Pub Date : 2026-02-12DOI: 10.1038/s41577-026-01279-1
Alexandra Flemming
Intracellular bacteria in cancer cells promote the recruitment of neutrophils and their polarization towards an immunosuppressive phenotype via a cGAS-STING-dependent pathway.
{"title":"Intracellular bacteria in cancer cells promote immunosuppression in the metastatic niche","authors":"Alexandra Flemming","doi":"10.1038/s41577-026-01279-1","DOIUrl":"10.1038/s41577-026-01279-1","url":null,"abstract":"Intracellular bacteria in cancer cells promote the recruitment of neutrophils and their polarization towards an immunosuppressive phenotype via a cGAS-STING-dependent pathway.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 3","pages":"166-166"},"PeriodicalIF":60.9,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146181179","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 : 2026-02-12DOI: 10.1038/s41577-026-01268-4
Peter T Bell, Gabrielle T Belz
Fibrosis is a complex disorder characterized by the excessive deposition of extracellular matrix, which disrupts normal tissue architecture and compromises organ function. Fibrosis can affect any organ, with pulmonary fibrosis being one of the most common and life-threatening forms. Despite marked research efforts, effective antifibrotic therapies remain limited, largely due to an incomplete understanding of the underlying disease mechanisms. At the centre of fibrotic processes are fibroblasts, which are tissue-resident mesenchymal cells responsible for extracellular matrix production, tissue remodelling, wound healing and fibrosis. For decades, the biology of fibroblasts remained poorly understood, but advances in single-cell sequencing have recently provided deeper insights into their heterogeneity, plasticity and functional diversity. These insights have prompted renewed efforts to identify the core regulatory programmes that govern fibroblast states in health and disease. In this Review, we examine how immunological, mechanical and metabolic regulators influence fibroblast function in fibrosing interstitial lung diseases. We show how loss of stromal regulation through chronic inflammation, immune dysfunction, altered tissue biomechanics and metabolic stress can tip the balance from successful tissue repair to progressive fibrosis.
{"title":"Fibroblasts as regulators of lung immunity, repair and fibrosis.","authors":"Peter T Bell, Gabrielle T Belz","doi":"10.1038/s41577-026-01268-4","DOIUrl":"https://doi.org/10.1038/s41577-026-01268-4","url":null,"abstract":"<p><p>Fibrosis is a complex disorder characterized by the excessive deposition of extracellular matrix, which disrupts normal tissue architecture and compromises organ function. Fibrosis can affect any organ, with pulmonary fibrosis being one of the most common and life-threatening forms. Despite marked research efforts, effective antifibrotic therapies remain limited, largely due to an incomplete understanding of the underlying disease mechanisms. At the centre of fibrotic processes are fibroblasts, which are tissue-resident mesenchymal cells responsible for extracellular matrix production, tissue remodelling, wound healing and fibrosis. For decades, the biology of fibroblasts remained poorly understood, but advances in single-cell sequencing have recently provided deeper insights into their heterogeneity, plasticity and functional diversity. These insights have prompted renewed efforts to identify the core regulatory programmes that govern fibroblast states in health and disease. In this Review, we examine how immunological, mechanical and metabolic regulators influence fibroblast function in fibrosing interstitial lung diseases. We show how loss of stromal regulation through chronic inflammation, immune dysfunction, altered tissue biomechanics and metabolic stress can tip the balance from successful tissue repair to progressive fibrosis.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":""},"PeriodicalIF":60.9,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146181223","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 : 2026-02-11DOI: 10.1038/s41577-026-01281-7
Yvonne Bordon
Intestinal macrophages that support the enteric nervous system may be involved in the spread of α-synuclein pathology from the gut to the brain.
