Pub Date : 2026-02-10DOI: 10.1016/j.immuni.2026.01.020
Victor Bosteels, Sophie Janssens
{"title":"Doping cDC1s for tolerance","authors":"Victor Bosteels, Sophie Janssens","doi":"10.1016/j.immuni.2026.01.020","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.01.020","url":null,"abstract":"","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"48 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146152841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-10DOI: 10.1016/j.immuni.2026.01.024
Christopher A. Polera, Alex M. Jaeger
{"title":"TCRAFT: A Rosetta Stone for T cell receptors","authors":"Christopher A. Polera, Alex M. Jaeger","doi":"10.1016/j.immuni.2026.01.024","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.01.024","url":null,"abstract":"","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"5 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146152844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-10DOI: 10.1016/j.immuni.2025.12.005
Nicholas M. Adams, Aleksandra Galitsyna, Ioanna Tiniakou, Eduardo Esteva, Ai C. Ra, Simon Ullrich, Stephen T. Yeung, Yanjun Tan, Joseph N. Pucella, Igor Dolgalev, David E. Levy, Kamal M. Khanna, Irina Solovei, Leonid A. Mirny, Boris Reizis
{"title":"Chromatin-mediated anticipatory control of type I interferon production in plasmacytoid dendritic cells","authors":"Nicholas M. Adams, Aleksandra Galitsyna, Ioanna Tiniakou, Eduardo Esteva, Ai C. Ra, Simon Ullrich, Stephen T. Yeung, Yanjun Tan, Joseph N. Pucella, Igor Dolgalev, David E. Levy, Kamal M. Khanna, Irina Solovei, Leonid A. Mirny, Boris Reizis","doi":"10.1016/j.immuni.2025.12.005","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.12.005","url":null,"abstract":"","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"18 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146152843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-10DOI: 10.1016/j.immuni.2026.01.003
Luisa Menezes-Silva, Mingeum Jeong, Charles Carr, Riley M. Schneider, Silvia Pires, Ana C. Codo, Jazib Uddin, Alexander Grier, Randy S. Longman, Niels Olsen Saraiva Camara, David Artis, Seong-Ji Han, Nicholas Collins
{"title":"Hormonal rewiring of immunity during dietary restriction ensures host defense and systemic glucose conservation","authors":"Luisa Menezes-Silva, Mingeum Jeong, Charles Carr, Riley M. Schneider, Silvia Pires, Ana C. Codo, Jazib Uddin, Alexander Grier, Randy S. Longman, Niels Olsen Saraiva Camara, David Artis, Seong-Ji Han, Nicholas Collins","doi":"10.1016/j.immuni.2026.01.003","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.01.003","url":null,"abstract":"","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"118 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146152846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-10DOI: 10.1016/j.immuni.2026.01.021
Juan Zhang, Qiang Liu
Immunotherapeutic approaches to brain aging remain largely preclinical and in early translational stages, and they have focused mostly on modulating innate immunity. In this issue of Immunity, Negredo et al. identify T cells bearing exhaustion-like signatures as a hallmark of brain aging and reveal the beneficial effects of an engineered IL-10 variant that functionally uncouples pro- and anti-inflammatory signaling in microglia.
{"title":"Shedding light on interventions for brain aging","authors":"Juan Zhang, Qiang Liu","doi":"10.1016/j.immuni.2026.01.021","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.01.021","url":null,"abstract":"Immunotherapeutic approaches to brain aging remain largely preclinical and in early translational stages, and they have focused mostly on modulating innate immunity. In this issue of <em>Immunity</em>, Negredo et al. identify T cells bearing exhaustion-like signatures as a hallmark of brain aging and reveal the beneficial effects of an engineered IL-10 variant that functionally uncouples pro- and anti-inflammatory signaling in microglia.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"57 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146145961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-09DOI: 10.1016/j.immuni.2025.12.011
Jeffrey Downey, Ana Oliveira-Coelho, Máté G. Kiss, Gabriel Laghlali, Alexander Leunig, Emir Radkevich, Laszlo Halasz, Martin Umali, Joana Ferreira da Silva, Madeline L. Eller, Matteo Gianeselli, Magdalena M. Żak, Haley E. Randolph, Gabriel Caumartin, Wolfram C. Poller, Henrike Janssen, Laura L. Koekkoek, Jamshid Abdul-Ghafar, Pacific Huynh, Darwin D’Souza, Vladimir Roudko, Sheqouia Nauta, Jazz Munitz, Xisheng Li, Thomas Rathner, Ziche Chen, Anh Phan, Abigail Glick, Katarzyna Cialowicz, Zhihong Chen, Seunghee Kim-Schulze, Seonghun Yoon, Matthias Nahrendorf, Susmita Sahoo, Miriam Merad, Adolfo García-Sastre, Cameron S. McAlpine, Gustav J. Strijkers, Viviana Simon, Rachel Brody, Saurabh Mehandru, Zahi A. Fayad, Benjamin P. Kleinstiver, Lior Zangi, Mandy M.T. van Leent, Michael Schotsaert, Filip K. Swirski
Abundant evidence has correlated influenza infection with cardiovascular disease, yet mechanisms linking infection with the heart remain poorly understood. Here, we show that influenza infection damaged the human and murine heart. In mice, we showed that shortly after pulmonary infection, the virus infected a circulating myeloid pro-dendritic cell 3 (pro-DC3) that expressed high concentrations of the chemokine receptor CCR2. The heart, which produces abundant CCL2, preferentially attracted infected pro-DC3. In the myocardium, the virus escaped pro-DC3, infected cardiomyocytes, and triggered production of type-I interferon (IFN-I). Engagement of the IFN-I receptor (IFNAR1) on cardiomyocytes caused tissue damage and compromised heart function. Genetically and therapeutically dampening IFNAR1 exclusively in cardiomyocytes protected the heart while preserving anti-viral immunity in the lung. Our results identify a series of host-pathogen interactions that propagate tissue damage and uncover an axis for intervention to mitigate cardiovascular risk following viral infection.
