{"title":"Microglial and TREM2 dialogues in the developing brain","authors":"Raffaella Morini, Erica Tagliatti, Matteo Bizzotto, Michela Matteoli","doi":"10.1016/j.immuni.2025.04.022","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.04.022","url":null,"abstract":"From the migration of precursor cells to the refinement of neural circuits, the immune system plays a critical role in the development of the central nervous system. As the brain resident macrophages, microglia are integral to these processes, influencing key developmental stages and contributing to circuit remodeling. Recent years have brought a wealth of new insights into how microglia regulate key stages of brain development, particularly through their continuous crosstalk with various brain cell types. In this review, we synthesize this growing body of literature on microglia and neurodevelopment, highlighting the involvement of the TREM2 receptor, known for its role in aging and neurodegeneration, which profoundly affects the state of microglia and guides target cells by shaping their transcriptional and functional fate. We examine microglial communication with four major cell types—neural precursors, neurons, astrocytes, and oligodendrocytes—also delving into the described mechanisms that underpin these interactions.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"34 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143909759","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 : 2025-05-04DOI: 10.1016/j.immuni.2025.04.017
Kun-Wei Song, Michael Lim, Michelle Monje
{"title":"Complex neural-immune interactions shape glioma immunotherapy","authors":"Kun-Wei Song, Michael Lim, Michelle Monje","doi":"10.1016/j.immuni.2025.04.017","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.04.017","url":null,"abstract":"Rich neural-immune interactions in the central nervous system (CNS) shape its function and create a unique immunological microenvironment for immunotherapy in CNS malignancies. Far from the now-debunked concept of CNS “immune privilege,” it is now understood that unique immunological niches and constant immune surveillance of the brain contribute in multifaceted ways to brain health and robustly influence immunotherapy approaches for CNS cancers. Challenges include immune-suppressive and neurotoxicity-promoting crosstalk between brain, immune, and tumor cells. Developing effective immunotherapies for cancers of the nervous system will require a deeper understanding of these neural-immune-malignant cell interactions. Here, we review progress and challenges in immunotherapy for gliomas of the brain and spinal cord in light of these unique neural-immune interactions and highlight future work needed to optimize promising immunotherapies for gliomas.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"18 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143909749","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 : 2025-05-04DOI: 10.1016/j.immuni.2025.03.018
Brian S. Kim, David Artis
{"title":"The sensory neuroimmune frontier","authors":"Brian S. Kim, David Artis","doi":"10.1016/j.immuni.2025.03.018","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.03.018","url":null,"abstract":"Sensing and recognition are key properties of both the immune and nervous systems. In the immune system, pattern recognition or antigen-specific receptors represent classic motifs in innate and adaptive immunity, respectively. In the nervous system, there is a major anatomic division between how we sense stimuli from within the body (vagal sensory nervous system) and the outside world (somatosensory nervous system). However, in the last 5 years, there has been an explosion of discoveries revealing interactions between the immune and the sensory nervous systems that govern an array of physiologic and pathologic processes including allergy, infection, autoimmunity, regeneration, cancer, and beyond. Herein, we highlight recent advances that demonstrate how peripheral sensory neuroimmunology has emerged as a powerful field that provides new insights into classic immunologic processes including immune hypersensitivity, inflammation, and tissue homeostasis.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"12 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143909756","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 : 2025-05-02DOI: 10.1016/j.immuni.2025.04.011
Jaeu Yi, Jisun Jung, David Horton, Patricia Hsieh, Yangqing Peng, Sean J. Wang, Rodney Newberry, Aaron C. Ericsson, Kwang Soon Kim, Andrew L. Kau, Chyi-Song Hsieh
