Annual review of immunology最新文献

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The Interplay Between Innate Immunity and Nonimmune Cells in Lung Damage, Inflammation, and Repair. 先天免疫和非免疫细胞在肺损伤、炎症和修复中的相互作用。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 Epub Date: 2025-03-04 DOI: 10.1146/annurev-immunol-082323-031852
Chrysante S Iliakis, Stefania Crotta, Andreas Wack
{"title":"The Interplay Between Innate Immunity and Nonimmune Cells in Lung Damage, Inflammation, and Repair.","authors":"Chrysante S Iliakis, Stefania Crotta, Andreas Wack","doi":"10.1146/annurev-immunol-082323-031852","DOIUrl":"10.1146/annurev-immunol-082323-031852","url":null,"abstract":"<p><p>As the site of gas exchange, the lung is critical for organismal survival. It is also subject to continual environmental insults inflicted by pathogens, particles, and toxins. Sometimes, these insults result in structural damage and the initiation of an innate immune response. Operating in parallel, the immune response aims to eliminate the threat, while the repair process ensures continual physiological function of the lung. The inflammatory response and repair processes are thus inextricably linked in time and space but are often studied in isolation. Here, we review the interplay of innate immune cells and nonimmune cells during lung insult and repair. We highlight how cellular cross talk can fine-tune the circuitry of the immune response, how innate immune cells can facilitate or antagonize proper organ repair, and the prolonged changes to lung immunity and physiology that can result from acute immune responses and repair processes.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":" ","pages":"395-422"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555713","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}
引用次数: 0
Macrophage Differentiation and Metabolic Adaptation in Mycobacterial Infections. 分枝杆菌感染中的巨噬细胞分化和代谢适应。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 Epub Date: 2025-02-27 DOI: 10.1146/annurev-immunol-082323-120757
Anne Kathrin Lösslein, Philipp Henneke
{"title":"Macrophage Differentiation and Metabolic Adaptation in Mycobacterial Infections.","authors":"Anne Kathrin Lösslein, Philipp Henneke","doi":"10.1146/annurev-immunol-082323-120757","DOIUrl":"10.1146/annurev-immunol-082323-120757","url":null,"abstract":"<p><p>The adaptation of macrophages-the most common tissue-resident immune cells-to metabolic and microbial cues with high local variability is essential for the maintenance of organ integrity. In homeostasis, macrophages show largely predictable tissue-specific differentiation, as recently revealed by multidimensional methods. However, chronic infections with human-adapted pathogens substantially contribute to the differentiation complexity of tissue macrophages, which has been only partially resolved. Specifically, the response to mycobacterial species-which range from <i>Mycobacterium tuberculosis</i> (with highest specificity for humans, broad organ tropism, yet tissue-specific disease phenotypes) to environmental mycobacteria with humans as accidental hosts-may serve as a paradigm of tissue macrophage adaptation mechanisms. While mycobacterial species-specific tissue preferences are partially related to the mode of acquisition and pathogen characteristics, evolutionary convergence with macrophages driven by metabolic features of the target organ likely contributes to infection resistance and immunopathology. In this review, we unravel the mechanisms of tissue-specific macrophage differentiation and its limitations in mycobacterial infections.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":" ","pages":"423-450"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522565","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}
引用次数: 0
Regulation of the cGAS-STING Pathway. cGAS-STING通路的调控。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 Epub Date: 2025-03-14 DOI: 10.1146/annurev-immunol-101721-032910
Bing Zhang, Pengbiao Xu, Andrea Ablasser
