ImmunityPub Date : 2025-02-28DOI: 10.1016/j.immuni.2025.02.009
Nicholas N. Jarjour, Talia S. Dalzell, Nicholas J. Maurice, Kelsey M. Wanhainen, Changwei Peng, Stephen D. O’Flanagan, Taylor A. DePauw, Katharine E. Block, William J. Valente, K. Maude Ashby, David Masopust, Stephen C. Jameson
{"title":"Collaboration between interleukin-7 and -15 enables adaptation of tissue-resident and circulating memory CD8+ T cells to cytokine deficiency","authors":"Nicholas N. Jarjour, Talia S. Dalzell, Nicholas J. Maurice, Kelsey M. Wanhainen, Changwei Peng, Stephen D. O’Flanagan, Taylor A. DePauw, Katharine E. Block, William J. Valente, K. Maude Ashby, David Masopust, Stephen C. Jameson","doi":"10.1016/j.immuni.2025.02.009","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.009","url":null,"abstract":"Interleukin-7 (IL-7) is considered a critical regulator of memory CD8<sup>+</sup> T cell homeostasis. However, this is primarily based on circulating memory populations, and the cell-intrinsic requirement for IL-7 signaling during memory homeostasis has not been directly tested. Here, we addressed the role for IL-7Rα in circulating and resident memory CD8<sup>+</sup> T cells (Trm) after their establishment. We found that inducible <em>Il7ra</em> deletion had only a modest effect on persistence of circulating memory and Trm subsets, causing reduced basal proliferation. Loss of IL-15 signaling imposed heightened IL-7Rα dependence on memory CD8<sup>+</sup> T cells, including Trm cells described as IL-15 independent. In the absence of IL-15 signaling, IL-7Rα was elevated, and loss of IL-7Rα signaling reduced IL-15-elicited proliferation, suggesting crosstalk between these pathways in memory CD8<sup>+</sup> T cells. Thus, across subsets and tissues, IL-7 and IL-15 act in concert to support memory CD8<sup>+</sup> T cells, conferring resilience to altered availability of either cytokine.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"40 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518547","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}
ImmunityPub Date : 2025-02-28DOI: 10.1016/j.immuni.2025.02.012
Adriana M. Mujal, Mark Owyong, Endi K. Santosa, John C. Sauter, Simon Grassmann, Anna-Marie Pedde, Philippa Meiser, Claire K. Wingert, Marine Pujol, Veit R. Buchholz, Colleen M. Lau, Jan P. Böttcher, Joseph C. Sun
{"title":"Splenic TNF-α signaling potentiates the innate-to-adaptive transition of antiviral NK cells","authors":"Adriana M. Mujal, Mark Owyong, Endi K. Santosa, John C. Sauter, Simon Grassmann, Anna-Marie Pedde, Philippa Meiser, Claire K. Wingert, Marine Pujol, Veit R. Buchholz, Colleen M. Lau, Jan P. Böttcher, Joseph C. Sun","doi":"10.1016/j.immuni.2025.02.012","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.012","url":null,"abstract":"Natural killer (NK) cells possess both innate and adaptive features. Here, we investigated NK cell activation across tissues during cytomegalovirus infection, which generates antigen-specific clonal expansion and long-lived memory responses. Longitudinal tracking and single-cell RNA sequencing of NK cells following infection revealed enhanced activation in the spleen, as well as early formation of a CD69<sup>lo</sup> precursor population that preferentially gave rise to adaptive NK cells. Splenic NK cells demonstrated heightened tumor necrosis factor alpha (TNF-α) signaling and increased expression of the receptor TNFR2, which coincided with elevated TNF-α production by splenic myeloid cells. TNFR2-deficient NK cells exhibited impaired interferon gamma (IFN-γ) production and expansion. TNFR2 signaling engaged two distinct nuclear factor κB (NF-κB) signaling arms—innate effector NK cell responses required canonical NF-κB signaling, whereas non-canonical NF-κB signaling enforced differentiation of CD69<sup>lo</sup> adaptive NK cell precursors. Thus, NK cell priming in the spleen during viral infection promotes an innate-to-adaptive transition, providing insight into avenues for generating adaptive NK cell immunity across diverse settings.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"28 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518149","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}
ImmunityPub Date : 2025-02-28DOI: 10.1016/j.immuni.2025.02.003
Yuxin Zhang, Yuchao Jing, Juan He, Rui Dong, Tongyang Li, Fang Li, Xiaoqing Zheng, Gaoyu Liu, Ran Jia, Jin Xu, Fan Wu, Chunhong Jia, Jin Song, Lijuan Zhang, Pan Zhou, Haitao Wang, Zhi Yao, Qiang Liu, Ying Yu, Jie Zhou
