Immunity & Ageing免疫与衰老
Immunity & Ageing(英文缩写 IMMUN AGEING),ISSN 1742-4933,eISSN 1742-4933,中文译名:免疫与衰老 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 | 9.701 | Q1 |
| 2022 | 7.900 | Q1 |
| 2023 | 5.200 | Q1 |
| 2024 | 5.600 | Q1 |
| 2025 | 8.300 | Q1 |
Immunity & Ageing 最新收录文献
-
1. Correction: Ageing results in an exacerbated inflammatory response to LPS by resident lung cells.
PMID:日期:2026-10-03该文献暂无摘要。
-
2. Acute viral respiratory infections are not associated with an increased IMMune Age indeX (IMMAX) four weeks after infection: a prospective observational cohort study.
2. 急性病毒性呼吸道感染与感染后四周免疫年龄指数（IMMAX）升高无关：一项前瞻性观察性队列研究PMID:日期:2026-09-22The factors that determine how quickly immunosenescence occurs in individuals are not yet fully understood. Viral infections throughout one's life span are suggested to be a relevant modulator. Latent chronic infections, such as CMV or EBV, occupy immune space and are associated with advanced immunological ageing as measured by biomarkers. The IMMune Age indeX (IMMAX) is a validated surrogate for the IMM-AGE metric based on flow cytometry. It is currently unknown whether light to moderate acute, community-acquired infections with common viruses in Western Europe provoke an increase in biomarkers assessing an individual's immunological age. Therefore, this study examined IMMAX changes from pre- to post-viral infection, while additionally exploring IMMAX responses during the acute phase of a respiratory illness. A prospective observational study was conducted involving a cohort of 77 participants aged between 21 and 65 years. Baseline assessment (t0) included recording demographic data and IMMAX calculation. In the event of symptoms of a respiratory infection, blood samples were taken within the first 72 h (t1), after one week (t2) and after four weeks (t3) for IMMAX follow-up assessment. Viral multiplex PCR was performed at t1 to identify the causative pathogen. Additionally, participants who remained clinically healthy for over 6 months underwent a second IMMAX assessment (t4) and acted as a control group. The primary outcome was the change in IMMAX from t0 to t3, while time- and etiology-dependent differences were evaluated using linear mixed-effects modeling. Twenty-six participants caught a respiratory infection including human rhinovirus (n = 9), SARS-CoV-2 (n = 9), parainfluenza virus (n = 1) and 7 cases of PCR-negative respiratory illness. Over the confirmed viral infection cohort (n = 19), IMMAX values transiently increased during the early acute phase of infection, which was no longer observed after recovery. However, subgroup analysis of all cases of acute respiratory illness (n = 26) revealed a remarkable difference: participants with SARS-CoV-2 infection exhibited significantly higher IMMAX values at t1 and lower IMMAX values at t3 compared to baseline, with all nine participants having fully recovered clinically by t3. This observational cohort study prospectively investigates community-acquired infections with concomitant immune age determination. Mild to moderate viral infections followed by complete recovery were not associated with an increased IMMAX score four weeks after infection, regardless of the underlying etiology. Nevertheless, acute SARS-CoV-2 infections lead to distinct shifts in systemic immune cell proportions, highlighting their immunological demands.
-
3. Aging-related immune phenotypes are associated with subclinical coronary atherosclerosis in a middle-aged population: a subcohort of the Swedish CArdioPulmonary bioImage Study.
3. 衰老相关免疫表型与中年人群亚临床冠状动脉粥样硬化相关：瑞典心肺生物影像研究的一个亚队列PMID:日期:2026-09-15Aging-related immune perturbations, including lower proportions of regulatory T (T) cells, shifts in naïve/memory T cells, and elevated monocyte and neutrophil counts, are well documented in patients with manifest coronary artery disease (CAD). In a cross-sectional study, we investigated whether these changes are present in subclinical coronary atherosclerosis.A total of 1078 participants aged 50-64 (49% female) were consecutively recruited from the Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort at Linköping University Hospital. Immune composition (25 subsets) was analyzed in fresh whole blood using flow cytometry. Atherosclerotic burden was assessed by coronary computed tomography angiography (CCTA) and coronary artery calcification (CAC) scoring. Subjects with a prior history of CAD (n = 11), active inflammation (n = 20), poor CCTA data (n = 19), missing CCTA data (n = 5), CT not performed (n = 5) or CCTA not performed (n = 51) were excluded.Individuals with CCTA-detected coronary atherosclerosis (n = 327) showed higher levels of monocytes and central memory (CM) CD4 T cells, and lower levels of naïve T and naïve CD8 T cells, compared to those without atherosclerosis (n = 640). Moreover, those with significant stenosis (≥50%, n = 40) had lower levels of naïve CD4 T and CD56 NK cells. After adjustment for age and sex, increases in CM CD4 T cells and reductions in effector memory (EM) CD4 T, naïve T, and CD56 NK cells remained associated with ≥50% stenosis. After exploratory adjustment for other covariates and type 1 errors, changes in the proportions of CM and EM CD4 T cells and naïve T cells continued to show significant associations with subclinical atherosclerosis when subjects with ≥50% stenosis and those without were compared. No associations were observed between any immune cell subsets and CAC scores.To conclude, immune perturbations, mainly related to an imbalance in naïve/memory CD4 T cells and a reduction of naïve T cells, are present already during the asymptomatic stage of CAD. The findings highlight the potential role of aging-related T cell phenotypes in the pathogenesis of atherosclerosis.
