TRENDS IN IMMUNOLOGY免疫学趋势
TRENDS IN IMMUNOLOGY(英文缩写 TRENDS IMMUNOL),ISSN 1471-4906,eISSN 1471-4981,中文译名:免疫学趋势 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 19.709 | Q1 |
| 2022 | 16.800 | Q1 |
| 2023 | 13.100 | Q1 |
| 2024 | 13.900 | Q1 |
| 2025 | 13.100 | Q1 |
TRENDS IN IMMUNOLOGY 最新收录文献
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1. {"_":"Coupling and uncoupling cell cycle and metabolism in CD8 T cells.","sup":["+"]}
PMID:日期:2026-09-29CD8 T cells eliminate infected and malignant cells through coordinated proliferation and effector differentiation, processes supported by metabolic reprogramming that together form an interconnected, cross-regulated network. Emerging evidence indicates, however, that cell cycle progression and effector programming can be transiently uncoupled, with implications for T cell function and fate. Short-term modulation of cell cycle dynamics creates a window for metabolic rewiring, reshaping nutrient utilization, cytokine responsiveness, and bioenergetic capacity. This uncoupling can enhance T cell expansion, effector function, and antitumor activity. Collectively, these findings indicate that the cell cycle functions as an instructive checkpoint integrating metabolic and differentiation programs, not merely supporting proliferation. Understanding this interplay provides a conceptual framework to optimize T cell-based immunotherapies and rationally design chemoimmunotherapy combinations.
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2. Beyond immunity: hematopoietic involvement in nonhematological inborn errors of immunity.
2. 超越免疫：非血液系统先天性免疫缺陷中的造血系统受累PMID:日期:2026-09-23Inborn errors of immunity (IEIs) are a group of disorders caused by defects in the immune system. Emerging evidence indicates that dysregulated interferon (IFN) signaling can perturb hematopoietic stem cells in nonhematological IEIs. This forum examines the role of IFNs in regulating hematopoiesis to inform prognosis and therapeutic strategies in IEI.
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3. Erythropoietin impacts immune adaptation through myeloid-cell programming.
3. 促红细胞生成素通过髓系细胞编程影响免疫适应PMID:日期:2026-09-16The immune system balances protective immunity against pathogens with tolerance to self and selected foreign antigens. Emerging evidence identifies erythropoietin (EPO) as a systemic immunoregulatory signal that links physiological stress to immune adaptation. Beyond its canonical role in erythropoiesis, EPO-EPO receptor (EPOR) signaling reprograms specialized myeloid cells, including macrophages and type 1 conventional dendritic cells (cDC1s), promoting efferocytosis, inflammatory restraint, and maturation-associated cDC1 fate. Through these mechanisms, EPO shapes antigen-specific T-cell responses across transplantation and cancer. We propose that the EPO-EPOR axis functions as a systemic regulator of immune adaptation through myeloid-cellprogramming.
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4. Dendritic cells as programmable platforms for cancer immunotherapy.
4. 树突状细胞作为癌症免疫治疗的可编程平台PMID:日期:2026-09-16Dendritic cells (DCs) are professional orchestrators of the immune system, integrating environmental signals to initiate, modulate, and sustain antitumor immunity. Although their therapeutic potential extends beyond antigen delivery, most clinical strategies have used DCs primarily as cellular vaccines. Here, we propose that DCs should be viewed as programmable therapeutic cells whose functions can be rationally controlled, either in situ or ex vivo, through four variables: DC identity, antigenic input, anatomical site of action, and immune-instructive output. Together, these variables determine how DCs establish tissue-level immune circuits for tumor control. We further discuss how tumor-associated barriers determine DC programming requirements and how matching DC programs to these microenvironmental or systemic barriers may improve tumor control in patients with cancer.
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5. Spatially instructed checkpoints in antitumor NK cell immunity.
5. 抗肿瘤NK细胞免疫中的空间指令性检查点PMID:日期:2026-09-14Natural killer (NK) cell immunotherapies remain less effective in solid tumors than in hematologic malignancies. Poor infiltration, checkpoint engagement, and metabolic stress contribute, but these mechanisms often operate within spatially organized niches. We develop the concept of spatially instructed checkpoints: inhibitory programs locally induced or maintained whose functional impact depends on position. We organize evidence across tissue-level exclusion, suppressive cellular neighborhoods, and the cytotoxic synapse, distinguishing causal findings from associations and hypotheses. Spatial organization is an integrating layer that interacts with, rather than replaces, intrinsic, soluble, metabolic, transcriptional, and epigenetic mechanisms. We propose a translational framework for converting spatial discoveries into deployable assays that identify the dominant barrier and guide mechanism-matched strategies to restore antitumor NK cell activity.
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6. Eating to heal: dietary interventions as emerging immune-based therapeutic strategies.
PMID:日期:2026-09-09Clinical immunology is increasingly recognizing diet not merely as baseline metabolic sustenance but as a tunable pharmacological tool. By targeting conserved nutrient-sensing networks and the microbiome, defined nutritional protocols-such as fasting mimetics and specific macronutrient titrations-can actively rewire immune responses. In this review, we examine how manipulating macronutrient stoichiometry, systemic energy availability, and chrononutrition can be strategically deployed to enhance antitumor immune efficacy, promote tissue regeneration, and drive the resolution of chronic inflammation. Finally, we dissect the translational bottlenecks that must be overcome to elevate dietary strategies from broad lifestyle guidelines to prescribable precision immunotherapies.
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8. Understanding HLA risk in immune-mediated inflammatory diseases requires antigen discovery.
8. 理解免疫介导炎症性疾病中的HLA风险需要抗原发现PMID:日期:2026-09-07Certain human leukocyte antigen (HLA) alleles occur more often in people with immune-mediated inflammatory diseases (IMIDs) than in unaffected individuals, making HLA one of the strongest inherited contributors to IMID risk. Yet how these alleles promote disease remains unclear. We argue that HLA risk has often been studied through allele-level properties or immunopeptidomic profiles without knowing which antigenic exposures matter. These approaches characterize peptide binding and presentation but rarely identify disease-relevant exposures. We propose that large-scale T cell receptor repertoire analysis provides a complementary route by identifying disease-associated clonotypes as antigenic footprints. When interpreted in their HLA context, these antigenic footprints can focus immunopeptidomic and functional studies on candidate antigens, turning HLA associations from statistical signals into testable mechanisms of disease.