{"title":"Regulation of the cGAS-STING Pathway.","authors":"Bing Zhang, Pengbiao Xu, Andrea Ablasser","doi":"10.1146/annurev-immunol-101721-032910","DOIUrl":"10.1146/annurev-immunol-101721-032910","url":null,"abstract":"<p><p>The cGAS-cGAMP-STING pathway is essential for immune defense against pathogens. Upon binding DNA, cGAS synthesizes cGAMP, which activates STING, leading to potent innate immune effector responses. However, lacking specific features to distinguish between self and nonself DNA, cGAS-STING immunity requires precise regulation to prevent aberrant activation. Several safeguard mechanisms acting on different levels have evolved to maintain tolerance to self DNA and ensure immune homeostasis under normal conditions. Disruption of these safeguards can lead to erroneous activation by self DNA, resulting in inflammatory conditions but also favorable antitumor immunity. Insights into structural and cellular checkpoints that control and terminate cGAS-STING signaling are essential for comprehending and manipulating DNA-triggered innate immunity in health and disease.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":" ","pages":"667-692"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630117","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}
引用次数: 0
Human Immune Responses to Epstein-Barr Virus Highlighted by Immunodeficiencies. 人类对eb病毒的免疫反应由免疫缺陷引起。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 DOI: 10.1146/annurev-immunol-082323-035455
Sylvain Latour
{"title":"Human Immune Responses to Epstein-Barr Virus Highlighted by Immunodeficiencies.","authors":"Sylvain Latour","doi":"10.1146/annurev-immunol-082323-035455","DOIUrl":"https://doi.org/10.1146/annurev-immunol-082323-035455","url":null,"abstract":"<p><p>Inborn errors of immunity (IEIs) represent unique in natura models that uncover key components of immunity in humans, in particular those that predispose to infections. Epstein-Barr virus (EBV) is one of the most common opportunistic infectious agents in humans and is responsible for several diseases, including infectious mononucleosis, nonmalignant and malignant lymphoproliferative disorders, hemophagocytic lymphohistiocytosis, and smooth muscle and epithelial tumors. For most individuals, EBV infection persists for life without pathological consequences. IEIs that do not predispose to EBV infection suggest that innate and humoral responses are not necessary or redundant for the immune response to EBV. IEIs associated with high susceptibility to EBV infection provide unequivocal genetic proof of the central role of CD8+ T cell responses in immunity to EBV. They also highlight the distinct steps and pathways required for, on the one hand, the effector cytotoxic functions of CD8+ T cells and, on the other hand, the expansion and maturation of cytotoxic CD8+ T cells.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":"43 1","pages":"723-749"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962108","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}
引用次数: 0
Using the Key Characteristics Framework to Unlock the Mysteries of Aryl Hydrocarbon Receptor-Mediated Effects on the Immune System. 利用关键特征框架解开芳基烃受体介导免疫系统作用的奥秘。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 Epub Date: 2025-01-15 DOI: 10.1146/annurev-immunol-083122-040107
Courtney E W Sulentic, Barbara L F Kaplan, B Paige Lawrence
{"title":"Using the Key Characteristics Framework to Unlock the Mysteries of Aryl Hydrocarbon Receptor-Mediated Effects on the Immune System.","authors":"Courtney E W Sulentic, Barbara L F Kaplan, B Paige Lawrence","doi":"10.1146/annurev-immunol-083122-040107","DOIUrl":"10.1146/annurev-immunol-083122-040107","url":null,"abstract":"<p><p>Initially discovered for its role mediating the deleterious effects of environmental contaminants, the aryl hydrocarbon receptor (AHR) is now known to be a crucial regulator of the immune system. The expanding list of AHR ligands includes synthetic and naturally derived molecules spanning pollutants, phytochemicals, pharmaceuticals, and substances derived from amino acids and microorganisms. The consequences of engaging AHR vary, depending on factors such as the AHR ligand, cell type, immune challenge, developmental state, dose, and timing of exposure relative to the immune stimulus. This review frames this complexity using the recently identified key characteristics of agents that affect immune system function (altered cell signaling, proliferation, differentiation, effector function, communication, trafficking, death, antigen presentation and processing, and tolerance). The use of these key characteristics provides a scaffold for continued discovery of how AHR and its myriad ligands influence the immune system, which will help harness the power of this enigmatic receptor to prevent or treat disease.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":" ","pages":"191-218"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142999127","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}
引用次数: 0
Genetic Regulation of Cell Death: Insights from Autoinflammatory Diseases. 细胞死亡的遗传调控:来自自身炎症性疾病的见解。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 DOI: 10.1146/annurev-immunol-090222-105848
