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 : 2026-02-10Epub Date: 2026-01-07DOI: 10.1016/j.immuni.2025.11.023
Nicole Hamagami, Dvita Kapadia, Kia M Barclay, Yanlong Huang, Nora Abduljawad, Zuolin Cheng, Liam McLaughlin, Darsh Singhania, Xukai Ding, Jin Yang, Zhixin Sun, Vikram Karra, Siling Du, Peter Bayguinov, Guoqiang Yu, Yang E Li, Harrison W Gabel, Qingyun Li
Single-cell transcriptomic studies have identified distinct microglial subpopulations with shared and divergent gene signatures across development, aging, and disease. Whether these microglial subsets represent ontogenically separate lineages of cells or are manifestations of plastic changes in microglial states downstream of some converging signals is unknown. Furthermore, despite the well-established role of enhancer landscapes underlying the identity of microglia, the extent to which histone modifications and DNA methylation regulate microglial state switches at enhancers has not been defined. Here, using genetic fate mapping, we demonstrated the common embryonic origin of proliferative-region-associated microglia enriched in developing white matter and tracked their dynamic transitions into disease-associated microglia and white matter-associated microglia in disease and aging contexts, respectively. This study links spatiotemporally discrete microglial states through their transcriptomic and epigenomic plasticity, while revealing state-specific enhancer histone modifications and transcription regulators that govern state transitions in health and disease.
{"title":"State-specific enhancer landscapes govern microglial plasticity.","authors":"Nicole Hamagami, Dvita Kapadia, Kia M Barclay, Yanlong Huang, Nora Abduljawad, Zuolin Cheng, Liam McLaughlin, Darsh Singhania, Xukai Ding, Jin Yang, Zhixin Sun, Vikram Karra, Siling Du, Peter Bayguinov, Guoqiang Yu, Yang E Li, Harrison W Gabel, Qingyun Li","doi":"10.1016/j.immuni.2025.11.023","DOIUrl":"10.1016/j.immuni.2025.11.023","url":null,"abstract":"<p><p>Single-cell transcriptomic studies have identified distinct microglial subpopulations with shared and divergent gene signatures across development, aging, and disease. Whether these microglial subsets represent ontogenically separate lineages of cells or are manifestations of plastic changes in microglial states downstream of some converging signals is unknown. Furthermore, despite the well-established role of enhancer landscapes underlying the identity of microglia, the extent to which histone modifications and DNA methylation regulate microglial state switches at enhancers has not been defined. Here, using genetic fate mapping, we demonstrated the common embryonic origin of proliferative-region-associated microglia enriched in developing white matter and tracked their dynamic transitions into disease-associated microglia and white matter-associated microglia in disease and aging contexts, respectively. This study links spatiotemporally discrete microglial states through their transcriptomic and epigenomic plasticity, while revealing state-specific enhancer histone modifications and transcription regulators that govern state transitions in health and disease.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":" ","pages":"288-305.e11"},"PeriodicalIF":26.3,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145933078","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号