支持肠神经系统的肠巨噬细胞可能参与了α-突触核蛋白病理从肠道向大脑的传播。
{"title":"Gut macrophages and Parkinson’s disease","authors":"Yvonne Bordon","doi":"10.1038/s41577-026-01281-7","DOIUrl":"10.1038/s41577-026-01281-7","url":null,"abstract":"Intestinal macrophages that support the enteric nervous system may be involved in the spread of α-synuclein pathology from the gut to the brain.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 3","pages":"167-167"},"PeriodicalIF":60.9,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146165608","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: 10.1038/s41577-026-01278-2
Amitava Sinha, Thomas Weichhart
{"title":"O-GlcNAcylation shapes macrophage tissue residency and alternative activation.","authors":"Amitava Sinha, Thomas Weichhart","doi":"10.1038/s41577-026-01278-2","DOIUrl":"https://doi.org/10.1038/s41577-026-01278-2","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":""},"PeriodicalIF":60.9,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146157876","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 : 2026-02-06DOI: 10.1038/s41577-026-01277-3
Annette Wu, Betty Y. S. Kim
A preprint by Yan et al. reports that local antibody production in germinal centres contributes to negative feedback on low-affinity B cells that target the same epitope.
Yan等人的预印本报告称，生发中心的局部抗体产生有助于针对相同表位的低亲和力B细胞的负反馈。
{"title":"Affinity-dependent local antibody feedback shapes germinal centre dynamics","authors":"Annette Wu, Betty Y. S. Kim","doi":"10.1038/s41577-026-01277-3","DOIUrl":"10.1038/s41577-026-01277-3","url":null,"abstract":"A preprint by Yan et al. reports that local antibody production in germinal centres contributes to negative feedback on low-affinity B cells that target the same epitope.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 3","pages":"169-169"},"PeriodicalIF":60.9,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146132427","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 : 2026-02-05DOI: 10.1038/s41577-026-01276-4
Ruslan Medzhitov
Empirical data and the theories that make sense of them are the twin pillars of scientific progress. When one pillar is raised much higher than the other, they cease to be good pillars. Ruslan Medzhitov shares his thoughts on the balance between generating data and developing theories in immunology, with a focus on exploring the rules that govern complex systems.
{"title":"On the balance of knowledge","authors":"Ruslan Medzhitov","doi":"10.1038/s41577-026-01276-4","DOIUrl":"10.1038/s41577-026-01276-4","url":null,"abstract":"Empirical data and the theories that make sense of them are the twin pillars of scientific progress. When one pillar is raised much higher than the other, they cease to be good pillars. Ruslan Medzhitov shares his thoughts on the balance between generating data and developing theories in immunology, with a focus on exploring the rules that govern complex systems.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 3","pages":"163-165"},"PeriodicalIF":60.9,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146125874","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 : 2026-01-28DOI: 10.1038/s41577-026-01275-5
Rachel Geltman, Dusan Bogunovic
A preprint by El-Daher et al. describes an interferonopathy-associated mutation in the chromatin remodeller ATRX, which identifies an unexpected role for nuclear cGAS in transcriptional regulation.
{"title":"Type I interferonopathy in ATR-X syndrome reveals a transcriptional role for cGAS","authors":"Rachel Geltman, Dusan Bogunovic","doi":"10.1038/s41577-026-01275-5","DOIUrl":"10.1038/s41577-026-01275-5","url":null,"abstract":"A preprint by El-Daher et al. describes an interferonopathy-associated mutation in the chromatin remodeller ATRX, which identifies an unexpected role for nuclear cGAS in transcriptional regulation.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 3","pages":"168-168"},"PeriodicalIF":60.9,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146069997","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 : 2026-01-27DOI: 10.1038/s41577-026-01274-6
Leon Baronijan, Alberto Martin
A preprint by Villazala-Merino et al. shows that allergen-specific memory B cells must re-enter germinal centres to differentiate into IgE-producing plasma cells, which occurs in lymph nodes but not at barrier sites.