Hirotsugu Oda, Alessandro Annibaldi, Daniel L Kastner, Ivona Aksentijevich
{"title":"Genetic Regulation of Cell Death: Insights from Autoinflammatory Diseases.","authors":"Hirotsugu Oda, Alessandro Annibaldi, Daniel L Kastner, Ivona Aksentijevich","doi":"10.1146/annurev-immunol-090222-105848","DOIUrl":"https://doi.org/10.1146/annurev-immunol-090222-105848","url":null,"abstract":"<p><p>Metazoans have evolved innate antimicrobial defenses that promote cellular survival and proliferation. Countering the inevitable molecular mechanisms by which microbes sabotage these pathways, multicellular organisms rely on an alternative, perhaps more ancient, strategy that is the immune equivalent of suicide bombing: Infection triggers cell death programs that summon localized or even systemic inflammation. The study of human genetics has now unveiled a level of complexity that refutes the naive view that cell death is merely a blunt instrument or an evolutionary afterthought. To the contrary, findings from patients with rare diseases teach us that cell death-induced inflammation is a sophisticated, tightly choreographed process. We herein review the emerging body of evidence describing a group of illnesses-inborn errors of cell death, which define many of the molecular building blocks and regulatory elements controlling cell death-induced inflammation in humans-and provide a possible road map to countering this process across the spectrum of rare and common illnesses.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":"43 1","pages":"313-342"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953115","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}
引用次数: 0
From Cytokines to Tuberculosis and Back: My Journey to Understanding the Immune Response to Infection. 从细胞因子到肺结核再回来:我理解感染免疫反应的旅程。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 DOI: 10.1146/annurev-immunol-010824-041601
Anne O'Garra
{"title":"From Cytokines to Tuberculosis and Back: My Journey to Understanding the Immune Response to Infection.","authors":"Anne O'Garra","doi":"10.1146/annurev-immunol-010824-041601","DOIUrl":"10.1146/annurev-immunol-010824-041601","url":null,"abstract":"<p><p>I felt honored by the invitation to write this autobiography, although it was an arduous task to describe my journey through science: first bacterial adhesion, then cytokine function, and then immune responses in tuberculosis. Since only seven women had been authors of autobiographies for the <i>Annual Review of Immunology</i>, I felt I couldn't refuse to contribute to Volume 43 of the journal. Moreover, this was a good occasion to record my appreciation to all the lab members and collaborators for their contributions over the last 40 years, to remember the exciting times, and to reflect on the obstacles we faced. I often reflect on this line that is commonly attributed to Winston Churchill: Success is not final; failure is not fatal: It is the courage to continue that counts. What kept me going was a burning desire to know how things work and find enjoyment in the discovery. This passion to understand immune responses to infection remains with me to this day. I thank all those I have interacted with for the support and friendship they provided.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":"43 1","pages":"1-28"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963055","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}
引用次数: 0
Catch Bonds in Immunology. 抓住免疫学中的化学键。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 Epub Date: 2025-03-14 DOI: 10.1146/annurev-immunol-082423-035904
Hyun-Kyu Choi, Cheng Zhu
{"title":"Catch Bonds in Immunology.","authors":"Hyun-Kyu Choi, Cheng Zhu","doi":"10.1146/annurev-immunol-082423-035904","DOIUrl":"10.1146/annurev-immunol-082423-035904","url":null,"abstract":"<p><p>Catch bonds are molecular bonds that last longer under force than slip bonds, which become shorter-lived under force. Although catch bonds were initially discovered in studies of leukocyte and bacterial adhesions two decades ago, they have since been found in many other contexts, including platelet binding to blood vessel walls during clotting, structural support within the cell and between cells, force transmission in the cell's machineries for motility and mechanotransduction, viral infection of host cells, and immunoreceptor mechanosensing. Catch bonds are strengthened by increasing force, which induces structural changes in one or both interacting molecules either locally or allosterically to enable additional contacts at their binding interface, thus lengthening bond lifetimes. They can be modeled by the kinetics of a system escaping from the energy well(s) of the bound state(s) over the energy barrier(s) to the free state by traversing along the dissociation path(s) across a hilly energy landscape modulated by force. Catch bond studies are important for understanding the mechanics of biological systems and developing treatment strategies for infectious diseases, immune disorders, cancer, and other ailments.