{"title":"Influenza hijacks myeloid cells to inflict type-I interferon-fueled damage in the heart","authors":"Jeffrey Downey, Ana Oliveira-Coelho, Máté G. Kiss, Gabriel Laghlali, Alexander Leunig, Emir Radkevich, Laszlo Halasz, Martin Umali, Joana Ferreira da Silva, Madeline L. Eller, Matteo Gianeselli, Magdalena M. Żak, Haley E. Randolph, Gabriel Caumartin, Wolfram C. Poller, Henrike Janssen, Laura L. Koekkoek, Jamshid Abdul-Ghafar, Pacific Huynh, Darwin D’Souza, Vladimir Roudko, Sheqouia Nauta, Jazz Munitz, Xisheng Li, Thomas Rathner, Ziche Chen, Anh Phan, Abigail Glick, Katarzyna Cialowicz, Zhihong Chen, Seunghee Kim-Schulze, Seonghun Yoon, Matthias Nahrendorf, Susmita Sahoo, Miriam Merad, Adolfo García-Sastre, Cameron S. McAlpine, Gustav J. Strijkers, Viviana Simon, Rachel Brody, Saurabh Mehandru, Zahi A. Fayad, Benjamin P. Kleinstiver, Lior Zangi, Mandy M.T. van Leent, Michael Schotsaert, Filip K. Swirski","doi":"10.1016/j.immuni.2025.12.011","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.12.011","url":null,"abstract":"Abundant evidence has correlated influenza infection with cardiovascular disease, yet mechanisms linking infection with the heart remain poorly understood. Here, we show that influenza infection damaged the human and murine heart. In mice, we showed that shortly after pulmonary infection, the virus infected a circulating myeloid pro-dendritic cell 3 (pro-DC3) that expressed high concentrations of the chemokine receptor CCR2. The heart, which produces abundant CCL2, preferentially attracted infected pro-DC3. In the myocardium, the virus escaped pro-DC3, infected cardiomyocytes, and triggered production of type-I interferon (IFN-I). Engagement of the IFN-I receptor (IFNAR1) on cardiomyocytes caused tissue damage and compromised heart function. Genetically and therapeutically dampening IFNAR1 exclusively in cardiomyocytes protected the heart while preserving anti-viral immunity in the lung. Our results identify a series of host-pathogen interactions that propagate tissue damage and uncover an axis for intervention to mitigate cardiovascular risk following viral infection.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"315 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146146750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-30DOI: 10.1016/j.immuni.2026.01.013
Dianyu Chen, Heping Xu
The meninges, long viewed as passive protective membranes, are now recognized as active immunological interfaces harboring diverse immune populations. Among them, B cells have emerged as dynamic participants in central nervous system (CNS) homeostasis and disorders. Recent studies have identified distinct B cell subsets in the meninges at different developmental and activation stages, including precursors supported by skull marrow-derived progenitors and immunoglobulin A (IgA)⁺ plasma cells influenced by gut microbiota. These meningeal B cells contribute to immune tolerance, barrier protection, and potentially neural development and repair, while also exhibiting context-dependent pathogenic roles in CNS autoimmunity, aging, and neurodegeneration. In this review, we discuss the current knowledge of meningeal B cells and highlight key future research directions aimed at understanding their cellular dynamics, activation and differentiation processes, and the balance between protective and deleterious functions.
{"title":"Meningeal B cells: Emerging players at the brain border","authors":"Dianyu Chen, Heping Xu","doi":"10.1016/j.immuni.2026.01.013","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.01.013","url":null,"abstract":"The meninges, long viewed as passive protective membranes, are now recognized as active immunological interfaces harboring diverse immune populations. Among them, B cells have emerged as dynamic participants in central nervous system (CNS) homeostasis and disorders. Recent studies have identified distinct B cell subsets in the meninges at different developmental and activation stages, including precursors supported by skull marrow-derived progenitors and immunoglobulin A (IgA)⁺ plasma cells influenced by gut microbiota. These meningeal B cells contribute to immune tolerance, barrier protection, and potentially neural development and repair, while also exhibiting context-dependent pathogenic roles in CNS autoimmunity, aging, and neurodegeneration. In this review, we discuss the current knowledge of meningeal B cells and highlight key future research directions aimed at understanding their cellular dynamics, activation and differentiation processes, and the balance between protective and deleterious functions.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"14 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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