Immune Network免疫网络
Immune Network(英文缩写 IMMUNE NETW),ISSN 1598-2629,eISSN 2092-6685,中文译名:免疫网络 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 | 5.851 | Q2 |
| 2022 | 6.000 | Q2 |
| 2023 | 4.300 | Q2 |
| 2024 | 4.100 | Q2 |
| 2025 | 5.900 | Q1 |
Immune Network 最新收录文献
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1. Homeostatic Regulation of Lung Dendritic Cells at Steady State.
1. 稳态下肺树突状细胞的内稳态调节PMID:日期:2026-08-13The lung immune system is uniquely adapted to sustain continuous exposure to environmental stimuli while avoiding excessive inflammation. Among lung-resident immune cells, alveolar macrophages are well recognized as key regulators of immune quiescence and tissue homeostasis under steady-state conditions. In contrast, the roles of dendritic cells (DCs), another population of resident immune cells, have received comparatively less attention, likely owing to their lower abundance within the lung tissue. Nevertheless, as professional antigen-presenting cells and central orchestrators of adaptive immunity, DCs are critically positioned to determine the balance between immune tolerance and activation in the lung. Recent studies have increasingly highlighted the contribution of lung DCs to the pathogenesis of inflammatory and neoplastic lung diseases, including allergy, asthma, and cancer. However, how DCs are positioned, conditioned, and functionally regulated under steady-state conditions remains incompletely understood. In this review, we focus on spatial organization, cellular interactions, and microenvironmental cues that shape lung DC behavior at steady-state and delineate how these homeostatic programs preserve immune tolerance while maintaining immune readiness.
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2. Mitochondrial Metabolic Reprogramming and Skin Immune Homeostasis: From Basic Mechanisms to Therapeutic Perspectives.
2. 线粒体代谢重编程与皮肤免疫稳态：从基础机制到治疗前景PMID:日期:2026-08-07Mitochondria have long been viewed as the "powerhouses" of the cell, but research over the past decade has established that they play a far more complex role in skin immune homeostasis beyond ATP production. The metabolic preferences of immune cells and skin parenchymal cells-glycolysis, oxidative phosphorylation, or fatty acid oxidation-determine their fate choices during inflammatory responses. When mitochondrial function is impaired, the release of damage-associated molecular patterns (DAMPs) such as mitochondrial DNA and mitochondrial ROS can activate the cGAS-STING and NOD-like receptor family pyrin domain-containing 3 inflammasome pathways, driving inflammatory cycles in various skin diseases including psoriasis, atopic dermatitis, lupus erythematosus, and vitiligo. This review systematically examines the key mechanisms of mitochondrial metabolic reprogramming in skin immune disorders, focusing on 3 typical scenarios: the metabolic preferences of immune cells, mitochondrial DAMP-mediated autoinflammation, and the impact of mitochondrial dynamics imbalance on tissue-resident memory T cell function. Furthermore, we evaluate clinical evidence for repurposing old drugs such as metformin and thiazolidinediones, and discuss the translational prospects of emerging strategies including Nrf2 agonists, mitophagy inducers, and targeted nanocarriers. Understanding the "dual identity" of mitochondria in skin immunity-as both metabolic regulators and signaling sensors-will lay the foundation for developing precise metabolic immunomodulatory therapies.
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4. Cancer Immunotherapy: Therapeutic Limitations and Next-Generation Precision Strategies.
4. 癌症免疫治疗：治疗局限性及下一代精准策略PMID:日期:2026-08-06Cancer immunotherapy has reshaped oncology, largely through immune checkpoint inhibitors that release the brakes on tumor-reactive T cells. Yet the benefit remains uneven, and that unevenness traces back to a few basic biological limits. Checkpoint blockade amplifies immunity that is already present; it does not create tumor specificity de novo. Poor Ag quality, defective Ag presentation, a suppressive microenvironment, and epigenetically fixed T-cell exhaustion together set a ceiling on what checkpoint release can achieve. Next-generation strategies try to move past these limits by reorganizing immunotherapy around the functional layers of the immune response. Cancer vaccines define tumor-specific neoantigens and expand the responses against them. Ab-based approaches tune inhibitory signaling, draw immune cells toward the tumor, and trigger immunogenic cell death. Cellular therapies-chimeric Ag receptor T cell, TCR-engineered T cells, and tumor-infiltrating lymphocytes (TILs)-boost effector potency, with TIL therapy notable for preserving tumor-reactive repertoires shaped . Rather than rivals, these modalities are best seen as complementary layers-Ag definition, immune priming, effector optimization, and microenvironmental conditioning-to be combined in a programmable way. As genomic profiling, immunopeptidomics, and high-dimensional immune monitoring mature, the field is shifting from checkpoint-centered release toward precision immunoengineering, in which tumor-specific immunity is deliberately designed, aligned, and sustained.
