Alain Fischer , Patrick Peretti-Watel , Jeremy Ward
{"title":"Vaccine policies in France and Europe","authors":"Alain Fischer , Patrick Peretti-Watel , Jeremy Ward","doi":"10.1016/j.coi.2024.102513","DOIUrl":"10.1016/j.coi.2024.102513","url":null,"abstract":"<div><div>This review outlines the outcome of the COVID-19 vaccination campaign in France and assesses the respective roles of information and coercion in its overall success. These data are then put into perspective of the evolution of vaccination acceptance in France.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"92 ","pages":"Article 102513"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142831493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Navigating the metabolic landscape of regulatory T cells: from autoimmune diseases to tumor microenvironments","authors":"Janika Härm , Yu-Tong Fan , Dirk Brenner","doi":"10.1016/j.coi.2024.102511","DOIUrl":"10.1016/j.coi.2024.102511","url":null,"abstract":"<div><div>Regulatory T cells (Tregs) are essential for maintaining immune homeostasis, playing crucial roles in modulating autoimmune conditions and contributing to the suppressive tumor microenvironment. Their cellular metabolism governs their generation, stability, proliferation, and suppressive function. Enhancing Treg metabolism to boost their suppressive function offers promising therapeutic potential for alleviating inflammatory symptoms in autoimmune diseases. Conversely, inhibiting Treg metabolism to reduce their suppressive function can enhance the efficacy of traditional immunotherapy in cancer patients. This review explores recent advances in targeting Treg metabolism in autoimmune diseases and the metabolic adaptations of Tregs within the tumor microenvironment that increase their immunosuppressive function.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"92 ","pages":"Article 102511"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of allergen-specific regulatory T cells in the control of allergic disease","authors":"Athanasios Stoumpos , Guido Heine , Carina Saggau , Alexander Scheffold","doi":"10.1016/j.coi.2024.102509","DOIUrl":"10.1016/j.coi.2024.102509","url":null,"abstract":"<div><div>Allergies result from an antigen-specific loss of tolerance against innocuous foreign substances. Allergen immunotherapy (AIT) aims to reverse the pathogenic response and to re-establish physiological tolerance. However, the tolerogenic mechanisms that prevent allergy in healthy and act during AIT are still obscure. Foxp3 expressing ‘regulatory’ CD4 T cells (Tregs) are essential mediators of tolerance against allergens. It remains controversial which antigen specificity of Tregs is required to prevent allergy and the role of allergen-specific Tregs during AIT. Recent work provided precise insight into physiological T cell responses against environmental and food compounds. This identified Treg responses mainly against peptides and proteins not involved in immune pathology, revealing an unexpected role of Treg antigen specificity for tolerance. This review will focus on antigen-specific Treg responses against food and airborne allergens, and the impact of the technological approach utilized for antigen-specific Treg characterization is discussed, with critical points to be addressed in future research.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"92 ","pages":"Article 102509"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142793022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chemokines that govern T cell activity in tumors","authors":"Thorsten R Mempel, Mohsen Malehmir","doi":"10.1016/j.coi.2024.102510","DOIUrl":"10.1016/j.coi.2024.102510","url":null,"abstract":"<div><div>Local regulation of T cell–mediated immunity to solid tumors occurs at multiple levels, including their recruitment from the bloodstream to the tumor microenvironment (TME), coordinated crosstalk with different subsets of antigen-presenting cells (APCs) controlling their local survival, proliferation, and effector differentiation, as well as their egress from tumors via lymphatics. At each level, chemokines play essential roles, for instance, by guiding directional T cell migration across blood and lymphatic endothelial barriers or by promoting their spatial proximity and direct physical interactions with APCs to enable functional crosstalk. In this article, we will review recent mechanistic insights into the chemokine axes that guide T cell functions in TMEs in light of the emerging functional state heterogeneity of CD8<sup>+</sup> effector T cells and our growing understanding of how regulatory T cells restrain antitumor activity.