Cell Reports MedicinePub Date : 2026-09-15Epub Date: 2026-08-28DOI: 10.1016/j.xcrm.2026.103011
Clara Helal, Léa Pinon, Juliette Jin, Niccolo Schintu, Ana Vazquez, Léna Domalain, Martin Nurmik, Gianni Antonelli, Ségolène Ladaigue, Maxime Simon, Elodie Montaudon, Laura Sourd, Heloise Derrien, Gérard Zalcman, Angela Bellini, Andreia Goncalves, Anne Vincent-Salomon, Toulsie Ramtohul, Elisabetta Marangoni, Maria Carla Parrini, Luc Cabel, Stéphanie Descroix
{"title":"Tumor-on-chip as a personalized platform for rapid drug testing in breast cancer.","authors":"Clara Helal, Léa Pinon, Juliette Jin, Niccolo Schintu, Ana Vazquez, Léna Domalain, Martin Nurmik, Gianni Antonelli, Ségolène Ladaigue, Maxime Simon, Elodie Montaudon, Laura Sourd, Heloise Derrien, Gérard Zalcman, Angela Bellini, Andreia Goncalves, Anne Vincent-Salomon, Toulsie Ramtohul, Elisabetta Marangoni, Maria Carla Parrini, Luc Cabel, Stéphanie Descroix","doi":"10.1016/j.xcrm.2026.103011","DOIUrl":"10.1016/j.xcrm.2026.103011","url":null,"abstract":"<p><p>Breast cancer (BC) continues to pose major therapeutic challenges, emphasizing the need for functional models that can rapidly inform treatment selection. Patient-derived xenografts (PDXs) and organoids (PDOs) are valuable tools for precision oncology, but their clinical utility is limited by inconsistent success rates and lengthy timelines. Here, we develop a tumor-on-chip (ToC) platform enabling functional drug sensitivity profiling within 4 days. ToC models show high reproducibility and a strong concordance with in vivo PDX responses. Drug sensitivity is correctly identified in 88% of PDX-responsive cases, while resistance was detected in 91%, with no false positives at clinically relevant concentrations. We design a chip compatible with minimal BC biopsy material. Proof-of-concept studies on patient samples show that the platform can distinguish sensitive and resistant profiles. These findings support the translational potential of ToC models for rapid personalized drug profiling in BC, laying the ground for their integration into clinical decision-making workflows.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"103011"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Discovery of antimicrobial peptides from incomplete biosynthetic gene clusters to combat multidrug-resistant bacteria.","authors":"Yao Tang, Xin Cheng, Jing Zhou, Yuqi Shi, Jiaying Zhou, Zaiyang Chen, Yan Zhang, Liucun Zhu, Jian-Qun Chen, Jiang Gu, Qiang Wang, Qihan Chen","doi":"10.1016/j.xcrm.2026.102982","DOIUrl":"10.1016/j.xcrm.2026.102982","url":null,"abstract":"<p><p>The escalating crisis of multidrug-resistant bacteria necessitates innovative antibiotic discovery platforms. Conventional antimicrobial peptide (AMP) mining often relies on complete biosynthetic gene clusters (BGCs), leaving fragmented genomic resources underexplored. Here, we present an evolution-inspired approach to reconstruct and predict AMPs from partial BGCs. Applying this strategy to 954 Paenibacillus genomes identifies five polymyxin-like peptides, NP001-NP005, with broad in vitro activity. Crucially, in murine models of polymyxin-resistant infection, NP001 reduced bacterial burdens by up to 1,000-fold in a thigh infection model and improved survival (50% vs. 0%) in a lethal peritonitis model. Structural simulations and biophysical assays revealed that NP001 maintains high affinity for bacterial membranes and effectively binds to MCR-1-modified lipid A, a key colistin-resistance mechanism. Moreover, Leu at position 10 of NP001 plays a key role in antibacterial activity against MCR-1-resistant bacteria. Our work establishes a generalizable framework for AMP discovery and introduces a promising therapeutic candidate, NP001, which effectively counteracts polymyxin-resistant pathogens.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"102982"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148720955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2026-09-15Epub Date: 2026-08-25DOI: 10.1016/j.xcrm.2026.103008