{"title":"A hierarchy of intestinal antigens instructs the CD4+ T cell receptor repertoire","authors":"Jaeu Yi, Jisun Jung, David Horton, Patricia Hsieh, Yangqing Peng, Sean J. Wang, Rodney Newberry, Aaron C. Ericsson, Kwang Soon Kim, Andrew L. Kau, Chyi-Song Hsieh","doi":"10.1016/j.immuni.2025.04.011","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.04.011","url":null,"abstract":"Intestinal CD4<sup>+</sup> T cells that are specific for self-, diet-, or commensal-derived antigens are critical for host tolerance but must also be tightly regulated to prevent aberrant activation and conditions like inflammatory bowel disease (IBD). However, it is unclear how the antigen source and location dictate the intestinal TCR repertoire. Here, we hierarchically classified self-, diet-, or microbiota-dependent TCRs using TCliβ TCRβ transgenic mice. This demonstrated that microbiota had a greater influence than diet on CD4<sup>+</sup> T cell responses throughout the intestine at homeostasis. Complex bi-directional interactions between microbes and diet were also observed. In the context of murine colitis as a model of IBD, we showed that antigen-free diet substantially altered the microbiota and associated T cell responses, which ameliorated intestinal inflammation. Collectively, these findings suggest how deconvoluting the gut immune interactome may facilitate identifying primary microbial and dietary drivers of T cell responses during health and disease.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"114 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143897520","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 : 2025-05-02DOI: 10.1016/j.immuni.2025.04.007
Kristine E. Zengeler, Ava Hollis, Tyler C.J. Deutsch, Joshua D. Samuels, Hannah Ennerfelt, Katelyn A. Moore, Eric J. Steacy, Vikram Sabapathy, Rahul Sharma, Manoj K. Patel, John R. Lukens
{"title":"Inflammasome signaling in astrocytes modulates hippocampal plasticity","authors":"Kristine E. Zengeler, Ava Hollis, Tyler C.J. Deutsch, Joshua D. Samuels, Hannah Ennerfelt, Katelyn A. Moore, Eric J. Steacy, Vikram Sabapathy, Rahul Sharma, Manoj K. Patel, John R. Lukens","doi":"10.1016/j.immuni.2025.04.007","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.04.007","url":null,"abstract":"Emerging evidence indicates that a baseline level of controlled innate immune signaling is required to support proper brain function. However, little is known about the function of most innate immune pathways in homeostatic neurobiology. Here, we report a role for astrocyte-dependent inflammasome signaling in regulating hippocampal plasticity. Inflammasomes are multiprotein complexes that promote caspase-1-mediated interleukin (IL)-1 and IL-18 production in response to pathogens and tissue damage. We observed that inflammasome complex formation was regularly detected under homeostasis in hippocampal astrocytes and that its assembly is dynamically regulated in response to learning and regional activity. Conditional ablation of caspase-1 in astrocytes limited hyperexcitability in an acute seizure model and impacted hippocampal plasticity via modulation of synaptic protein density, neuronal activity, and perineuronal net coverage. Caspase-1 and IL-18 regulated hippocampal IL-33 production and related plasticity. These findings reveal a homeostatic function for astrocyte inflammasome activity in regulating hippocampal physiology in health and disease.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"13 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143897531","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 : 2025-05-01DOI: 10.1016/j.immuni.2025.04.003
Hannah Van Hove, Chaim Glück, Wiebke Mildenberger, Ekaterina Petrova, Upasana Maheshwari, Philipp Häne, Victor Kreiner, Mitchell Bijnen, Caroline Mussak, Sebastian G. Utz, Jeanne Droux, Florian Ingelfinger, Christian Ashworth, Sebastian A. Stifter, Elsa Roussel, Iva Lelios, Marijne Vermeer, Sheng-Fu Huang, Quanyu Zhou, Zhenyue Chen, Melanie Greter
{"title":"Interleukin-34-dependent perivascular macrophages promote vascular function in the brain","authors":"Hannah Van Hove, Chaim Glück, Wiebke Mildenberger, Ekaterina Petrova, Upasana Maheshwari, Philipp Häne, Victor Kreiner, Mitchell Bijnen, Caroline Mussak, Sebastian G. Utz, Jeanne Droux, Florian Ingelfinger, Christian Ashworth, Sebastian A. Stifter, Elsa Roussel, Iva Lelios, Marijne Vermeer, Sheng-Fu Huang, Quanyu Zhou, Zhenyue Chen, Melanie Greter","doi":"10.1016/j.immuni.2025.04.003","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.04.003","url":null,"abstract":"The development of most macrophages depends on the colony-stimulating factor 1 (CSF-1) receptor, which has two ligands: CSF-1 and interleukin-34 (IL-34). While IL-34 is required for the homeostasis of microglia, the parenchymal macrophages in the central nervous system (CNS), it is unclear whether brain border-associated macrophages (BAMs) also depend on this cytokine. Here, we demonstrated that the embryonic development of murine BAMs in the choroid plexus, leptomeninges, and perivascular spaces required CSF-1, while IL-34 was critical for their maintenance in adulthood. In the brain, <em>Il34</em> was expressed by mural cells and perivascular fibroblasts, and its transgenic deletion in these cells interrupted BAM maintenance. <em>Il34</em> deficiency coincided with transcriptional changes in vascular cells, leading to increased flow velocity and vasomotion in pial and penetrating arterioles. Similarly, <em>Mrc1</em><sup>Cre</sup><em>Csf1r</em><sup>fl/fl</sup> mice lacking CD206<sup>+</sup> perivascular BAMs exhibited increased hemodynamics in arterial networks. These findings reveal a crosstalk between vascular cells and CNS macrophages regulating cerebrovascular function.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"24 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143893159","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 : 2025-04-30DOI: 10.1016/j.immuni.2025.04.006