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5. Rosa26-INDIA Identifies Early Apoptotic B Cells Before Macrophage-Mediated Efferocytosis.
5. Rosa26-INDIA 在巨噬细胞介导的胞葬作用之前识别早期凋亡 B 细胞PMID:日期:2026-08-06Apoptotic cells are removed by efferocytosis, raising the possibility that apoptotic cell frequencies underestimate cell death. Rosa26-INDIA is an apoptosis reporter that detects activated caspase-3 (Casp3) via Förster resonance energy transfer (FRET) loss, but the relationship between Casp3 activation, phosphatidylserine exposure, membrane permeabilization, and efferocytic clearance remains unclear. We combined live-cell imaging and macrophage depletion to evaluate apoptotic B cell detection by Rosa26-INDIA. Live-cell imaging revealed that FRET loss preceded loss of detectable INDIA, Annexin-V positivity, and DAPI uptake. Loss of detectable INDIA occurred on average 6 and 12 min before Annexin-V and DAPI positivity, respectively, indicating that Rosa26-INDIA preferentially identifies early apoptotic cells. Consistently, macrophage depletion had limited effects on Rosa26-INDIA-based detection of apoptotic B cells under both steady-state and dexamethasone-induced conditions. These findings demonstrate that Rosa26-INDIA reports early apoptosis and suggest that macrophage-mediated efferocytosis does not substantially limit Rosa26-INDIA-based detection of apoptotic B cells under the conditions examined.
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6. NLRP3 Deficiency Enhances Neutrophil Motility and Phagocytic Function in the Inflamed Kidney.
6. NLRP3缺陷增强炎症肾脏中中性粒细胞的运动性和吞噬功能PMID:日期:2026-08-06Neutrophils serve host defense through phagocytic activity in acute kidney injury. However, excessive neutrophil activation drives tissue damage during systemic inflammation. NOD-like receptor family pyrin domain-containing 3 (NLRP3) has been reported to regulate neutrophil function in inflammatory conditions, but it remains unclear how NLRP3 modulates neutrophil function in the kidney. We investigated the role of NLRP3 in regulating neutrophil phagocytic activity and infiltration in the kidney. knockout (KO) and KO/lysozyme M-GFP mice were analyzed by time-lapse imaging and intravital imaging under naïve and LPS-treated conditions. KO neutrophils exhibited enhanced motility and phagocytic activity against pHrodo particles. The enhanced phagocytic activity was confirmed at both cellular and tissue levels in deficient kidneys . deficient kidneys showed increased neutrophil infiltration accompanied by upregulation of and and downregulation of and under naïve and LPS-treated conditions. Despite increased infiltration, deficient kidneys under LPS treatment displayed reduced and expression and attenuated tissue damage. Collectively, these findings suggest that NLRP3 suppresses neutrophil effector function at the cellular level. At the tissue level, NLRP3 amplifies inflammatory tissue injury in the kidney.
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7. Conserved Influenza Epitopes Delivered via MHC-I-Functionalized Nanocarriers Induce Influenza-Specific CTL Responses.
PMID:日期:2026-07-30Seasonal influenza evades vaccine-induced immunity via ongoing antigenic drift, highlighting the critical necessity for universal vaccines that elicit broadly cross-reactive CD8 T cell responses targeting conserved internal viral epitopes. In pursuit of this objective, we prepared biocompatible and biodegradable poly(lactic-co-glycolic acid) (PLGA) nanocarriers (NCs) and functionalized them with MHC-I molecules. Among various murine and human epitopes tested, PB1 and M1 showed the highest stabilization of H-2K and HLA-A2.1 molecules, respectively, thereby promoting sustained Ag presentation. These NCs exhibited specific peptide-loading onto MHC-I molecules while minimizing non-specific peptide surface binding. immunization of C57BL/6 mice with PB1-loaded NCs elicited epitope-specific CD8 T cell responses. Furthermore, the successful specific peptide-loading of HLA-A2.1-attached NCs highlighted the system's human translational applicability. Ultimately, by combining effective Ag delivery with specific CTL induction, this designed NC platform provides a promising strategy for developing next-generation universal vaccines.
