along with a tEGFR gene suicide system.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf022"},"PeriodicalIF":4.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12306182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144746375","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 cell spheroid-induced suppression of primary human cytotoxic T cells as a scalable <i>in vitro</i> model of exhaustion.","authors":"Amal Alsubaiti, Hanin Alamir, Lan Huynh, Tressan Grant, Abdullah Aljohani, Po Han Chou, Yiwei Shi, Maryam Alismail, Lydia R Mason, Andrew Herman, John S Bridgeman, Christopher J Holland, Christoph Wülfing","doi":"10.1093/immadv/ltaf023","DOIUrl":"10.1093/immadv/ltaf023","url":null,"abstract":"<p><strong>Background: </strong>Cytotoxic T lymphocytes (CTL) are key effectors in the antitumor immune response. However, their function is commonly suppressed in tumors in the form of exhausted CTL. Understanding mechanisms of suppression and of therapeutics to overcome them is of substantial basic and translational importance yet hindered by limited access to large numbers of exhausted CTL in vitro.</p><p><strong>Methods: </strong>Here we use three-dimensional tissue culture to generate primary human CTL with suppressed function. Using functional assays, a 21-antibody flow cytometry panel and determination of calcium signaling and CTL tumor cell couple maintenance, we have characterized their phenotype.</p><p><strong>Results: </strong>We show that these cells closely resemble exhausted CTL from tumors. For a better understanding of in vitro human primary CTL as key tools in therapeutic development, before and after induction of suppression, we have determined the dependence of CTL function on methodology of generation, antigen dose, and affinity across two T-cell receptors and multiple tumor cell lines. As a further determination of their phenotype, we have investigated the morphology and subcellular F-actin distributions of CTL as key regulators of effector function. Primary human CTL formed cell couples with tumor target cells even in the absence of antigen. Yet, the gradual stabilization of such cell couples was associated with increasing CTL effector function. Induction of suppression substantially destabilized CTL tumor cell couples.</p><p><strong>Conclusion: </strong>This comprehensive characterization of the phenotype of in vitro primary human CTL, including a suppressed state, should facilitate their use in basic research, the development of CTL-targeting therapeutics and the determination of their mechanism of action.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf023"},"PeriodicalIF":4.1,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12207883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144531348","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":"Applying population mechanistic modelling to find determinants of chimeric antigen receptor T-cells dynamics in month-one lymphoma patients.","authors":"Liam V Brown, Mark McConnell, Robert Rosler, Leanne Peiser, Brian J Schmidt, Alexander V Ratushny, Eamonn A Gaffney, Mark C Coles","doi":"10.1093/immadv/ltaf001","DOIUrl":"10.1093/immadv/ltaf001","url":null,"abstract":"<p><strong>Background: </strong>Chimeric antigen receptor (CAR) T-cells have been utilized for the treatment of several malignancies, including Non-Hodgkin lymphomas. A myriad of product- and patient-specific factors determines the extent of patient response, and determining which are most impactful requires analysis of clinical data.</p><p><strong>Methods: </strong>We used population-level ordinary differential equation models to fit clinical flow cytometry and tumour biopsy data from the TRANSCEND-NHL-001 (NCT02631044) study [1]. We analyzed the impact of lymphodepletion, CAR T-cell phenotypes, and other factors on CAR T-cell dynamics for 30 days after infusion.</p><p><strong>Results: </strong>We quantified the relative contribution of antigen-dependent and independent sources of proliferation on CAR T-cell dynamics, finding that both make a large contribution and that antigen-independent proliferation was highly correlated with patient IL-15 and IL-7 blood concentrations. The proportion of CAR T-cells in naïve, memory, or effector cells was found to have a limited impact on CAR T-cell dynamics, compared with lymphodepletion and tumour burden.</p><p><strong>Conclusions: </strong>This study shows how models can be used to link endogenous T-cells, CAR T-cells, and their phenotypes, and may be useful for determining whether a given patient may be responding poorly to treatment, by observing the dynamics of their endogenous T-cells. The framework we developed can be utilized for other CAR T constructs and indications, to test product alterations or biological hypotheses at the population level.