Nature Reviews Immunology最新文献

{"title":"In vivo enhancement of tumour-specific T cells via peptide–MHC-pseudotyped retroviral gene delivery","authors":"Hugo Kwong, Persephone Borrow","doi":"10.1038/s41577-024-01128-z","DOIUrl":"https://doi.org/10.1038/s41577-024-01128-z","url":null,"abstract":"A preprint by Xu et al. shows that MHC-pseudotyped retroviruses can reprogramme, activate and expand tumour-specific T cell populations in vivo.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"98 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142935889","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":"How macrophage heterogeneity affects tuberculosis disease and therapy","authors":"David G. Russell, Nelson V. Simwela, Joshua T. Mattila, JoAnne Flynn, Henry C. Mwandumba, Davide Pisu","doi":"10.1038/s41577-024-01124-3","DOIUrl":"https://doi.org/10.1038/s41577-024-01124-3","url":null,"abstract":"<p>Macrophages are the primary host cell type for infection by <i>Mycobacterium tuberculosis</i> in vivo. Macrophages are also key immune effector cells that mediate the control of bacterial growth. However, the specific macrophage phenotypes that are required for optimal immune control of <i>M. tuberculosis</i> infection in vivo remain poorly defined. There are two distinct macrophage lineages in the lung, comprising embryonically derived, tissue-resident alveolar macrophages and recruited, blood monocyte-derived interstitial macrophages. Recent studies have shown that these lineages respond divergently to similar immune environments within the tuberculosis granuloma. Here, we discuss how the differing responses of macrophage lineages might affect the control or progression of tuberculosis disease. We suggest that the ability to reprogramme macrophage responses appropriately, through immunological or chemotherapeutic routes, could help to optimize vaccines and drug regimens for tuberculosis.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"28 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142934995","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":"Regulation of cGAS–STING signalling and its diversity of cellular outcomes","authors":"Zhengyin Zhang, Conggang Zhang","doi":"10.1038/s41577-024-01112-7","DOIUrl":"https://doi.org/10.1038/s41577-024-01112-7","url":null,"abstract":"<p>The cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) signalling pathway, which recognizes both pathogen DNA and host-derived DNA, has emerged as a crucial component of the innate immune system, having important roles in antimicrobial defence, inflammatory disease, ageing, autoimmunity and cancer. Recent work suggests that the regulation of cGAS–STING signalling is complex and sophisticated. In this Review, we describe recent insights from structural studies that have helped to elucidate the molecular mechanisms of the cGAS–STING signalling cascade and we discuss how the cGAS–STING pathway is regulated by both activating and inhibitory factors. Furthermore, we summarize the newly emerging understanding of crosstalk between cGAS–STING signalling and other signalling pathways and provide examples to highlight the wide variety of cellular processes in which cGAS–STING signalling is involved, including autophagy, metabolism, ageing, inflammation and tumorigenesis.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"24 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142935014","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":"Endogenous thymic regeneration: restoring T cell production following injury","authors":"David Granadier, Dante Acenas, Jarrod A. Dudakov","doi":"10.1038/s41577-024-01119-0","DOIUrl":"https://doi.org/10.1038/s41577-024-01119-0","url":null,"abstract":"<p>Despite its importance for generating and maintaining a healthy and broad T cell repertoire, the thymus is exquisitely sensitive to acute damage. Marked thymic involution occurs in response to stimuli as diverse as infection, stress, pregnancy, malnutrition, drug use and cytoreductive chemotherapy. However, the thymus also has a remarkable capacity for repair, although this regenerative capacity declines with age. Endogenous thymic regeneration is a crucial process that allows for the recovery of immune competence after