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8. {"_":"Qualitative Superiority, Not Magnitude, of Lung-Resident CD8 T Cells Determines Protective Efficacy of Influenza NP Versus PB1 Vaccines.","sup":["+"]}
8. {"_":"决定流感NP疫苗与PB1疫苗保护效力的是肺驻留CD8 T细胞的质性优势而非数量优势。","sup":["+"]}PMID:日期:2026-07-28T cell-based universal influenza vaccines aim to generate robust lung-resident memory CD8 T cells (T), yet it remains unclear whether conserved Ags elicit equally protective T pools. We compared recombinant adenoviral vectors expressing the influenza A nucleoprotein (rAd/NP) or polymerase basic protein 1 (PB1). After intranasal immunization, both induced comparable magnitudes of respiratory Ag-specific CD8 T cells, yet only rAd/NP provided 100% survival after lethal influenza challenge. This disparity reflected qualitative differences in the T pool; nucleoprotein (NP)-specific cells were predominantly CD103CD49a, a phenotype associated with superior cytotoxicity, whereas PB1-specific cells were mainly CD103CD49a. Furthermore, NP-specific CD8 T cells showed 100-fold higher functional avidity and stronger lung-local CTL activity than PB1-specific cells. Our findings demonstrate that T quality-specifically phenotypic bias and functional avidity-rather than magnitude, are the primary determinants of vaccine-mediated protection. This study underscores the critical importance of Ag selection in optimizing T cell-based universal vaccine strategies.
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9. Regulation of T Cell Senescence in Health and Diseases.
PMID:日期:2026-06-10Aging is accompanied by a progressive decline in immune function, a process termed immunosenescence, which affects both innate and adaptive immune compartments. Among these, the adaptive immune system-and particularly T cells-undergoes the most profound functional and phenotypic alterations, critically impairing host defense against infections, cancer, and vaccination responses. The age-associated decline of adaptive immunity is shaped by the divergent senescence pathways of CD4 helper and CD8 cytotoxic T cells. While both lineages enter a state of cell-cycle arrest, their distinct immunological roles dictate fundamentally different molecular triggers, metabolic adaptations, and functional outcomes. This review synthesizes these subset-specific differences, highlighting how DNA damage-dependent mechanisms and DNA damage-independent processes drive distinct senescence phenotypes. Furthermore, we discuss how these differences contribute to immune system remodeling during aging and explore emerging therapeutic strategies targeting metabolic and signaling pathways to mitigate T cell senescence.
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10. {"_":"Apoptotic-Cell Accumulation and Mertk Expression Are Linked to Diminished Antiviral CD8 T Cell Immunity in Chronic Infections.","sup":["+"]}
PMID:日期:2026-06-10Exhaustion of antiviral immunity driven by inhibitory signals is one hallmark of persistent viral infection. Notably, PD-1 and IL-10 are two major contributors to CD8 T cell dysfunction. How these molecules are specifically induced during chronic viral infection remains mainly unknown. Using the lymphocytic choriomeningitis virus model, we show that the apoptotic-cell accumulation and expression of tyrosine kinase Mertk are linked to the outcome of chronic viral infection. Early CD8 T cell activation correlated with increased dead-cell deposition, rapid induction of IL-10 and TGF-β in macrophages and dendritic cells (DCs), and a pronounced upregulation of PD-1 on CD8 T cells and its ligand PD-L1. In TCR-β-deficient mice lacking CD8 T cells, dead-cell generation and expression of IL-10, TGF-β, PD-1, and PD-L1 were markedly restricted. Our findings suggest that CD8 T cell-mediated killing of infected targets generates large quantities of apoptotic cells, which activate the phosphatidylserine-binding kinase Mertk on macrophages and DCs. This signalling cascade subsequently promotes expression of IL-10, TGF-β, PD-1, and partially PD-L1. Consistent with this model, loss of Mertk in mice reduced inhibitory cytokines and PD-1 expression, accelerated antiviral CD8 T cell responses, and improved viral control. Collectively, our study provides important insight into cellular basis of T cell regulation identifying apoptotic cells and Mertk activation as key mechanisms initiating the suppression of CD8 T cell immunity during chronic viral infection.