{"title":"Germinal centre IL-4 enforces tissue confinement of IgE memory","authors":"Leon Baronijan, Alberto Martin","doi":"10.1038/s41577-026-01274-6","DOIUrl":"10.1038/s41577-026-01274-6","url":null,"abstract":"A preprint by Villazala-Merino et al. shows that allergen-specific memory B cells must re-enter germinal centres to differentiate into IgE-producing plasma cells, which occurs in lymph nodes but not at barrier sites.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 3","pages":"168-168"},"PeriodicalIF":60.9,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146056549","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 : 2026-01-23DOI: 10.1038/s41577-026-01266-6
Jaroslav Zak,John R Teijaro
JAK inhibitors target a large group of cytokines that signal through the JAK-STAT pathway and are typically used clinically as immunosuppressive agents. However, recent work has demonstrated the paradoxical ability of JAK inhibitors to enhance antitumour and antiviral immune responses and established their synergy with immune checkpoint inhibitors in early-stage clinical trials. In this Perspective, we consider why JAK inhibitors, which are typically used as immunosuppressive drugs, can have immune-enhancing effects, exploring the potential mechanistic basis and the opportunities to harness this effect to improve cancer immunotherapy.
{"title":"Beyond suppression: the paradox of JAK inhibitors as amplifiers of cancer immunotherapy.","authors":"Jaroslav Zak,John R Teijaro","doi":"10.1038/s41577-026-01266-6","DOIUrl":"https://doi.org/10.1038/s41577-026-01266-6","url":null,"abstract":"JAK inhibitors target a large group of cytokines that signal through the JAK-STAT pathway and are typically used clinically as immunosuppressive agents. However, recent work has demonstrated the paradoxical ability of JAK inhibitors to enhance antitumour and antiviral immune responses and established their synergy with immune checkpoint inhibitors in early-stage clinical trials. In this Perspective, we consider why JAK inhibitors, which are typically used as immunosuppressive drugs, can have immune-enhancing effects, exploring the potential mechanistic basis and the opportunities to harness this effect to improve cancer immunotherapy.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"186 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146033855","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 : 2026-01-21DOI: 10.1038/s41577-025-01262-2
Noa B Martín-Cófreces,Diego Calzada-Fraile,Francisco Sánchez-Madrid
In the context of adaptive immunity, T cells are activated by professional antigen-presenting cells (APCs) in a process that begins with peptide-MHC complexes on the APC being recognized by T cell receptor and CD3 co-receptor complexes on the T cell. This triggers a reorganization of T cell morphology, formation of an immune synapse, and the delivery of signals that ultimately culminate in nuclear activation. The interaction between T cells and APCs, such as dendritic cells (DCs), was originally viewed as a unidirectional information highway in which the APC instructs the T cell. It is now clear that bidirectional crosstalk occurs at the immune synapse and that T cells also shape APC functions. The concept of 'DC licensing' originally suggested an instructive role for T cells in modifying DC functions. More recent studies have provided important insight into the changes that occur in DCs during antigen-driven contacts with T cells at the immune synapse. In this Review, we discuss our current understanding of the bidirectional T cell-DC crosstalk that occurs at the IS and its relevance for immune responses and immunotherapies.
{"title":"How crosstalk at the immune synapse shapes T cell and dendritic cell biologys.","authors":"Noa B Martín-Cófreces,Diego Calzada-Fraile,Francisco Sánchez-Madrid","doi":"10.1038/s41577-025-01262-2","DOIUrl":"https://doi.org/10.1038/s41577-025-01262-2","url":null,"abstract":"In the context of adaptive immunity, T cells are activated by professional antigen-presenting cells (APCs) in a process that begins with peptide-MHC complexes on the APC being recognized by T cell receptor and CD3 co-receptor complexes on the T cell. This triggers a reorganization of T cell morphology, formation of an immune synapse, and the delivery of signals that ultimately culminate in nuclear activation. The interaction between T cells and APCs, such as dendritic cells (DCs), was originally viewed as a unidirectional information highway in which the APC instructs the T cell. It is now clear that bidirectional crosstalk occurs at the immune synapse and that T cells also shape APC functions. The concept of 'DC licensing' originally suggested an instructive role for T cells in modifying DC functions. More recent studies have provided important insight into the changes that occur in DCs during antigen-driven contacts with T cells at the immune synapse. In this Review, we discuss our current understanding of the bidirectional T cell-DC crosstalk that occurs at the IS and its relevance for immune responses and immunotherapies.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"258 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146015330","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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