{"title":"Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis","authors":"Yuxin Zhang, Yuchao Jing, Juan He, Rui Dong, Tongyang Li, Fang Li, Xiaoqing Zheng, Gaoyu Liu, Ran Jia, Jin Xu, Fan Wu, Chunhong Jia, Jin Song, Lijuan Zhang, Pan Zhou, Haitao Wang, Zhi Yao, Qiang Liu, Ying Yu, Jie Zhou","doi":"10.1016/j.immuni.2025.02.003","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.003","url":null,"abstract":"Necrotizing enterocolitis (NEC) is a common pediatric emergency primarily afflicting preterm infants, yet its mechanisms remain to be fully understood. Here, we report that plasma fibroblast growth factor (FGF)19, a target of farnesoid X receptor (FXR), was positively correlated with the clinical parameters of NEC. NEC patients and the NEC murine model displayed abundant FXR in intestinal epithelial cells (IECs), which was restricted by microbiota-derived short-chain fatty acids (SCFAs) under homeostasis. Genetic deficiency of FXR in IECs caused remission of NEC. Mechanistically, FXR facilitated ferroptosis of IECs via targeting acyl-coenzyme A synthetase long-chain family member 4 (<em>Acsl4</em>). Lipid peroxides released by ferroptotic IECs suppressed interleukin (IL)-22 secretion from type 3 innate lymphoid cells (ILC3s), thereby exacerbating NEC. Intestinal FXR antagonist, ACSL4 inhibitor, and ferroptosis inhibitor ameliorated murine NEC. Furthermore, the elevated lipid peroxides in NEC patients were positively correlated with FGF19 and disease parameters. These observations demonstrate the therapeutic value of targeting intestinal FXR and ferroptosis in NEC treatment.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"66 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518150","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}
ImmunityPub Date : 2025-02-28DOI: 10.1016/j.immuni.2025.02.011
{"title":"The polyamine-regulating enzyme SSAT1 impairs tissue regulatory T cell function in chronic cutaneous inflammation","authors":"","doi":"10.1016/j.immuni.2025.02.011","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.011","url":null,"abstract":"Regulatory T (Treg) cells are a critical immune component guarding against excessive inflammation. Treg cell dysfunction can lead to chronic inflammat…","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"11 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518155","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}
ImmunityPub Date : 2025-02-28DOI: 10.1016/j.immuni.2025.02.004
Abby Spangler, Geoffrey D. Shimberg, Grace E. Mantus, Rory Malek, Lauren Y. Cominsky, Yaroslav Tsybovsky, Ning Li, Rebecca A. Gillespie, Michelle Ravichandran, Adrian Creanga, Julie E. Raab, Suprabhath R. Gajjala, Floreliz Mendoza, Katherine V. Houser, Lesia Dropulic, Adrian B. McDermott, Masaru Kanekiyo, Sarah F. Andrews
{"title":"Early influenza virus exposure shapes the B cell response to influenza vaccination in individuals 50 years later","authors":"Abby Spangler, Geoffrey D. Shimberg, Grace E. Mantus, Rory Malek, Lauren Y. Cominsky, Yaroslav Tsybovsky, Ning Li, Rebecca A. Gillespie, Michelle Ravichandran, Adrian Creanga, Julie E. Raab, Suprabhath R. Gajjala, Floreliz Mendoza, Katherine V. Houser, Lesia Dropulic, Adrian B. McDermott, Masaru Kanekiyo, Sarah F. Andrews","doi":"10.1016/j.immuni.2025.02.004","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.004","url":null,"abstract":"Pre-existing immunity impacts vaccine responses to influenza, but directly connecting influenza infections early in life with immune responses decades later is difficult. However, H2N2 stopped circulating in the human population in 1968, creating the opportunity to directly evaluate the impact of early H2N2 exposure on vaccine responses 50 years later. Here, we vaccinated individuals born before (H2 exposed) or after (H2 naive) 1968 with an H2 hemagglutinin (HA) DNA plasmid and/or a ferritin nanoparticle vaccine. H2-exposed individuals generated a rapid B cell recall response that was more potent, targeted more conserved epitopes, and differed phenotypically from the <em>de novo</em> response in H2-naive individuals. Furthermore, vaccinating with a DNA versus a protein nanoparticle vaccine altered the response in H2-naive but not H2-exposed individuals. This study establishes and describes the lifelong impact of influenza HA-specific memory B cells formed early in life on vaccine responses decades later.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"85 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517814","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}
ImmunityPub Date : 2025-02-28DOI: 10.1016/j.immuni.2025.02.007
Ce Luo, Rui Zhang, Rui Guo, Lijian Wu, Teng Xue, Yufeng He, Yiteng Jin, Yanping Zhao, Zongxu Zhang, Peng Zhang, Sitong Ye, Xiaohong Li, Dian Li, Wubing Zhang, Chenfei Wang, Luhua Lai, Qiang Pan-Hammarström, Kai W. Wucherpfennig, Zhidong Gao, Deng Pan, Zexian Zeng