Jonathan Bastos, Carleigh O’Brien, Mónica Vara-Pérez, Myrthe Mampay, Lynn van Olst, Liam Barry-Carroll, Daliya Kancheva, Sophia Leduc, Ayla Line Lievens, Leen Ali, Vladislav Vlasov, Laura Meysman, Hadis Shakeri, Ria Roelandt, Hannah Van Hove, Karen De Vlaminck, Isabelle Scheyltjens, Fazeela Yaqoob, Sonia I. Lombroso, Maria Breugelmans, Kiavash Movahedi
{"title":"Monocytes can efficiently replace all brain macrophages and fetal liver monocytes can generate bona fide SALL1+ microglia","authors":"Jonathan Bastos, Carleigh O’Brien, Mónica Vara-Pérez, Myrthe Mampay, Lynn van Olst, Liam Barry-Carroll, Daliya Kancheva, Sophia Leduc, Ayla Line Lievens, Leen Ali, Vladislav Vlasov, Laura Meysman, Hadis Shakeri, Ria Roelandt, Hannah Van Hove, Karen De Vlaminck, Isabelle Scheyltjens, Fazeela Yaqoob, Sonia I. Lombroso, Maria Breugelmans, Kiavash Movahedi","doi":"10.1016/j.immuni.2025.04.006","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.04.006","url":null,"abstract":"Microglia and border-associated macrophages (BAMs) are critical for brain health, and their dysfunction is associated to disease. Replacing brain macrophages holds substantial therapeutic promise but remains challenging. Here, we demonstrate that monocytes can efficiently replace all brain macrophages. Monocytes readily replaced embryonal BAMs upon their depletion and engrafted as monocyte-derived microglia (Mo-Microglia) upon more sustained niche availability. Mo-Microglia expanded comparably to their embryonic counterparts and showed similar longevity. However, monocytes were unable to replicate the distinct identity of embryonically derived BAMs and microglia. Using xenotransplantation, we found that human monocytes exhibited similar behavior, enabling identification of putative Mo-Microglia in Alzheimer’s disease individuals. In mice and humans, monocyte ontogeny shaped their identity as brain macrophages. Importantly, mouse fetal liver monocytes exhibited a distinct epigenetic landscape and could develop a bona fide microglial identity. Our results illuminate brain macrophage development and highlight monocytes as an abundant progenitor source for brain macrophage replacement therapies.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"71 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143889895","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 : 2025-04-30DOI: 10.1016/j.immuni.2025.03.019
William H. Aisenberg, Carleigh A. O’Brien, Madison Sangster, Fazeela Yaqoob, Yuanchao Zhang, Brian Temsamrit, Searlait Thom, Luca Gosse, Sai Chaluvadi, Bilal Elfayomi, Gavin Lee, Vidhur Polam, Eli M. Levitt, Gary Liu, Sonia I. Lombroso, Kelsey M. Nemec, Gavin Clowry, Cassaundra Nieves, Priyanka Rawat, Emily Church, F. Chris Bennett
{"title":"Direct microglia replacement reveals pathologic and therapeutic contributions of brain macrophages to a monogenic neurological disease","authors":"William H. Aisenberg, Carleigh A. O’Brien, Madison Sangster, Fazeela Yaqoob, Yuanchao Zhang, Brian Temsamrit, Searlait Thom, Luca Gosse, Sai Chaluvadi, Bilal Elfayomi, Gavin Lee, Vidhur Polam, Eli M. Levitt, Gary Liu, Sonia I. Lombroso, Kelsey M. Nemec, Gavin Clowry, Cassaundra Nieves, Priyanka Rawat, Emily Church, F. Chris Bennett","doi":"10.1016/j.immuni.2025.03.019","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.03.019","url":null,"abstract":"Krabbe disease, also named globoid cell (GC) leukodystrophy (GLD) for its distinct lipid-laden macrophages, is a severe leukodystrophy caused by galactosylceramidase (GALC) mutations. Hematopoietic stem cell transplant (HSCT) ameliorates disease and is associated with central nervous system (CNS) engraftment of GALC<sup>+</sup> donor macrophages. Yet, the role of macrophages in GLD pathophysiology and HSCT remains unclear. Using single-cell sequencing, we revealed early interferon response signatures that preceded progressively severe macrophage dyshomeostasis and identified a molecular signature of GCs, which we validated in human brain specimens. Genetic depletion and direct microglia replacement by CNS monocyte injection rapidly replaced >80% of endogenous microglia with healthy macrophages in the twitcher (<em>Galc</em><sup>W355</sup><sup>∗</sup>) mouse model of GLD. Perinatal microglia replacement completely normalized transcriptional signatures, rescued histopathology, and doubled average survival. Overall, we uncovered distinct forms of microglial dysfunction and evidence that direct, CNS-limited microglia replacement improves a monogenic neurodegenerative disease, identifying a promising therapeutic target.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"18 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143889896","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 : 2025-04-29DOI: 10.1016/j.immuni.2025.04.004