-
4. Toll-like receptor 2 modulates age-associated insulitis and fibrotic remodeling of Langerhans islets.
PMID:日期:2026-09-12The steadily increasing aging population highlights the importance of maintaining health at an advanced age. Metabolic diseases are among the most prevalent age-related disorders, and the Langerhans islets, critical regulators of glucose homeostasis, are particularly susceptible to disturbed insulin secretion and functional decline. Multiple stimuli contribute to islet dysfunction during aging, including bacterial products that increase with age and can activate Toll-like receptor (TLR) signaling. TLR2, which recognizes a broad spectrum of microbial ligands including components from Gram-positive bacteria, has been implicated in type 2 diabetes; however, its role in β-cell function during aging remains unclear. Accordingly, we hypothesize that TLR2 signaling contributes to inflammation and remodeling during aging in Langerhans islets. To determine the role of TLR2 in islet aging, we compared young and old male TLR2-deficient mice with age-matched C57BL/6J controls. Old TLR2 mice showed an altered ex vivo glucose-stimulated insulin secretory response, together with attenuated age-related islet hypertrophy and β-cell mass expansion. Immunohistochemical analysis further revealed that this was accompanied by decreased intra-islet immune cell accumulation, in particular macrophages, but also reduced fibrosis. In a complementary approach, 17-month-old C57BL/6J mice with elevated levels of TLR2 ligands were pharmacologically treated with the TLR2 inhibitor ortho-vanillin (60 mg/kg bodyweight) for four months. This intervention attenuated insulitis by reducing intra-islet leukocyte accumulation, particularly macrophage infiltration, and significantly reduced islet fibrosis, as indicated by decreased collagen and αSMA staining. Since mice at the investigated age-time points do not show metabolic impairments of glucose handling, these histological improvements were not yet reflected by improved glucose tolerance. Overall, our results suggest that TLR2 signaling contributes to immune cell accumulation and fibrotic remodeling during aging, linking inflammation to pancreatic islet aging in mice. These findings identify TLR2 as a potential mediator of age-related islet dysfunction and a candidate target for further investigation.
-
5. {"_":"CD8 effector memory and regulatory T cell dynamics predict subclinical atherosclerotic plaque formation in healthy aging.","sup":["+"]}
5. CD8+效应记忆和调节性T细胞动力学预测健康衰老中亚临床动脉粥样硬化斑块的形成PMID:日期:2026-08-15Subclinical atherosclerotic plaque (SAP) develops silently in older adults. Biological changes that predict plaque formation are not well defined. We examined whether circulating immunological, metabolic, and functional measures identify vascular vulnerability before clinical disease. In a three-year longitudinal study, 49 healthy older adults (63.8 ± 3.8 years) underwent carotid ultrasound, T cell phenotyping, serum protein profiling, body composition assessment, and fitness testing at baseline and follow-up. At follow-up, participants were classified as no SAP, new SAP or persistent SAP. We analyzed baseline determinants and within-person changes to predict incident plaque formation. New SAP occurred in 30.3% of those initially plaque-free. At baseline, lower frequencies of CD8 effector memory (EM) T cells and higher frequencies of CD8 effector memory re-expressing CD45RA (EMRA) T cells and regulatory T cells (Tregs) were associated with higher odds of new SAP. Over time, expansion of CD8 EM T cells was the most consistently associated independent variable of new SAP, accompanied by declines in Tregs and in the Treg/Teff ratio. Vascular cell adhesion molecule-1 (VCAM-1) at baseline was an additional independent predictor. Increases in visceral fat and declines in VOpeak were linked to new SAP, but immune markers were more robust than metabolic variables or serum cytokines. Adaptive immune remodeling follows a phase-dependent pattern in which CD8 EM reductions and later CD8 EM expansion with Treg decline signal emerging vascular vulnerability. These immune signatures, together with VCAM-1, may help characterize vascular vulnerability during the subclinical phase of plaque development.