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf001"},"PeriodicalIF":4.9,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12362351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981218","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":"High level of anti-drug antibodies is associated with shorter survival in advanced solid cancer patients treated with Immune checkpoint inhibitors.","authors":"Rui Zhao, Weihao Wang, Jingliang Wang, Yahui Wang, Liying Pan, Pancen Ran, Fang Luan, Guobin Fu","doi":"10.1093/immadv/ltaf019","DOIUrl":"10.1093/immadv/ltaf019","url":null,"abstract":"<p><strong>Background: </strong>Camrelizumab has become the first-line treatment for most patients with advanced tumors. Among advanced tumor patients undergoing camrelizumab, the majority develop immunogenicity, resulting in the production of anti-drug antibodies (ADA). The impact of ADA on the efficacy and safety of camrelizumab treatment is currently unknown.</p><p><strong>Method: </strong>Hematologic samples from 31 tumor patients treated with camrelizumab were collected to serve as an experimental cohort for ADA levels detection. Concurrently, a separate validation cohort consisting of 16 patients was established. Follow-up data on patients' OS and PFS were collected and analyzed.</p><p><strong>Results: </strong>High ADA levels (≥1200 ng/ml) after the three cycles camrelizumab treatment were linked to poorer patient outcomes, as shown by significant differences between PD and PR (<i>P</i> = 0016) and PR and SD (<i>P</i> = .0439). This trend was also present in the validation cohort (PD vs PR, <i>P</i> = .0413). More importantly, high ADA levels after the three cycles camrelizumab treatment were associated with a significant reduction in OS (<i>P</i> = .0128) and PFS (<i>P</i> = .0004), with the validation cohort reporting comparable findings (OS: <i>P</i> = .0009; PFS: <i>P</i> = .0007). Additionally, camrelizumab concentration was negatively correlated with ADA levels (experimental cohort: <i>R</i> ² = 0.3876; validation cohort: <i>R</i> ² = 0.3702). Patients had higher ADA levels after the early phase of camrelizumab treatment.</p><p><strong>Conclusion: </strong>High ADA levels were associated with shorter OS and PFS in patients after three cycles of camrelizumab therapy. Furthermore, patients had higher ADA levels after the early phase of treatment, specifically in the first three cycles with camrelizumab. It found that the higher the ADA concentration, the lower the serum camrelizumab concentration.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf019"},"PeriodicalIF":4.1,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12167428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144303845","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":"Comparing DC subsets in solid tumors: what about DC3s?","authors":"Casper J Pachocki, Marianne Boes, Alsya J Affandi","doi":"10.1093/immadv/ltaf021","DOIUrl":"10.1093/immadv/ltaf021","url":null,"abstract":"<p><p>Dendritic cells (DCs) are critical sentinels of the immune system, serving as indispensable bridges between innate and adaptive immune responses. DCs are a heterogeneous population, with subsets playing specialized roles in immune defense, tolerance, or disease development. Among these, the recently redefined DC3 subset has gained attention for its unique features and potential roles in health and disease. This review focuses on the phenotypic, functional, and developmental diversity of DC subsets-primarily DC3s-and their contributions to cancer. The tumor microenvironment (TME) in solid tumors is characterized by varying degrees of immune cell infiltration, including DCs. Within the TME, DCs play diverse roles, either promoting anti-tumor responses or facilitating immune evasion. Key subsets include conventional type 1 and type 2 DCs (cDC1s and cDC2s), as well as plasmacytoid DCs (pDCs). DC3s share certain features with cDC2s and monocytes but are distinct in their phenotype, function, and ontogeny. Functionally, DC3s can prime and activate T cells, skewing CD4⁺ T cells towards Th17 and stimulating CD8⁺ T cells with a tissue-resident memory phenotype. In cancer, their presence correlates with diverse outcomes depending on the TME: DC3 presence is linked to increased survival in patients with pancreatic ductal adenocarcinoma and oropharyngeal cancer while in non-small-cell lung cancer and melanoma it is associated with immunosuppression. The emerging understanding of DC3s highlights the complexity of DC biology and its relevance to diseases. The dynamic immunomodulatory functions of DC3s open new avenues for developing targeted therapies against cancer and immune-mediated disorders.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf021"},"PeriodicalIF":4.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144531347","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}