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"92 ","pages":"Article 102510"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142815203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tuberculosis as an unconventional interferonopathy","authors":"Russell E Vance","doi":"10.1016/j.coi.2024.102508","DOIUrl":"10.1016/j.coi.2024.102508","url":null,"abstract":"<div><div>Tuberculosis is caused by <em>Mycobacterium tuberculosis</em>, a bacterium that accounts for more human mortality than any other. Evidence is accumulating for the view that tuberculosis is an interferonopathy — a disease driven by type I interferons. However, how type I interferons exacerbate tuberculosis remains poorly understood. As an infection, tuberculosis is distinct from conventional interferonopathies, which are autoinflammatory diseases. Here I consider the hypothesis that type I interferons promote bacterial replication by impairing key antibacterial immune responses, including those orchestrated by interleukin-1 and interferon γ. Paradoxically, during tuberculosis, the underlying state of impaired antibacterial immunity co-exists with overt (but ineffective) inflammation. Conceiving of tuberculosis as an unconventional interferonopathy may suggest fruitful avenues for therapeutic intervention.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"92 ","pages":"Article 102508"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142788193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Macrophage barrier responses to oncogenic transformation","authors":"J Magarian Blander","doi":"10.1016/j.coi.2024.102524","DOIUrl":"10.1016/j.coi.2024.102524","url":null,"abstract":"<div><div>The well-documented protumorigenic roles of macrophages in advanced cancers can sometimes overshadow their beneficial functions in the earlier stages of tumor development. This essay explores the hypothesis that macrophages play a crucial protective role in premalignant tissues by sensing and responding to early oncogenic transformation. Their activity is closely intertwined with cell-intrinsic barriers to transformation — such as apoptosis, senescence, and DNA repair — which collectively work to suppress malignant progression. Thus, an integrated cell-intrinsic and macrophage response constitutes effective ‘oncogenic monitoring’. In premalignant tissues, macrophages interpret outputs of cell-intrinsic tumor suppression as oncogenic stress signals detected through innate immune sensors, initiating a protective, homeostatic response that mitigates potential progression to malignancy. By recontextualizing macrophage roles in the early immune landscape, it becomes evident that these cells can serve as key protectors, preventing or delaying tumor formation. Understanding this dual role of macrophages — protective in early tumorigenesis and protumorigenic in established cancers — offers new perspectives on harnessing their immune functions for cancer prevention and therapy.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"92 ","pages":"Article 102524"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143097282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Nucleic acid triggers of autoimmunity and autoinflammation","authors":"Kaiyuan Hao, Ann Marshak-Rothstein","doi":"10.1016/j.coi.2025.102535","DOIUrl":"10.1016/j.coi.2025.102535","url":null,"abstract":"<div><div>The key role of nucleic acid sensing receptors in the development of autoimmune and autoinflammatory diseases is becoming increasingly apparent. Activation of these sensors has been attributed to the failure of professional scavenger cells to adequately clear cell debris, in many cases due to defective scavenger receptors. However, as now summarized in this review, numerous gain-of-function mutations in the nucleic acid sensing receptors, or in molecules that regulate sensor activity, have now been evaluated in gene-targeted murine strains, and critical components of their downstream pathways have been identified as therapeutic targets. In addition, we are beginning to understand how DNases and RNases play crucial roles in both generating and eliminating the distinct ligands that engage the various nucleic acid sensors. Murine models of disease have further provided important insights regarding the function of and synergy between individual endosomal and cytosolic receptors, as well as cell type restricted functions.