-
6. IL-35 promotes synovial fibroblast senescence via activation of cGAS-STING-TBK1-IRF3 pathway in rheumatoid arthritis.
6. IL-35通过激活类风湿性关节炎中的cGAS-STING-TBK1-IRF3通路促进滑膜成纤维细胞衰老PMID:日期:2026-07-28Interleukin-35 (IL-35) exerts immunosuppressive effects in rheumatoid arthritis (RA), but its direct impact on synovial fibroblasts (SFs) remains unclear. This study aimed to redefine the role of IL-35 in RA by uncovering its therapeutic mechanism through the induction of STING-dependent synovial fibroblast senescence. We first observed dysregulated IL-35 signaling in RA patients. In a collagen-induced arthritis (CIA) mouse model, recombinant IL-35 treatment effectively alleviated disease severity, reducing clinical scores, joint swelling, and pro-inflammatory cytokines. The pivotal discovery emerged from in vitro experiments: IL-35, but not TNF-α, directly promoted cellular senescence in RA synovial fibroblasts (RASFs). Mechanistically, IL-35 signaled through the glycoprotein 130 (GP130) receptor to activate the cGAS-STING-TBK1-IRF3 pathway, leading to upregulated senescence markers (p16, p21, p53). This STING activation was essential, as its inhibition abolished the pro-senescent effect. Crucially, in vivo knockdown of endogenous IL-35 exacerbated arthritis, and this aggravation was rescued by co-treatment with an IRF3 agonist. Our findings establish a novel protective axis in which IL-35 activates the STING pathway to drive RASFs into a senescent state, thereby inhibiting their pathogenic activity and ameliorating RA progression. Our work identifies IL-35 as a unique cytokine that confers protection by driving STING-dependent senescence in RASFs, highlighting this axis as a novel therapeutic target for RA.
-
7. Cellular senescence: the "hidden driver" in chronic inflammatory skin disorders.
7. 细胞衰老：慢性炎症性皮肤疾病中的“隐藏驱动因素”PMID:日期:2026-07-24Chronic inflammatory skin disorders are characterized by persistent skin inflammation, impaired barrier function, and frequent recurrence, all of which substantially reduce patients' quality of life. Traditional studies attribute the pathogenesis of these diseases to immune dysregulation, whereas new evidence indicates that cellular senescence is a key risk factor and a mechanism underlying disease progression. Cellular senescence, defined by irreversible cell cycle arrest, is accompanied by a senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, and DNA damage. This review systematically outlines the hallmarks, regulatory mechanisms, and inducers of cellular senescence, elucidates its pathological role in representative inflammatory skin disorders, and evaluates emerging therapeutic strategies that target senescent cells. By elucidating the dynamic crosstalk between cellular senescence and inflammatory skin diseases, this review aims to identify novel therapeutic targets and provide new insights into their diagnosis, treatment, and prevention.
-
8. Reduced NK cell frequency in older patients with evolving fractures is linked to a distinct inflammatory cytokine profile.
8. 老年骨折进展期患者自然杀伤细胞频率降低与独特的炎症细胞因子谱相关PMID:日期:2026-07-24Proximal hip fractures represent a profound acute physiological stress in older adults and are often followed by infections, delayed recovery, and functional decline. These complications occur more frequently in frail individuals with reduced physiological resilience and impaired immune responses. As natural killer (NK) cells are central to early immune defense, we aimed to define how acute fracture, hospitalization and frailty shape NK cell homeostasis and function in older patients. We conducted a prospective study including older patients (> 65 years) with acute fractures (SMART cohort; n = 103) and compared them to matched healthy older people from the RESIST senior individuals (SI) cohort (n = 550). A subset of SMART patients (n = 55) was longitudinally followed-up post-surgery. NK cell frequency, phenotype and function were investigated using multiparametric flow cytometry, and plasma soluble immune mediators (SIMs) were analyzed. SMART patients were clinically frailer than matched SI individuals, as indicated by reduced grip strength and lower Barthel scores, and exhibited an inflammatory state with elevated CRP levels and leukocyte counts. NK cell frequencies were significantly reduced in SMART patients and inversely correlated with grip strength and systemic inflammation. Furthermore, NK cells from SMART patients showed a distinct immune phenotype and altered chemokine receptor expression compared with SI individuals. Of note, differences between frail and non-frail patients within the SMART cohort were modest and substantially smaller than those observed between SMART patients and SI individuals. Functionally, frail patients displayed reduced baseline expression of cytotoxic molecules, whereas cytokine-induced NK cell responses were preserved. Furthermore, longitudinal analyses revealed stable NK cell frequencies but surgical intervention remodeled NK cell subset distribution and marker expression. In conclusion, our findings indicate that NK cell alterations in older patients with fractures are likely driven by the combined impact of acute injury, hospitalization and surgery rather than by frailty alone.
-
9. Virtual memory CD8⁺ T cells in aging: heterogeneity, bystander protection, inflammatory potential, and inhibitory regulation.