Seung Hyeon Kim, Zachary White, Anastasiia Gainullina, Soeun Kang, Jiseon Kim, Joseph R. Dominguez, Yeonwoo Choi, Ivan Cabrera, Madison Plaster, Michihiro Takahama, Rafael S. Czepielewski, Jinki Yeom, Matthias Gunzer, Nissim Hay, Odile David, Nicolas Chevrier, Teruyuki Sano, Ki-Wook Kim
{"title":"IL-10 sensing by lung interstitial macrophages prevents bacterial dysbiosis-driven pulmonary inflammation and maintains immune homeostasis","authors":"Seung Hyeon Kim, Zachary White, Anastasiia Gainullina, Soeun Kang, Jiseon Kim, Joseph R. Dominguez, Yeonwoo Choi, Ivan Cabrera, Madison Plaster, Michihiro Takahama, Rafael S. Czepielewski, Jinki Yeom, Matthias Gunzer, Nissim Hay, Odile David, Nicolas Chevrier, Teruyuki Sano, Ki-Wook Kim","doi":"10.1016/j.immuni.2025.04.004","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.04.004","url":null,"abstract":"Crosstalk between the immune system and the microbiome is critical for maintaining immune homeostasis. Here, we examined this communication and the impact of immune-suppressive IL-10 signaling on pulmonary homeostasis. We found that IL-10 sensing by interstitial macrophages (IMs) is required to prevent spontaneous lung inflammation. Loss of IL-10 signaling in IMs initiated an inflammatory cascade through the activation of classical monocytes and CD4<sup>+</sup> T cell subsets, leading to chronic lung inflammation with age. Analyses of antibiotic-treated and germ-free mice established that lung inflammation in the animals lacking IL-10 signaling was triggered by commensal bacteria. 16S rRNA sequencing revealed <em>Delftia acidovorans</em> and <em>Rhodococcus erythropolis</em> as potential drivers of lung inflammation. Intranasal administration of these bacteria or transplantation of human fecal microbiota elicited lung inflammation in gnotobiotic <em>Il10</em>-deficient mice. These findings highlight that IL-10 sensing by IMs contributes to pulmonary homeostasis by preventing lung inflammation caused by commensal dysbiosis.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"137 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143885425","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 : 2025-04-25DOI: 10.1016/j.immuni.2025.04.001
Stephen T. Yeung, Payal Damani-Yokota, Sara A. Thannickal, Eric Bartnicki, Eduardo D. Bernier, Clea R. Barnett, Camille Khairallah, Ralf Duerr, Maria G. Noval, Leopoldo N. Segal, Kenneth A. Stapleford, Kamal M. Khanna
{"title":"Nerve- and airway-associated interstitial macrophages mitigate SARS-CoV-2 pathogenesis via type I interferon signaling","authors":"Stephen T. Yeung, Payal Damani-Yokota, Sara A. Thannickal, Eric Bartnicki, Eduardo D. Bernier, Clea R. Barnett, Camille Khairallah, Ralf Duerr, Maria G. Noval, Leopoldo N. Segal, Kenneth A. Stapleford, Kamal M. Khanna","doi":"10.1016/j.immuni.2025.04.001","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.04.001","url":null,"abstract":"Despite vaccines, rapidly mutating viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continue to threaten human health due to an impaired immunoregulatory pathway and a hyperactive immune response. Our understanding of the local immune mechanisms used by tissue-resident macrophages to safeguard the host from excessive inflammation during SARS-CoV-2 infection remains limited. Here, we found that nerve- and airway-associated interstitial macrophages (NAMs) are required to control mouse-adapted SARS-CoV-2 (MA-10) infection. Control mice restricted lung viral distribution and survived infection, whereas NAM depletion enhanced viral spread and inflammation and led to 100% mortality. Mechanistically, type I interferon receptor (IFNAR) signaling by NAMs was critical for limiting inflammation and viral spread, and IFNAR deficiency in CD169<sup>+</sup> macrophages mirrored NAM-depleted outcomes and abrogated their expansion. These findings highlight the essential protective role of NAMs in regulating viral spread and inflammation, offering insights into SARS-CoV-2 pathogenesis and underscoring the importance of NAMs in mediating host immunity and disease tolerance.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"32 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143872397","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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