{"title":"Integrated computational analysis identifies therapeutic targets with dual action in cancer cells and T cells","authors":"Ce Luo, Rui Zhang, Rui Guo, Lijian Wu, Teng Xue, Yufeng He, Yiteng Jin, Yanping Zhao, Zongxu Zhang, Peng Zhang, Sitong Ye, Xiaohong Li, Dian Li, Wubing Zhang, Chenfei Wang, Luhua Lai, Qiang Pan-Hammarström, Kai W. Wucherpfennig, Zhidong Gao, Deng Pan, Zexian Zeng","doi":"10.1016/j.immuni.2025.02.007","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.007","url":null,"abstract":"Many cancer drugs that target cancer cell pathways also impair the immune system. We developed a computational target discovery platform to enable examination of both cancer and immune cells so as to identify pathways that restrain tumor progression and potentiate anti-tumor immunity. Immune-related CRISPR screen analyzer of functional targets (ICRAFT) integrates immune-related CRISPR screen datasets, single-cell RNA sequencing (scRNA-seq) data, and pre-treatment RNA-seq data from clinical trials, enabling a systems-level approach to therapeutic target discovery. Using ICRAFT, we identified numerous targets that enhance both cancer cell susceptibility to immune attack and T cell activation, including tumor necrosis factor (TNF) alpha-induced protein 3 (TNFAIP3), protein tyrosine phosphatase non-receptor type 2 (PTPN2), and suppressor of cytokine signaling 1 (SOCS1). In cancer cells, Tnfaip3 (A20) deletion activated the TNF-nuclear factor kappa-B (NF-κB) pathway, promoting chemokine expression and T cell recruitment to the tumor. T cell-mediated elimination of Tnaifp3-null cancer cells was primarily driven by TNF-induced apoptosis. Inactivation of Tnfaip3 in T cells enhanced anti-tumor efficacy. By integrating diverse functional genomics and clinical datasets, ICRAFT provides an interactive resource toward a deeper understanding of anti-tumor immunity and immuno-oncology drug development.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"11 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518152","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}
ImmunityPub Date : 2025-02-27DOI: 10.1016/j.immuni.2025.02.001
Leena Abdullah, Francesco E. Emiliani, Chinmay M. Vaidya, Hannah Stuart, Shawn C. Musial, Fred W. Kolling, Joshua J. Obar, Pamela C. Rosato, Margaret E. Ackerman, Li Song, Aaron McKenna, Yina H. Huang
{"title":"The endogenous antigen-specific CD8+ T cell repertoire is composed of unbiased and biased clonotypes with differential fate commitments","authors":"Leena Abdullah, Francesco E. Emiliani, Chinmay M. Vaidya, Hannah Stuart, Shawn C. Musial, Fred W. Kolling, Joshua J. Obar, Pamela C. Rosato, Margaret E. Ackerman, Li Song, Aaron McKenna, Yina H. Huang","doi":"10.1016/j.immuni.2025.02.001","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.001","url":null,"abstract":"Generating balanced populations of CD8<sup>+</sup> effector and memory T cells is necessary for immediate and durable immunity to infections and cancer. Yet, a definitive understanding of how a diverse CD8<sup>+</sup> T cell repertoire differentiates remains unclear. We identified several hundred T cell receptor (TCR) clonotypes that constitute the polyclonal response against a single antigen and found that a majority of TCR clonotypes were highly biased toward memory or effector fates. TCR-intrinsic biases were not stochastic and were dominant over environmental cues. Differential gene expression analysis of memory- or effector-biased TCR clonotypes showed bifurcation of differential fates at the early effector stage. Additionally, phylogenetic analysis revealed that memory-biased clonotypes retain their fate preferences in subclonal populations but effector-biased subclones can switch to a memory fate. Our study highlights that the polyclonal CD8<sup>+</sup> T cell response is a composite of unbiased and biased clonotypes with varying capacity to incorporate environmental cues in their cell fate decisions.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"28 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506909","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}
ImmunityPub Date : 2025-02-26DOI: 10.1016/j.immuni.2025.02.002
Lu Li, Qiancheng Jiao, Qianqian Yang, Haisen Lu, Xia Zhou, Qing Zhang, Futing Zhang, Hai Li, Zhigang Tian, Zhutian Zeng
{"title":"A bladder-blood immune barrier constituted by suburothelial perivascular macrophages restrains uropathogen dissemination","authors":"Lu Li, Qiancheng Jiao, Qianqian Yang, Haisen Lu, Xia Zhou, Qing Zhang, Futing Zhang, Hai Li, Zhigang Tian, Zhutian Zeng","doi":"10.1016/j.immuni.2025.02.002","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.002","url":null,"abstract":"Urinary tract infections (UTIs) predominantly occur in the bladder and can potentially progress into life-threatening sepsis if uropathogens spread unconstrainedly into the bloodstream. Here, we identified a subset of suburothelial perivascular macrophages (suPVMs) in the bladder that exerted a pivotal barrier function to prevent systemic bacterial