Nature Reviews Immunology最新文献

{"title":"IL-22 protects against stress-induced anxiety","authors":"Lucy Bird","doi":"10.1038/s41577-024-01127-0","DOIUrl":"10.1038/s41577-024-01127-0","url":null,"abstract":"Stress-induced gut leakage and immune activation lead to the release of IL-22, which acts directly on septal neurons in the brain to dampen their activation and protect against anxiety behaviour.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 2","pages":"75-75"},"PeriodicalIF":67.7,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911456","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}

{"title":"Transposon-derived decoy fine-tunes IFN responses","authors":"Yvonne Bordon","doi":"10.1038/s41577-024-01126-1","DOIUrl":"10.1038/s41577-024-01126-1","url":null,"abstract":"A transposon-derived isoform of the type I interferon (IFN) receptor IFNAR2 can serve as a decoy receptor to regulate IFN signalling.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 2","pages":"74-74"},"PeriodicalIF":67.7,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142857808","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}

{"title":"Muscle spindle macrophages regulate motor coordination","authors":"Kirsty Minton","doi":"10.1038/s41577-024-01125-2","DOIUrl":"10.1038/s41577-024-01125-2","url":null,"abstract":"Yan et al. report the identification of a population of muscle spindle macrophages, which regulate the muscle stretch reflex through glutamate production.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 2","pages":"73-73"},"PeriodicalIF":67.7,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142825555","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}

{"title":"Systematic identification of cell state-specific transcription factors in T cells","authors":"Didem Ağaç Çobanoğlu","doi":"10.1038/s41577-024-01118-1","DOIUrl":"10.1038/s41577-024-01118-1","url":null,"abstract":"A preprint by Chung et al. presents a framework for the use of transcriptomic and epigenomic data to identify novel transcription factors driving CD8+ T cell states.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 1","pages":"4-4"},"PeriodicalIF":67.7,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142790465","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}

{"title":"Neuroinflammation in Alzheimer disease","authors":"Michael T. Heneka, Wiesje M. van der Flier, Frank Jessen, Jeroen Hoozemanns, Dietmar Rudolf Thal, Delphine Boche, Frederic Brosseron, Charlotte Teunissen, Henrik Zetterberg, Andreas H. Jacobs, Paul Edison, Alfredo Ramirez, Carlos Cruchaga, Jean-Charles Lambert, Agustin Ruiz Laza, Jose Vicente Sanchez-Mut, Andre Fischer, Sergio Castro-Gomez, Thor D. Stein, Luca Kleineidam, Michael Wagner, Jonas J. Neher, Colm Cunningham, Sim K. Singhrao, Marco Prinz, Christopher K. Glass, Johannes C. M. Schlachetzki, Oleg Butovsky, Kilian Kleemann, Philip L. De Jaeger, Hannah Scheiblich, Guy C. Brown, Gary Landreth, Miguel Moutinho, Jaime Grutzendler, Diego Gomez-Nicola, Róisín M. McManus, Katrin Andreasson, Christina Ising, Deniz Karabag, Darren J. Baker, Shane A. Liddelow, Alexei Verkhratsky, Malu Tansey, Alon Monsonego, Ludwig Aigner, Guillaume Dorothée, Klaus-Armin Nave, Mikael Simons, Gabriela Constantin, Neta Rosenzweig, Alberto Pascual, Gabor C. Petzold, Jonathan Kipnis, Carmen Venegas, Marco Colonna, Jochen Walter, Andrea J. Tenner, M. Kerry O’Banion, Joern R. Steinert, Douglas L. Feinstein, Magdalena Sastre, Kiran Bhaskar, Soyon Hong, Dorothy P. Schafer, Todd Golde, Richard M. Ransohoff, David Morgan, John Breitner, Renzo Mancuso, Sean-Patrick Riechers","doi":"10.1038/s41577-024-01104-7","DOIUrl":"10.1038/s41577-024-01104-7","url":null,"abstract":"Increasing evidence points to a pivotal role of immune processes in the pathogenesis of Alzheimer disease, which is the most prevalent neurodegenerative and dementia-causing disease of our time. Multiple lines of information provided by experimental, epidemiological, neuropathological and genetic studies suggest a pathological role for innate and adaptive immune activation in this disease. Here, we review the cell types and pathological mechanisms involved in disease development as well as the influence of genetics and lifestyle factors. Given the decade-long preclinical stage of Alzheimer disease, these mechanisms and their interactions are driving forces behind the spread and progression of the disease. The identification of treatment opportunities will require a precise understanding of the cells and mechanisms involved as well as a clear definition of their temporal and topographical nature. We will also discuss new therapeutic strategies for targeting neuroinflammation, which are now entering the clinic and showing promise for patients. This Review provides an in-depth examination of how inflammation contributes to neurodegeneration in Alzheimer disease. The authors explore the impact of extrinsic factors, such as brain trauma, diet and infections, and host-intrinsic factors, such as the activity of microglial cells and other immune, vascular and neuronal cell populations, on disease development. They also highlight emerging drugs that target this inflammatory component for therapy of Alzheimer disease.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"1-32"},"PeriodicalIF":67.7,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142793588","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}

{"title":"Author Correction: Inflammasome components as new therapeutic targets in inflammatory disease","authors":"Rebecca C. Coll, Kate Schroder","doi":"10.1038/s41577-024-01123-4","DOIUrl":"10.1038/s41577-024-01123-4","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 2","pages":"153-153"},"PeriodicalIF":67.7,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41577-024-01123-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142778641","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":"Publisher Correction: Inflammasome components as new therapeutic targets in inflammatory disease","authors":"Rebecca C. Coll, Kate Schroder","doi":"10.1038/s41577-024-01122-5","DOIUrl":"10.1038/s41577-024-01122-5","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 2","pages":"153-153"},"PeriodicalIF":67.7,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41577-024-01122-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142778548","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":"Guardians of immune privilege","authors":"Yvonne Bordon","doi":"10.1038/s41577-024-01121-6","DOIUrl":"10.1038/s41577-024-01121-6","url":null,"abstract":"Endogenous self-peptides derived from CNS antigens are presented on MHC class II molecules at the borders of the CNS and expand suppressive populations of CD4+ T cells.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 1","pages":"1-1"},"PeriodicalIF":67.7,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142760544","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}

{"title":"Sialylated IgG restrains lung inflammation","authors":"Lucy Bird","doi":"10.1038/s41577-024-01120-7","DOIUrl":"10.1038/s41577-024-01120-7","url":null,"abstract":"Sialylated IgG protects against severe influenza by inducing the transcriptional repressor REST, which dampens the inflammatory response and preserves lung tissue function.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 1","pages":"2-2"},"PeriodicalIF":67.7,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142753189","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}

{"title":"Mitochondria in monocyte-derived cells promote tissue damage in multiple sclerosis","authors":"Zi Yan Chen, Arthur Mortha","doi":"10.1038/s41577-024-01116-3","DOIUrl":"10.1038/s41577-024-01116-3","url":null,"abstract":"A preprint by Villar-Vesga et al. shows that monocyte-derived cells in the central nervous system produce mitochondrial reactive oxygen species to promote neuroinflammation.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 1","pages":"3-3"},"PeriodicalIF":67.7,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142712525","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}