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":" ","pages":"641-666"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630088","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}
引用次数: 0
TNF/TNFR Superfamily Members in Costimulation of T Cell Responses-Revisited. TNF/TNFR超家族成员在共同刺激T细胞反应中的作用
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 Epub Date: 2025-01-02 DOI: 10.1146/annurev-immunol-082423-040557
Tania H Watts, Karen K M Yeung, Tianning Yu, Seungwoo Lee, Razieh Eshraghisamani
{"title":"TNF/TNFR Superfamily Members in Costimulation of T Cell Responses-Revisited.","authors":"Tania H Watts, Karen K M Yeung, Tianning Yu, Seungwoo Lee, Razieh Eshraghisamani","doi":"10.1146/annurev-immunol-082423-040557","DOIUrl":"10.1146/annurev-immunol-082423-040557","url":null,"abstract":"<p><p>Prosurvival tumor necrosis factor receptor (TNFR) superfamily (TNFRSF) members on T cells, including 4-1BB, CD27, GITR, and OX40, support T cell accumulation during clonal expansion, contributing to T cell memory. During viral infection, tumor necrosis factor superfamily (TNFSF) members on inflammatory monocyte-derived antigen-presenting cells (APCs) provide a postpriming signal (signal 4) for T cell accumulation, particularly in the tissues. Patients with loss-of-function mutations in TNFR/TNFSF members reveal a critical role for 4-1BB and CD27 in CD8 T cell control of Epstein-Barr virus and other childhood infections and of OX40 in CD4 T cell responses. Here, on the 20th anniversary of a previous <i>Annual Review of Immunology</i> article about TNFRSF signaling in T cells, we discuss the effects of endogenous TNFRSF signals in T cells upon recognition of TNFSF members on APCs; the role of TNFRSF members, including TNFR2, on regulatory T cells; and recent advances in the incorporation of TNFRSF signaling in T cells into immunotherapeutic strategies for cancer.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":" ","pages":"113-142"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920715","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}
引用次数: 0
Decoding Immunobiology Through Genetic Errors of Immunity. 通过免疫基因错误解码免疫生物学。
IF 26.9 1区 医学
Annual review of immunology Pub Date : 2025-04-01 Epub Date: 2025-02-14 DOI: 10.1146/annurev-immunol-082323-124920
Mackenzie J Bender, Carrie L Lucas
{"title":"Decoding Immunobiology Through Genetic Errors of Immunity.","authors":"Mackenzie J Bender, Carrie L Lucas","doi":"10.1146/annurev-immunol-082323-124920","DOIUrl":"10.1146/annurev-immunol-082323-124920","url":null,"abstract":"<p><p>Throughout biology, the pursuit of genotype-phenotype relationships has provided foundational knowledge upon which new concepts and hypotheses are built. Genetic perturbation, whether occurring naturally or in experimental settings, is the mainstay of mechanistic dissection in biological systems. The unbiased discovery of causal genetic lesions via forward genetics in patients who have a rare disease elucidates a particularly impactful set of genotype-phenotype relationships. Here, we review the field of genetic errors of immunity, often termed inborn errors of immunity (IEIs), in a framework aimed at highlighting the powerful real-world immunology insights provided collectively and individually by these (approximately) 500 disorders. By conceptualizing essential immune functions in a model of the adaptive arsenal of rapid defenses, we organize IEIs based on immune circuits in which sensors, relays, and executioners cooperate to carry out pathogen clearance functions in an effective yet regulated manner. We review and discuss findings from IEIs that not only reinforce known immunology concepts but also offer surprising phenotypes, prompting an opportunity to refine our understanding of immune system function.</p>","PeriodicalId":8271,"journal":{"name":"Annual review of immunology","volume":" ","pages":"285-311"},"PeriodicalIF":26.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424767","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}
引用次数: 0
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