{"title":"Faulty mitochondria jump between tumours and T cells","authors":"Lucy Bird","doi":"10.1038/s41577-025-01143-8","DOIUrl":"10.1038/s41577-025-01143-8","url":null,"abstract":"To evade elimination by T cells, tumour cells transfer mutant mitochondria to T cells, which reprogrammes their metabolism and compromises their antitumour activity.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 3","pages":"155-155"},"PeriodicalIF":67.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257886","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}
Abrar Samiea, George Celis, Rashi Yadav, Lauren B. Rodda, Joshua M. Moreau
{"title":"B cells in non-lymphoid tissues","authors":"Abrar Samiea, George Celis, Rashi Yadav, Lauren B. Rodda, Joshua M. Moreau","doi":"10.1038/s41577-025-01137-6","DOIUrl":"https://doi.org/10.1038/s41577-025-01137-6","url":null,"abstract":"<p>B cells have long been understood to be drivers of both humoral and cellular immunity. Recent advances underscore this importance but also indicate that in infection, inflammatory disease and cancer, B cells function directly at sites of inflammation and form tissue-resident memory populations. The spatial organization and cellular niches of tissue B cells have profound effects on their function and on disease outcome, as well as on patient response to therapy. Here we review the role of B cells in peripheral tissues in homeostasis and disease, and discuss the newly identified cellular and molecular signals that are involved in regulating their activity. We integrate emerging data from multi-omic human studies with experimental models to propose a framework for B cell function in tissue inflammation and homeostasis.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"79 2 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143192154","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}
Martyna Szpakowska, Daniel F. Legler, Stefan Offermanns, Silvano Sozzani, Antal Rot, Marcus Thelen, Andy Chevigné
{"title":"Inclusion of ACKR5 in the systematic nomenclature of atypical chemokine receptors","authors":"Martyna Szpakowska, Daniel F. Legler, Stefan Offermanns, Silvano Sozzani, Antal Rot, Marcus Thelen, Andy Chevigné","doi":"10.1038/s41577-025-01135-8","DOIUrl":"10.1038/s41577-025-01135-8","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 3","pages":"225-226"},"PeriodicalIF":67.7,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41577-025-01135-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143077293","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":"Podoplanin mediates stromal–immune crosstalk in the lymph node","authors":"Erika E. McCartney, Matthew B. Buechler","doi":"10.1038/s41577-025-01140-x","DOIUrl":"10.1038/s41577-025-01140-x","url":null,"abstract":"A preprint by Makris et al. shows that podoplanin is a key regulator of the functions of fibroblastic reticular cells in lymph nodes, by modulating interactions with immune cells.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 3","pages":"160-160"},"PeriodicalIF":67.7,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143071395","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}
Mariángeles Kovacs, Amaia Dominguez-Belloso, Samir Ali-Moussa, Aleksandra Deczkowska
{"title":"Immune control of brain physiology","authors":"Mariángeles Kovacs, Amaia Dominguez-Belloso, Samir Ali-Moussa, Aleksandra Deczkowska","doi":"10.1038/s41577-025-01129-6","DOIUrl":"https://doi.org/10.1038/s41577-025-01129-6","url":null,"abstract":"<p>The peripheral immune system communicates with the brain through complex anatomical routes involving the skull, the brain borders, circumventricular organs and peripheral nerves. These immune–brain communication pathways were classically considered to be dormant under physiological conditions and active only in cases of infection or damage. Yet, peripheral immune cells and signals are key in brain development, function and maintenance. In this Perspective, we propose an alternative framework for understanding the mechanisms of immune–brain communication. During brain development and in homeostasis, these anatomical structures allow selected elements of the peripheral immune system to affect the brain directly or indirectly, within physiological limits. By contrast, in ageing and pathological settings, detrimental peripheral immune signals hijack the existing communication routes or alter their structure. We discuss why a diversity of communication channels is needed and how they work in relation to one another to maintain homeostasis of the brain.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"74 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143071406","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}
George Hajishengallis, Mihai G. Netea, Triantafyllos Chavakis
