Immunological Reviews最新文献_第6页

The T Cell Receptor: Molecular Sensor, Therapeutic Mediator and Probabilistic Driver of Adaptive Immunity T细胞受体：分子传感器、治疗介质和适应性免疫的概率驱动。

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-06-04 DOI: 10.1111/imr.70136

Kilian Schober

{"title":"The T Cell Receptor: Molecular Sensor, Therapeutic Mediator and Probabilistic Driver of Adaptive Immunity","authors":"Kilian Schober","doi":"10.1111/imr.70136","DOIUrl":"10.1111/imr.70136","url":null,"abstract":"<p>Advances in high-throughput sequencing, single-cell profiling, and genome engineering have transformed the study of T cell receptors (TCRs), enabling the identification and functional interrogation of antigen-specific repertoires at an unprecedented scale. This review discusses how recent methodological developments—including high-dimensional TCR discovery strategies, physiological receptor engineering, and longitudinal in vivo analyses—have reshaped our understanding of TCR-driven immune responses. Recruitment into immune responses originates from diverse naïve precursor pools and results in polyclonal populations in which multiple clonotypes contribute to antigen recognition. Within such populations, receptor properties, such as TCR avidity, influence the likelihood of recruitment, expansion, and persistence. However, the impact of these parameters depends strongly on biological context, including antigen availability, cellular competition, and tissue environment. Physiological engineering approaches, such as orthotopic TCR replacement, now enable causal interrogation of receptor function while preserving endogenous regulatory control. Together with advances in spatial and longitudinal profiling of human immune responses, these approaches allow increasingly precise analyses of connections between TCR identity and T cell fate. Integrating insights across antigen discovery, receptor engineering, and in vivo dynamics suggests that TCR biology is shaped by the interplay of receptor sequence, regulatory context, and tissue environment across time. Understanding these relationships will be essential for interpreting immune responses and for guiding the rational design of T cell-based immunotherapies.</p>","PeriodicalId":178,"journal":{"name":"Immunological Reviews","volume":"340 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imr.70136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148160989","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}

引用次数: 0

Tissue-Resident Memory T Cells in the Heart: An Emerging Role in Chronic Inflammation 心脏组织常驻记忆T细胞：在慢性炎症中的新作用。

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-06-04 DOI: 10.1111/imr.70134

Priyanka Manandhar, Ashley Yan, Javid J. Moslehi

{"title":"Tissue-Resident Memory T Cells in the Heart: An Emerging Role in Chronic Inflammation","authors":"Priyanka Manandhar, Ashley Yan, Javid J. Moslehi","doi":"10.1111/imr.70134","DOIUrl":"10.1111/imr.70134","url":null,"abstract":"<div>\u0000 \u0000 <p>T lymphocytes are increasingly recognized as central regulators of cardiac inflammation, contributing to both tissue repair and disease progression across conditions such as myocardial infarction, heart failure, and myocarditis. While traditionally viewed as transient responders to injury, emerging evidence indicates that cardiac T cell responses are often antigen-driven, clonally expanded, and sustained over time. In particular, α-myosin heavy chain (α-MyHC, encoded by MYH6) has emerged as a dominant cardiac autoantigen capable of eliciting pathogenic T cell responses in both experimental models and human disease. In parallel, tissue-resident memory T cells (Trm) have been established as a distinct population of memory T cells that persist within non-lymphoid tissues and provide rapid, localized responses upon antigen re-exposure. Although extensively studied in non-lymphoid and barrier tissues, Trm are now increasingly implicated in chronic inflammatory and autoimmune diseases, where they can act as long-lived reservoirs of antigen-experienced T cells. Here, we propose that cardiac injury seeds antigen-specific T cell populations that acquire tissue-resident phenotypes within the myocardium, thereby linking acute immune activation to chronic, relapsing inflammation. We first review the role of T cells in cardiac homeostasis, aging, and disease, highlighting features of antigen specificity, persistence, and local adaptation. We then outline the defining characteristics and developmental pathways of Trm and integrate emerging evidence for their presence and function in the heart. Particular emphasis is placed on α-MyHC-specific Trm as potential drivers of cardiac autoimmunity and immune-related adverse events of cancer immunotherapies, including immune checkpoint inhibitor–associated myocarditis. Finally, we discuss the implications of this framework for understanding chronic cardiac inflammation and for developing therapeutic strategies targeting tissue-resident immune populations.</p>\u0000 </div>","PeriodicalId":178,"journal":{"name":"Immunological Reviews","volume":"340 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161138","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}

引用次数: 0

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-05-27

引用次数: 0

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-05-27

引用次数: 0

Inflammation-Driven Lymphoid Structures: Organization, Function, and Clinical Impact Across Autoimmunity, Cancer, and Checkpoint Toxicity 炎症驱动的淋巴结构：组织、功能和自身免疫、癌症和检查点毒性的临床影响。

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-05-17 DOI: 10.1111/imr.70127

Marie Frutoso, Emie Delmas, Rudolf Corty, Eleonore Bettacchioli, Divi Cornec, Sophie Hillion, Soizic Garaud