Adeleye O Adeshakin, Hao Shi, S Scott Perry, Heather Sheppard, Phuong Nguyen, Xiang Sun, Peipei Zhou, Jean-Yves Métais, Trevor Cunningham, Anil Kc, Liqing Tian, Vivek Peche, Mollie S Prater, Deanna M Langfitt, Carla O'Reilly, Jeoungeun J Park, Ashley Chabot, Sheng Zhou, Azusa Matsubara, GaHyun Lee, Shengdar Q Tsai, Shondra M Pruett-Miller, Lindsay J Talbot, Jason T Yustein, Giedre Krenciute, Christopher DeRenzo, Hongbo Chi, Stephen Gottschalk
{"title":"Targeting Regnase-1 in B7-H3-CAR T cells reprograms the tumor microenvironment and enhances antitumor efficacy for osteosarcoma.","authors":"Adeleye O Adeshakin, Hao Shi, S Scott Perry, Heather Sheppard, Phuong Nguyen, Xiang Sun, Peipei Zhou, Jean-Yves Métais, Trevor Cunningham, Anil Kc, Liqing Tian, Vivek Peche, Mollie S Prater, Deanna M Langfitt, Carla O'Reilly, Jeoungeun J Park, Ashley Chabot, Sheng Zhou, Azusa Matsubara, GaHyun Lee, Shengdar Q Tsai, Shondra M Pruett-Miller, Lindsay J Talbot, Jason T Yustein, Giedre Krenciute, Christopher DeRenzo, Hongbo Chi, Stephen Gottschalk","doi":"10.1016/j.xcrm.2026.103008","DOIUrl":"10.1016/j.xcrm.2026.103008","url":null,"abstract":"<p><p>The microenvironment in solid tumors represents an immunosuppressive therapeutic barrier to CAR T cell therapy, and it is currently unknown whether it can be reshaped by the deletion of negative regulators in CAR T cells. To address this knowledge gap, we evaluated the intrinsic and extrinsic effects of deleting the negative regulator Regnase-1 (Reg-1) in B7-H3-CAR T cells for the immunotherapy of osteosarcoma. Reg-1 knockout (KO) improved the antitumor activity of human and murine B7-H3-CAR T cells in vivo. In immune-competent models, Reg-1 KO also endowed murine B7-H3-CAR T cells with the ability to create a proinflammatory landscape characterized by an influx of interferon gamma (IFN-γ)-producing endogenous T cells and natural killer (NK) cells and a reduction of inhibitory myeloid cells, including M2-like macrophages. Thus, deleting Reg-1 has cell- and non-cell-autonomous benefits, nominating Reg-1 KO B7-H3-CAR T cells as a promising cell product for early-phase clinical testing in patients with solid tumors.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"103008"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2026-09-15Epub Date: 2026-08-27DOI: 10.1016/j.xcrm.2026.103010
Rozita Bagheri-Yarmand, Gabriel M Pagnotti, Joseph L Kidd, David Avila Ramirez, Trupti Trivedi, Leah Guerra, Zhongya Wang, Lucia Martinez Cruz, Jade M Moehle, Yaashmin S Jebaraj, Xinhai Wan, Jian H Song, Roland L Bassett, Sue-Hwa Lin, Mimi I Hu, Steven I Sherman, Marie-Claude Hofmann, Theresa A Guise
{"title":"RET-driven osteoprotegerin expression links medullary thyroid cancer to osteoblastic bone metastases.","authors":"Rozita Bagheri-Yarmand, Gabriel M Pagnotti, Joseph L Kidd, David Avila Ramirez, Trupti Trivedi, Leah Guerra, Zhongya Wang, Lucia Martinez Cruz, Jade M Moehle, Yaashmin S Jebaraj, Xinhai Wan, Jian H Song, Roland L Bassett, Sue-Hwa Lin, Mimi I Hu, Steven I Sherman, Marie-Claude Hofmann, Theresa A Guise","doi":"10.1016/j.xcrm.2026.103010","DOIUrl":"10.1016/j.xcrm.2026.103010","url":null,"abstract":"<p><p>Development of bone metastases increases mortality in patients with