9. 虚拟内存CD8⁺ 衰老中的T细胞：异质性、旁观者保护、炎症潜能和抑制性调节PMID:日期:2026-07-10[中文摘要] 衰老通过初始细胞库的收缩和记忆表型群体的扩增重塑CD8⁺ T细胞区室，其中包括抗原未经历型虚拟记忆（virtual memory，VM）CD8⁺ T细胞的进行性积累。VM CD8⁺ T细胞在缺乏外源抗原致敏的情况下产生，并获得类记忆表型。在衰老宿主中，VM CD8⁺ T细胞构成抗原未经历型记忆表型CD8⁺ T细胞库的相当大一部分，其分化受自身反应性、稳态细胞因子以及与IL-15和EOMES相关的转录程序所塑造。在衰老过程中，VM CD8⁺ T细胞数量积累，表现出改变的增殖反应，保留对稳态和炎症细胞因子的敏感性，并可在感染期间维持效应功能。这些特征提示，VM CD8⁺ T细胞可能通过提供快速的类效应反应，部分代偿与年龄相关的初始CD8⁺ T细胞丢失。与此同时，衰老的VM CD8⁺ T细胞似乎由异质性亚群组成，包括具有细胞毒性和炎症潜能的群体。新出现的证据提示，抑制性受体可能在衰老过程中标记不同的VM状态，尽管其功能意义和潜在的调控作用仍有待确立。
[英文摘要] Aging reshapes the CD8⁺ T cell compartment through contraction of the naïve pool and expansion of memory-phenotype populations, including the progressive accumulation of antigen-inexperienced virtual memory (VM) CD8⁺ T cells. VM CD8⁺ T cells arise in the absence of foreign antigen priming and acquire a memory-like phenotype. In aged hosts, VM CD8⁺ T cells constitute a substantial fraction of the antigen-inexperienced memory-phenotype CD8⁺ T cell pool, and their differentiation is shaped by self-reactivity, homeostatic cytokines, and transcriptional programs linked to IL-15 and EOMES. During aging, VM CD8⁺ T cells accumulate numerically, display altered proliferative responses, retain sensitivity to homeostatic and inflammatory cytokines, and can preserve effector function during infection. These features suggest that VM CD8⁺ T cells may partially compensate for the age-associated loss of naïve CD8⁺ T cells by providing rapid effector-like responses. At the same time, aged VM CD8⁺ T cells appear to comprise heterogeneous subsets, including populations with cytotoxic and inflammatory potential. Emerging evidence suggests that inhibitory receptors may mark distinct VM states during aging, although their functional significance and potential regulatory role remain to be established.
-
10. Clinical rationale for thymic restoration in adult immunosenescence.
10. 成人免疫衰老胸腺恢复的临床理论基础PMID:日期:2026-07-08Age-related thymic involution is a central feature of immunosenescence and intersects with multiple "hallmarks of aging", including genomic instability, telomere attrition, mitochondrial dysfunction, and chronic inflammation. The decline in thymic epithelial integrity and FOXN1-driven thymopoiesis reduces naïve T-cell output, contracts TCR repertoire diversity, and perturbs central tolerance, contributing to increased susceptibility to infection, cancer, and autoimmunity. These changes occur alongside broader immune-aging phenomena such as inflammaging and frailty and are reflected in poorer vaccine responses and altered outcomes to novel pathogens such as SARS-CoV‑2. This review integrates mechanistic, preclinical, and human data to reassess the adult thymus as a therapeutic target. Higher-confidence domains for thymic restoration include cancer immunosurveillance, infectious disease vulnerability, vaccine responsiveness, and post-treatment immune reconstitution, supported by modeling of age-related disease incidence, transplant and HIV cohorts, and new observational links between radiographic thymic health, mortality, and immunotherapy outcomes. High-plausibility but less directly validated domains include autoimmunity, chronic herpesvirus control, HIV immunological non-responders, and post-acute infection syndromes such as long COVID, which share convergent patterns of T-cell dysfunction and persistent immune activation. The translational landscape spans hormonal and somatotropic modulation (sex steroid ablation, growth hormone/ghrelin), cytokine and growth-factor strategies (IL‑7, IL‑22, KGF/BMP4, FGF21), cell- and tissue-engineering approaches leveraging thymic epithelial stem cells and FOXN1-reprogrammed stromal cells, and gene-therapy concepts such as intrathymic AAV delivery of FOXN1, AIRE, chemokines, and stromal-support pathways. Collectively, these data support the biological plausibility of adult thymus restoration but highlight that robust, domain-specific clinical benefits have not yet been demonstrated in controlled trials. Future work should prioritize harmonized structural and functional biomarkers, domain-focused interventional studies in high-risk populations, and combined strategies that situate thymus-directed interventions within broader efforts to modify immune and organismal aging.