{"title":"Trained immunity in chronic inflammatory diseases and cancer","authors":"George Hajishengallis, Mihai G. Netea, Triantafyllos Chavakis","doi":"10.1038/s41577-025-01132-x","DOIUrl":"https://doi.org/10.1038/s41577-025-01132-x","url":null,"abstract":"<p>A decade after the term ‘trained immunity’ (TRIM) was coined to reflect the long-lasting hyper-responsiveness of innate immune cells with an epigenetically imprinted ‘memory’ of earlier stimuli, our understanding has broadened to include the potential implications of TRIM in health and disease. Here, after summarizing the well-documented beneficial effects of TRIM against infections, we discuss emerging evidence that TRIM is also a major underlying mechanism in chronic inflammation-related disorders such as periodontitis, rheumatoid arthritis and cardiovascular disease. Furthermore, mounting evidence indicates that the induction of TRIM by certain agonists confers protective antitumour responses. Although the mechanisms underlying TRIM require further study, the current knowledge enables the experimental development of innovative therapeutic approaches to stimulate or inhibit TRIM in a context-appropriate manner, such as the stimulation of TRIM in cancer or its inhibition in inflammatory disorders.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"122 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143071396","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}
Christian Kurts, Sibylle von Vietinghoff, Christian F. Krebs, Ulf Panzer
{"title":"Kidney immunology from pathophysiology to clinical translation","authors":"Christian Kurts, Sibylle von Vietinghoff, Christian F. Krebs, Ulf Panzer","doi":"10.1038/s41577-025-01131-y","DOIUrl":"https://doi.org/10.1038/s41577-025-01131-y","url":null,"abstract":"<p>Kidney diseases are widespread and represent a considerable medical, social and economic burden. However, there has been marked progress in understanding the immunological aspects of kidney disease. This includes the identification of distinct intrarenal immunological niches and characterization of kidney disease endotypes according to the underlying molecular immunopathology, as well as a better understanding of the pathological roles for T cells, mononuclear phagocytes and B cells and the renal elements they target. These insights have improved the diagnosis of kidney disease. Here, we discuss new developments in our understanding of kidney immunology, focusing on immune mechanisms of disease and their translational implications for the diagnosis and treatment of kidney disease. We also describe the immune-mediated crosstalk between the kidney and other organs that influences kidney disease and extrarenal inflammation.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"28 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143057117","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}
Srikanth Kodali, Caroline M. Sands, Lei Guo, Yun Huang, Bruno Di Stefano
{"title":"Biomolecular condensates in immune cell fate","authors":"Srikanth Kodali, Caroline M. Sands, Lei Guo, Yun Huang, Bruno Di Stefano","doi":"10.1038/s41577-025-01130-z","DOIUrl":"https://doi.org/10.1038/s41577-025-01130-z","url":null,"abstract":"<p>Fate decisions during immune cell development require temporally precise changes in gene expression. Evidence suggests that the dynamic modulation of these changes is associated with the formation of diverse, membrane-less nucleoprotein assemblies that are termed biomolecular condensates. These condensates are thought to orchestrate fate-determining transcriptional and post-transcriptional processes by locally and transiently concentrating DNA or RNA molecules alongside their regulatory proteins. Findings have established a link between condensate formation and the gene regulatory networks that ensure the proper development of immune cells. Conversely, condensate dysregulation has been linked to impaired immune cell fates, including ageing and malignant transformation. This Review explores the putative mechanistic links between condensate assembly and the gene regulatory frameworks that govern normal and pathological development in the immune system.</p>","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"67 1","pages":""},"PeriodicalIF":100.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049989","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":"Beyond bacteria: Phanta adds flavour to microbiome profiling with a focus on phages","authors":"Yishay Pinto","doi":"10.1038/s41577-025-01138-5","DOIUrl":"10.1038/s41577-025-01138-5","url":null,"abstract":"In this Tools of the Trade article, Yishay Pinto describes a tool, called Phanta, that profiles phages alongside their bacterial hosts in microbiome analysis.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 3","pages":"159-159"},"PeriodicalIF":67.7,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049988","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":"An inter-organ neuro–immuno–endocrine circuit for glucose homeostasis","authors":"Kirsty Minton","doi":"10.1038/s41577-025-01139-4","DOIUrl":"10.1038/s41577-025-01139-4","url":null,"abstract":"A study in Science reports that intestinal innate lymphoid cells migrate to the pancreas in response to low blood glucose levels to promote glucagon production.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 3","pages":"158-158"},"PeriodicalIF":67.7,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049987","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}