medullary thyroid cancer (MTC), with ∼50% survival at 5 years after diagnosis, but the underlying mechanisms of action are unknown. We show that patient-derived MTC cells (RET<sup>C634W</sup> mutant TT and RET<sup>M918T</sup> mutant MZCRC1 cells) promote osteoblastic phenotypes due to reduced osteoclastic bone resorption. Mechanistically, activated RET increases osteoprotegerin (OPG) expression, an inhibitor of bone resorption, leading to decreased osteoclast differentiation. Furthermore, RET knockdown or pharmacological RET inhibition attenuates tumor burden and osteoblastic lesions in MTC-bearing mouse femurs. Circulating levels of OPG in humans increase in the plasma of patients with MTC and MTC bone metastases, and these levels are associated with poor overall survival. Patients who receive multi-kinase inhibitors have lower circulating OPG levels. These findings reveal a potential link between RET signaling and aberrant osteoblastic bone formation during tumor metastasis and suggest OPG as a potential biomarker for MTC bone metastases.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"103010"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2026-09-15Epub Date: 2026-09-04DOI: 10.1016/j.xcrm.2026.103023
Federica Tavaglione, Rohit Loomba
{"title":"Emerging role of GLP-1 mono, dual, and triple agonists in the management of MASH-related fibrosis.","authors":"Federica Tavaglione, Rohit Loomba","doi":"10.1016/j.xcrm.2026.103023","DOIUrl":"10.1016/j.xcrm.2026.103023","url":null,"abstract":"<p><p>Recent therapeutic advances have resulted in US Food and Drug Administration (FDA) approval of the first pharmacological agents-resmetirom and semaglutide-for advanced metabolic dysfunction-associated steatohepatitis (MASH) without cirrhosis, reshaping the therapeutic landscape of the disease. Within this evolving framework, incretin-based pharmacotherapies-including glucagon-like peptide-1 (GLP-1) receptor agonists and their dual and triple combinations with glucose-dependent insulinotropic peptide (GIP) and/or glucagon receptor agonists-have emerged as promising options, particularly for individuals with coexisting obesity or type 2 diabetes. These agents exert pleiotropic effects across multiple organs, modulating glucose and lipid metabolism, while providing cardiovascular and renal benefits. Despite these advances, key challenges remain regarding treatment duration, tolerability, and interindividual variability in therapeutic response. This review summarizes the emerging role of GLP-1 mono, dual, and triple agonists in MASH-related fibrosis, focusing on their mechanisms of action and evidence from phase 2 and phase 3 clinical trials with histology-assessed hepatic endpoints.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"103023"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2026-09-15Epub Date: 2026-08-24DOI: 10.1016/j.xcrm.2026.103006
Steven Wang, Parisa Mapar, Norbert Moldovan, Ymke van der Pol, Aram Safrastyan, Erik van Werkhoven, Normastuti Adhini Tantyo, Bart Snieder, André F Do Brito Valente, A Vera de Jonge, Avinash Dinmohamed, Esther E E Drees, Margaretha G M Roemer, Bauke Ylstra, Clara P W Klerk, Leonie Strobbe, Yorick Sandberg, Rinske S Boersma, Harry Koene, Hans Pruijt, Koen de Heer, Rozemarijn van Rijn, Yavuz M Bilgin, Eva de Jongh, Marcel Nijland, Marjolein van der Poel, Ad Koster, Laurens Nieuwenhuizen, Rob Fijnheer, Aart Beeker, Rogier Mous, Vibeke K J Vergote, Joost S P Vermaat, D Michiel Pegtel, Martine E D Chamuleau, Florent Mouliere