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"93 ","pages":"Article 102535"},"PeriodicalIF":6.6,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolism and metabolites regulating hematopoiesis","authors":"Baihao Zhang , Sidonia Fagarasan","doi":"10.1016/j.coi.2025.102525","DOIUrl":"10.1016/j.coi.2025.102525","url":null,"abstract":"<div><div>Energy metabolism of immune cells, such as glycolysis and mitochondrial activity, requires strict regulation. This is especially critical in the complex environment of the bone marrow (BM), where there is a need to both preserve the quiescence of hematopoietic stem cells (HSCs) and guarantee timed and effective lineage differentiation of the HSCs. Recent advances highlight the critical roles played by bioactive metabolites in regulating hematopoiesis. In particular, secreted immune metabolites (SIMets), such as γ-aminobutyric acid (GABA) and acetylcholine, secreted by B-lineage cells, act as potent modulators of hematopoietic processes, influencing HSC differentiation and emergency hematopoiesis. In this review, we provide an overview and discuss mechanisms by which energy metabolism and SIMets regulate hematopoiesis. We propose that biochemical communication facilitated by these metabolites is essential for maintaining the BM niche and suggest potential therapeutic strategies using SIMets in hematological disorders.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"93 ","pages":"Article 102525"},"PeriodicalIF":6.6,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Functional subsets of tumor-specific CD8+ T cells in draining lymph nodes and tumor microenvironment","authors":"Qizhao Huang , Lifan Xu , Lilin Ye","doi":"10.1016/j.coi.2024.102506","DOIUrl":"10.1016/j.coi.2024.102506","url":null,"abstract":"<div><div>Accumulating evidence demonstrates that tumor-specific CD8<sup>+</sup> T cells in tumor-draining lymph nodes (TdLNs) act as an upstream reservoir of exhausted subsets within tumor microenvironment (TME). This reservoir primarily consists of progenitor exhausted CD8<sup>+</sup> T (T<sub>PEX</sub>) cells and newly defined tumor-specific memory subsets (T<sub>TSM</sub>). We propose that these two subsets work together to mediate the antitumor effects of PD-1/PD-L1 immune checkpoint blockade (ICB) in a spatiotemporal manner. Although PD-1/PD-L1 ICB monotherapy drives the proliferation and further differentiation of these subsets, it does not alter the programmed differentiation trajectory from T<sub>TSM</sub> cells to T<sub>PEX</sub> cells, ultimately leading to the development of terminally exhausted CD8<sup>+</sup> T cells. This phenomenon may partly explaining the frequent relapse in patients following initial ICB therapy. In this review, we focus on the phenotypic and functional heterogeneity of tumor-specific CD8<sup>+</sup> T cells in both TdLNs and the TME and discuss the implications of these studies for ICB. Our insights aim to illuminate new strategies for advancing tumor immunotherapies.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"92 ","pages":"Article 102506"},"PeriodicalIF":6.6,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142701942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Decoding the neuroimmune axis in the atopic march: mechanisms and implications","authors":"Laura Brabenec , Surbhi Gupta , Tuany Eichwald , Moutih Rafei , Sebastien Talbot","doi":"10.1016/j.coi.2024.102507","DOIUrl":"10.1016/j.coi.2024.102507","url":null,"abstract":"<div><div>The immune and nervous systems have co-evolved complex mechanisms to sense environmental dangers and orchestrate a concerted response to safeguard tissue and mobilize host defenses. This sophisticated interplay, marked by a shared repertoire of receptors and ligands, influences disease pathogenesis. Neuro-immune interactions in allergic diseases are pivotal for symptom development, from anaphylaxis to chronic conditions like asthma and atopic dermatitis. This review explores the neuro-immune interplay within the atopic march, emphasizing its role in host defense, inflammation resolution, and tissue repair. We delve into the multifaceted functions of nociceptors in orchestrating type 2 immune responses and the progression of allergic disorders, focusing on key regulators such as CGRP-RAMP1 and SP-MRGPRB2/A2. Additionally, we discuss the potential of nociceptor neuron-blocking drugs to target neuro-immunity, offering the possibility of reversing the progression of the atopic march. Altogether, we underscore the need for targeted interventions to disrupt the pathological processes and enhance therapeutic outcomes at various stages of the atopic march.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"91 ","pages":"Article 102507"},"PeriodicalIF":6.6,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}