{"title":"Inflammation-Driven Lymphoid Structures: Organization, Function, and Clinical Impact Across Autoimmunity, Cancer, and Checkpoint Toxicity","authors":"Marie Frutoso, Emie Delmas, Rudolf Corty, Eleonore Bettacchioli, Divi Cornec, Sophie Hillion, Soizic Garaud","doi":"10.1111/imr.70127","DOIUrl":"10.1111/imr.70127","url":null,"abstract":"<p>Lymphoid structures (LS) arising in nonlymphoid tissues are increasingly recognized as active immune niches rather than simple consequences of chronic inflammation. In this review, we propose a framework that distinguishes inflammatory lymphoid structures (ILS) from mature tertiary lymphoid structures (mTLS), while acknowledging that these entities may form a continuum in some settings and represent distinct inflammatory states in others. We discuss how LS develop across autoimmunity, cancer, transplantation, immune-related adverse events, and aging, and how differences in architecture, stromal organization, antigen persistence, and tolerance checkpoints shape their biological outputs. Whereas mTLS are typically associated with follicular organization, germinal center-like reactions, and local clonal diversification, ILS may instead sustain inflammation through extrafollicular activation, survival niche formation, and tissue-adapted immune specialization. Importantly, the functional impact of LS is highly context dependent: they may promote pathogenic autoreactivity in autoimmune disease, support protective antitumor immunity in cancer, or acquire regulatory or suppressive features depending on the microenvironment. We also review current therapeutic strategies targeting LS and discuss how spatial transcriptomics and artificial intelligence may refine their detection, classification, and functional interpretation. Altogether, this perspective supports viewing LS as heterogeneous tissue immune niches rather than a binary TLS category, with major implications for pathogenesis, biomarker development, and therapeutic intervention.</p>","PeriodicalId":178,"journal":{"name":"Immunological Reviews","volume":"339 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13181160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147961571","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}

引用次数: 0

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-05-17

引用次数: 0

In Defense of Homeostasis: Innate Immunity in Cardiac Injury and Repair 保护体内平衡：心脏损伤和修复中的先天免疫。

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-04-28 DOI: 10.1111/imr.70126

Douglas L. Mann

{"title":"In Defense of Homeostasis: Innate Immunity in Cardiac Injury and Repair","authors":"Douglas L. Mann","doi":"10.1111/imr.70126","DOIUrl":"10.1111/imr.70126","url":null,"abstract":"<div>\u0000 \u0000 <p>The ability of the heart to compensate for and adapt to a superimposed environmental stress determines whether the heart will maintain preserved structure and function or decompensate and fail. In mammalian tissues, sterile tissue injury activates a suite of stress-activated programs that integrate cytoprotective stress responses that are tightly coupled with carefully regulated and precisely timed inflammatory signaling, thereby promoting tissue repair while simultaneously limiting collateral damage. Although the terminology for this phenomenon is still evolving, the recently described concept of “disease tolerance” has been proposed to explain tissue-intrinsic cell autonomous molecular programs that couple cytoprotective stress responses with tightly regulated inflammatory signaling that minimizes collateral damage while also activating tissue repair mechanisms. Emerging evidence reviewed here suggests that sterile cardiac injury (e.g., myocardial ischemia or hemodynamic pressure overload) elicits an acquired stress-tolerant state that sustains cytoprotective programs in cardiac myocytes and constrains collateral immune-mediated tissue injury. However, these stress-activated pathways are highly context-dependent and are shaped by the magnitude and duration of the ensuing inflammatory response. When tissue injury-induced inflammation is sustained and/or excessive, it can also lead to unwanted collateral tissue damage and cardiac decompensation.</p>\u0000 </div>","PeriodicalId":178,"journal":{"name":"Immunological Reviews","volume":"339 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147758332","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}

引用次数: 0

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-04-28

引用次数: 0

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-04-24

引用次数: 0

B Cell Subsets and Atherosclerosis: Updates and Emerging Concepts B细胞亚群和动脉粥样硬化：更新和新兴概念。

IF 8.3 2区医学

Immunological Reviews Pub Date : 2026-04-24 DOI: 10.1111/imr.70124

Sophieke Lems, Megan Grace Mazzei, Amanda C. Foks, Coleen A. McNamara

{"title":"B Cell Subsets and Atherosclerosis: Updates and Emerging Concepts","authors":"Sophieke Lems, Megan Grace Mazzei, Amanda C. Foks, Coleen A. McNamara","doi":"10.1111/imr.70124","DOIUrl":"10.1111/imr.70124","url":null,"abstract":"<p>Atherosclerotic cardiovascular disease (ASCVD) is increasingly recognized not just as a lipid-driven disease, but as a complex interplay between vascular cells and the immune system. Accumulating evidence highlights a central, yet heterogeneous role for B cells in atherogenesis, with distinct subsets displaying opposing roles. In this review, we provide an in-depth overview of the contributions of B cell subsets to ASCVD, including emerging insights into the roles and pathways of atheroprotective innate B cells producing IgM against oxidation-specific epitopes (IgM<sup>OSE</sup>) and newly appreciated age-associated B cells (ABCs), a distinct subset that accumulates with aging and potentially exacerbates atherosclerosis. By integrating insights from preclinical models and human studies, we describe the mechanisms through which B cell subsets influence ASCVD, including antigen presentation and immune checkpoint-mediated communication, secretion of cytokines and chemokines, and we highlight that humoral immunity in atherosclerosis reflects a context-dependent interplay between antibody effector properties and antigenic targets rather than antibody class alone. Finally, we explore how the advances in our understanding of B cells may guide the development of more targeted immunomodulatory therapies that enhance atheroprotective B cell functions while limiting atherogenic responses.</p>","PeriodicalId":178,"journal":{"name":"Immunological Reviews","volume":"339 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147758260","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}

引用次数: 0