{"title":"Cell-free DNA genomic and fragmentomic features for early outcome prediction in large B cell lymphoma.","authors":"Steven Wang, Parisa Mapar, Norbert Moldovan, Ymke van der Pol, Aram Safrastyan, Erik van Werkhoven, Normastuti Adhini Tantyo, Bart Snieder, André F Do Brito Valente, A Vera de Jonge, Avinash Dinmohamed, Esther E E Drees, Margaretha G M Roemer, Bauke Ylstra, Clara P W Klerk, Leonie Strobbe, Yorick Sandberg, Rinske S Boersma, Harry Koene, Hans Pruijt, Koen de Heer, Rozemarijn van Rijn, Yavuz M Bilgin, Eva de Jongh, Marcel Nijland, Marjolein van der Poel, Ad Koster, Laurens Nieuwenhuizen, Rob Fijnheer, Aart Beeker, Rogier Mous, Vibeke K J Vergote, Joost S P Vermaat, D Michiel Pegtel, Martine E D Chamuleau, Florent Mouliere","doi":"10.1016/j.xcrm.2026.103006","DOIUrl":"10.1016/j.xcrm.2026.103006","url":null,"abstract":"<p><p>Curative-intent immunochemotherapy fails in ∼30% of patients with large B cell lymphoma (LBCL), yet no validated molecular tool enables early identification of high-risk individuals to guide treatment intensification. Using shallow whole-genome sequencing (sWGS) of plasma cell-free DNA from 190 LBCL patients, we develop and validate the ACT score (aberrations, composition of fragments, and terminal motif analyses), a composite classifier integrating genomic and fragmentomic features from a single post-cycle-1 sample. ACT-positive patients have worse 2-year outcomes versus ACT-negative patients: time-to-progression 29% vs. 83% (hazard ratio [HR]: 4.4, 95% confidence interval [CI]: 1.9-10.0; p = 1.5 × 10<sup>-4</sup>) and overall survival 47% vs. 93% (HR: 8.7, 95% CI: 3.0-25.4; p = 1.8 × 10<sup>-6</sup>). The ACT score is independently prognostic of the International Prognostic Index, and their combination identifies the highest risk patients. Unlike mutation-based approaches, this assay requires neither tumor tissue, germline control, nor a baseline plasma sample. Built on open-source tools and sWGS, the ACT score offers a feasible, scalable strategy for early risk stratification in aggressive LBCL.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"103006"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Capsid inclusion in a CHIKV mRNA vaccine impairs adaptive immune responses.","authors":"Hongyu Chen, Longhai Yuan, Hao Yang, Qing Huang, Yun Yang, Cong Tang, Junbin Wang, Yanan Zhou, Wenhai Yu, Haixuan Wang, Wenqi Quan, Yuxia Yuan, Youchun Wang, Shuaiyao Lu","doi":"10.1016/j.xcrm.2026.102965","DOIUrl":"10.1016/j.xcrm.2026.102965","url":null,"abstract":"<p><p>Two mRNA vaccines (V1 and V2) from our previous study, encoding different CHIKV structural proteins, exhibit distinct immune effects and protective efficacy. However, the immune mechanisms underlying these differences remain unclear. In this study, we use an integrated multi-omics approach (single-cell RNA sequencing, immune repertoire sequencing, and Olink cytokine profiling) to elucidate the differential immune cell activation states induced by the two vaccines and the potential structural basis of the antigens that may account for these differences. We find that V2 induces sustained B cell activation, predominantly IgG-type memory antibodies, and a robust recall response following viral challenge. By contrast, V1 elicits only transient B cell activation and relatively weak T cell responses. These findings delineate a mechanistic pathway linking mRNA antigen structure to immune activation, functional differentiation, immunological memory, and protective efficacy. This work enhances our understanding of the immunological mechanisms underlying CHIKV mRNA vaccination and offers insights for rational vaccine antigen design.