acute damage and delay to this recovery can have important clinical effects. Until recently, the mechanisms that drive endogenous thymic regeneration were not well understood, but recent work in mice has revealed multiple distinct pathways of regeneration and the molecular mechanisms that trigger these pathways after damage. In this Review, we discuss the effects of different types of damage to the thymus, with a focus on an emerging body of work in mice that provides insight into the cellular and molecular mechanisms that regulate endogenous tissue regeneration in the thymus. We also highlight some of the clinical challenges that are presented by dysregulated thymic regeneration.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"36 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929718","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":"Cancer immune evasion, immunoediting and intratumour heterogeneity","authors":"Malte Roerden, Stefani Spranger","doi":"10.1038/s41577-024-01111-8","DOIUrl":"https://doi.org/10.1038/s41577-024-01111-8","url":null,"abstract":"<p>Cancers can avoid immune-mediated elimination by acquiring traits that disrupt antitumour immunity. These mechanisms of immune evasion are selected and reinforced during tumour evolution under immune pressure. Some immunogenic subclones are effectively eliminated by antitumour T cell responses (a process known as immunoediting), which results in a clonally selected tumour. Other cancer cells arise to resist immunoediting, which leads to a tumour that includes several distinct cancer cell populations (referred to as intratumour heterogeneity (ITH)). Tumours with high ITH are associated with poor patient outcomes and a lack of responsiveness to immune checkpoint blockade therapy. In this Review, we discuss the different ways that cancer cells evade the immune system and how these mechanisms impact immunoediting and tumour evolution. We also describe how subclonal antigen presentation in tumours with high ITH can result in immune evasion.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"6 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911457","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":"IL-22 protects against stress-induced anxiety","authors":"Lucy Bird","doi":"10.1038/s41577-024-01127-0","DOIUrl":"https://doi.org/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":"20 1","pages":""},"PeriodicalIF":100.3,"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":" ","pages":"1-1"},"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":" ","pages":"1-1"},"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,&nbsp;Wiesje M. van der Flier,&nbsp;Frank Jessen,&nbsp;Jeroen Hoozemanns,&nbsp;Dietmar Rudolf Thal,&nbsp;Delphine Boche,&nbsp;Frederic Brosseron,&nbsp;Charlotte Teunissen,&nbsp;Henrik Zetterberg,&nbsp;Andreas H. Jacobs,&nbsp;Paul Edison,&nbsp;Alfredo Ramirez,&nbsp;Carlos Cruchaga,&nbsp;Jean-Charles Lambert,&nbsp;Agustin Ruiz Laza,&nbsp;Jose Vicente Sanchez-Mut,&nbsp;Andre Fischer,&nbsp;Sergio Castro-Gomez,&nbsp;Thor D. Stein,&nbsp;Luca Kleineidam,&nbsp;Michael Wagner,&nbsp;Jonas J. Neher,&nbsp;Colm Cunningham,&nbsp;Sim K. Singhrao,&nbsp;Marco Prinz,&nbsp;Christopher K. Glass,&nbsp;Johannes C. M. Schlachetzki,&nbsp;Oleg Butovsky,&nbsp;Kilian Kleemann,&nbsp;Philip L. De Jaeger,&nbsp;Hannah Scheiblich,&nbsp;Guy C. Brown,&nbsp;Gary Landreth,&nbsp;Miguel Moutinho,&nbsp;Jaime Grutzendler,&nbsp;Diego Gomez-Nicola,&nbsp;Róisín M. McManus,&nbsp;Katrin Andreasson,&nbsp;Christina Ising,&nbsp;Deniz Karabag,&nbsp;Darren J. Baker,&nbsp;Shane A. Liddelow,&nbsp;Alexei Verkhratsky,&nbsp;Malu Tansey,&nbsp;Alon Monsonego,&nbsp;Ludwig Aigner,&nbsp;Guillaume Dorothée,&nbsp;Klaus-Armin Nave,&nbsp;Mikael Simons,&nbsp;Gabriela Constantin,&nbsp;Neta Rosenzweig,&nbsp;Alberto Pascual,&nbsp;Gabor C. Petzold,&nbsp;Jonathan Kipnis,&nbsp;Carmen Venegas,&nbsp;Marco Colonna,&nbsp;Jochen Walter,&nbsp;Andrea J. Tenner,&nbsp;M. Kerry O’Banion,&nbsp;Joern R. Steinert,&nbsp;Douglas L. Feinstein,&nbsp;Magdalena Sastre,&nbsp;Kiran Bhaskar,&nbsp;Soyon Hong,&nbsp;Dorothy P. Schafer,&nbsp;Todd Golde,&nbsp;Richard M. Ransohoff,&nbsp;David Morgan,&nbsp;John Breitner,&nbsp;Renzo Mancuso,&nbsp;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}