dissemination during acute cystitis. During the initial phase of uropathogenic <em>Escherichia coli</em> (UPEC) infection, suPVMs actively captured UPEC invading the laminal propria and maintained the integrity of inflamed vessels. They subsequently underwent METosis to expel macrophage extracellular DNA traps (METs) into the urothelium to sequester bacteria within this avascular compartment. Matrix metallopeptidase-13 was released along with METs to promote neutrophil transuroepithelial migration. Replenished suPVMs from monocytes following a prior infection were functionally competent to confer protection against recurrent UTIs. Our study thus uncovers a bladder-blood immune barrier in restraining uropathogen dissemination, which could have implications for the prevention and treatment of urosepsis.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"12 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143495776","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}
ImmunityPub Date : 2025-02-25DOI: 10.1016/j.immuni.2025.01.016
Wanwan Huai, Kun Yang, Cong Xing, Kun Song, Heng Lyu, Noelle S. Williams, Jianjun Wu, Nan Yan
{"title":"OAS cross-activates RNase L intercellularly through cell-to-cell transfer of 2-5A to spread innate immunity","authors":"Wanwan Huai, Kun Yang, Cong Xing, Kun Song, Heng Lyu, Noelle S. Williams, Jianjun Wu, Nan Yan","doi":"10.1016/j.immuni.2025.01.016","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.01.016","url":null,"abstract":"The 2′,5′-oligoadenylate synthetase (OAS)-RNase L pathway is a classical antiviral innate immune pathway. Upon sensing dsRNA, OAS produces 2′,5′-oligoadenylate (2-5A) as a second messenger to activate RNase L. Whether 2-5A can be transported to extend the reach of innate immune signaling has not been established. Here, we showed that 2-5A was transferred from cell to cell through connexin (CX43/CX45) gap junctions. 2-5A was also transferred through importers and exporters, allowing OAS to remotely activate RNase L and protect neighboring cells from viral infection. We identified ABCC10 as a 2-5A exporter. Loss of ABCC10 had no effect on 2-5A production but reduced 2-5A export and protection of neighboring cells. Furthermore, OAS<sup>hi</sup> tumors such as MC38 naturally produced 2-5A <em>in vivo</em>, which was secreted via ABCC10 to activate host—not tumor—RNase L-mediated antitumor response. Therefore, 2-5A is an immunotransmitter that mediates short-range communication between cells in infection and cancer.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"16 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143486526","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}
ImmunityPub Date : 2025-02-24DOI: 10.1016/j.immuni.2025.01.017
Irving Estevez, Benjamin D. Buckley, Marissa Lindman, Nicholas Panzera, Tsui-Wen Chou, Micheal McCourt, Brandon J. Vaglio, Colm Atkins, Bonnie L. Firestein, Brian P. Daniels
{"title":"The kinase RIPK3 promotes neuronal survival by suppressing excitatory neurotransmission during central nervous system viral infection","authors":"Irving Estevez, Benjamin D. Buckley, Marissa Lindman, Nicholas Panzera, Tsui-Wen Chou, Micheal McCourt, Brandon J. Vaglio, Colm Atkins, Bonnie L. Firestein, Brian P. Daniels","doi":"10.1016/j.immuni.2025.01.017","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.01.017","url":null,"abstract":"While recent work has identified roles for immune mediators in regulating neural activity, how innate immune signaling within neurons influences neurotransmission remains poorly understood. Emerging evidence suggests that the modulation of neurotransmission may serve important roles in host protection during infection of the central nervous system. Here, we showed that receptor-interacting protein kinase-3 (RIPK3) preserved neuronal survival during flavivirus infection through the suppression of excitatory neurotransmission. These effects occurred independently of the traditional functions of RIPK3 in promoting necroptosis and inflammatory transcription. Instead, RIPK3 promoted phosphorylation of the neuronal regulatory kinase calcium/calmodulin-dependent protein kinase II (CaMKII), which in turn activated the transcription factor cyclic AMP response element-binding protein (CREB) to drive a neuroprotective transcriptional program and suppress deleterious glutamatergic signaling. These findings identify an unexpected function for a canonical cell death protein in promoting neuronal survival during viral infection through the modulation of neuronal activity, highlighting mechanisms of neuroimmune crosstalk.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"30 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477750","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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