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"102965"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Preclinical evaluation of nitrated α-synuclein-specific CAR-Treg therapy in Parkinson's disease.","authors":"Valentina Ugalde, Daniela Elgueta, Sandra Espinoza, Ornella Chovar-Vera, Ernesto López, Alejandra Catenaccio, Francisca Álvarez-Astudillo, Dafne Franz, Vanesa Sanchez-Guajardo, María Inés Becker, Diego Figueroa, Zulmary Manjarres, Sofía Hidalgo, Álvaro Lladser, Cheril Tapia-Rojas, Alejandra Loyola, Sergio A Quezada, Roque Villagra, Rodrigo Pacheco","doi":"10.1016/j.xcrm.2026.102983","DOIUrl":"10.1016/j.xcrm.2026.102983","url":null,"abstract":"<p><p>Current evidence indicates that Parkinson's disease (PD) involves T cell-mediated inflammation, which plays a fundamental role in promoting neuroinflammation and neurodegeneration in patients and animal models. These T cells are specific to α-synuclein-derived antigens, including nitrated α-synuclein (NαSyn). Here, we sought to develop an experimental immunotherapy for PD based on the generation of regulatory T cells (Treg) specific to NαSyn, using the chimeric antigen receptor (CAR) technology. Accordingly, we first obtained an antibody specific to human α-synuclein containing three nitrated tyrosine residues (3NY-hαSyn), which displayed specific immunoreactivity in the serum of PD patients which correlated with the clinical score. Afterward, we generated CAR-Treg specific to 3NY-hαSyn and tested them in two PD models involving human α-synuclein. The CAR-Treg therapy substantially inhibited the inflammatory T cell response specific to α-synuclein-derived antigens, neuroinflammation, neurodegeneration, and the motor decline. This preclinical study indicates that the CAR-Treg therapy represents a promising therapeutic strategy for treating PD patients.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"102983"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148719991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A single-dose inhalable rAAV-vectored vaccine against mpox virus.","authors":"Zhouguang Jiao, Zhihui Zheng, Yue Xue, Hongjie Wang, Meng Zou, Peijie Qu, Guangzhi Zhang, Jiabo Ding, Yang Liu, Wenjun Liu, Lei Sun, Pengtao Jiao","doi":"10.1016/j.xcrm.2026.103019","DOIUrl":"10.1016/j.xcrm.2026.103019","url":null,"abstract":"<p><p>In response to the global mpox outbreak, an inhalable vaccine platform based on rAAV/DJ vectors is developed. This platform represents a needle-free, single-dose, highly immunogenic defense against monkeypox virus (MPXV) and related orthopoxviruses (OPXVs). Two multivalent vaccines, MV-A (encoding M1R/A35R) and MV-B (encoding A29L/B6R), are engineered, and MV-A, MV-B, and their combination (MV-C) are assessed preclinically. The vector integrates the mucosal adjuvant cholera toxin subunit B (CTB) at the 3' terminus of antigen genes, enabling the sustained production of self-assembled antigen-adjuvant nanoparticles. A single dose induces potent activation of antigen-presenting cells and pulmonary T cell responses, generating lung tissue-resident memory T cells. MV-C induces strong, durable MPXV-specific antibodies in mice and non-human primates, with sera and bronchoalveolar lavage fluid showing high neutralizing activity. Single pulmonary immunization with MV-C establishes a protective mucosal barrier in MPXV-susceptible CAST/EiJ mice and confers protection against OPXVs via respiratory or genital routes. These vaccines hold promise for combating future MPXV variants.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":"7 9","pages":"103019"},"PeriodicalIF":14.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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