Immunity免疫
Immunity(英文缩写 IMMUNITY),ISSN 1074-7613,eISSN 1097-4180,中文译名:免疫 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 | 43.474 | Q1 |
| 2022 | 32.400 | Q1 |
| 2023 | 25.500 | Q1 |
| 2024 | 26.300 | Q1 |
| 2025 | 30.600 | Q1 |
Immunity 最新收录文献
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1. Distant lymph nodes compensate for resected tumor-draining lymph nodes during cancer immunotherapy.
1. 在癌症免疫治疗中，远处淋巴结可代偿被切除的肿瘤引流淋巴结PMID:日期:2026-10-01Surgical removal of tumor-draining lymph nodes (tdLNs) is commonly performed in cancer patients. Here, we investigated whether immune checkpoint blockade (ICB) responses persist after resection of tdLNs, important sites for the initiation and maintenance of anti-cancer immunity. Melanoma patients remained responsive to programmed death 1 (PD-1) blockade after regional LN dissection. Similarly, ICB efficacy persisted after tdLN resection in orthotopic murine melanoma and mammary carcinoma models. Following tdLN removal, interstitial fluid containing soluble antigen was diverted through interstitial spaces across lymphosome boundaries to distant LNs, wherein cancer-derived antigen was acquired and presented to T cells by LN-resident type I conventional dendritic cells. These responses persisted after primary tumor resection and supported ICB-induced systemic immunity. Locoregional delivery of ICB to compensatory LNs enhanced anti-cancer responses after tdLN resection. Consistently, ICB responses in head and neck cancer patients were associated with reactive LNs at distant sites. Thus, antigen rerouting enables distant LNs to compensate for resected tdLNs and sustain anti-cancer immunity, including responses enhanced by immunotherapy.
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2. Functional evaluation of TCR-pMHC pairs at scale allows in silico TCR reactivity prediction.
2. 大规模TCR-pMHC配对的功能评估可实现计算机模拟TCR反应性预测PMID:日期:2026-10-01Accurate prediction of T cell receptor (TCR) reactivity is a long-standing goal in immunology. Here, we asked whether functional validation of TCR-peptide-major histocompatibility complex (MHC) (TCR-pMHC) pairs at scale alters performance estimates of TCR-pMHC reactivity prediction models. We developed a TCR rapid assembly platform (T-RAP) that allowed the generation of large and uniform TCR libraries. T-RAP enabled evaluation of TCR signaling or MHC multimer binding of thousands of previously reported TCR-pMHC pairs under standardized conditions. In this setting of systematic standardized evaluation, only ∼50% of these TCRs showed the previously reported TCR reactivity. Notably, AlphaFold3 structural predictions showed good performance in identifying reactive TCR-pMHC pairs within the set of TCRs that experimentally validated without any task-specific training. AlphaFold3 structural predictions could likewise be used to shortlist TCRs reactive to patient-specific cancer neoantigens. In silico prediction of TCR-pMHC reactivity thus has greater feasibility than previously assumed, with implications for basic research and clinical application.
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3. Glucose-deprived tumor microenvironment activates AMP-activated protein kinase to drive adoptively transferred T helper 9 cell senescence.
3. 葡萄糖缺乏的肿瘤微环境激活AMP活化蛋白激酶，驱动过继转移的辅助性T细胞9衰老PMID:日期:2026-10-01T helper 9 (Th9) cells show promise for adoptive cell therapy (ACT) against solid tumors. However, clinical application faces challenges regarding their persistence in the tumor microenvironment (TME). We observed that tumor growth gradually reduced glucose concentrations in the TME, accompanied by a decline in transferred Th9 cells and their effector functions, due to Th9 cell senescence. Restoring glucose concentrations suppressed Th9 cell senescence, thereby improving their persistence. Mechanistically, glucose-deprivation-activated AMP-activated protein kinase (AMPK), triggering downstream leucine-zipper and sterile-α motif kinase (ZAK)-nuclear factor κB (NF-κB)-inducing kinase (NIK) cascades that suppressed noncanonical NF-κB signaling and interleukin (IL)-9 production, ultimately driving Th9 cell senescence. ZAK-associated chimeric antigen receptor (CAR)-T cell senescence was linked to compromised therapeutic efficacy in human cancers. Targeting ZAK rejuvenated Th9 cells and enhanced CAR-Th9 cell efficacy against solid tumors. Our study uncovers a mechanism by which nutrient deprivation promotes Th9 cell senescence to compromise persistence, highlights the potential of targeting ZAK to rejuvenate CAR-Th9 cells for solid tumor therapy.
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4. Microglia with distinct origins and non-canonical phenotypes coexist within the border-like niche of the brain's circumventricular organs.
4. 具有不同起源和非经典表型的小胶质细胞共存于大脑室周器官的边界样微环境中PMID:日期:2026-09-29Circumventricular organs (CVOs) are small brain regions lacking a blood-brain barrier, giving neurons direct access to blood-borne signals, yet how these microenvironments shape the origin and phenotype of local macrophages remains unclear. Using multi-omics, we characterized the immune landscape of two CVOs, the area postrema (AP) and median eminence (ME), revealing brain-border-like environments with a unique macrophage compartment. CVO microglia showed a distinct, heterogeneous phenotype, including a CLEC7A myelin-associated subset in the ME, shaped by ageing and metabolism. CVO microglia were ontogenically diverse: fetal monocytes entered the CVOs perinatally and generated long-lived monocyte-derived microglia that fully adopted a yolk-sac-derived microglia identity. After depletion, CVO microglia were repopulated by local Sall1 cells but also by monocytes in the AP. Similarly, perivascular CVO border-associated macrophages displayed a distinct phenotype and origin. Our findings establish CVOs as specialized immune niches that shape local macrophages, reflecting the immune and metabolic demands of these environments.
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5. Targeting a site of vulnerability on circumsporozoite protein inhibits Plasmodium vivax malaria infection.
PMID:日期:2026-09-24Circumsporozoite protein (CSP) is the most abundant Plasmodium sporozoite surface antigen. It is the major component of licensed Plasmodium falciparum vaccines and, hence, is the logical lead candidate for Plasmodium vivax (P. vivax) vaccines. However, our limited knowledge of protective B cell epitopes on P. vivax CSP remains a major roadblock. Here we identified two Plasmodium vivax CSP (PvCSP) B cell epitopes, PvCSP-A and PvCSP-B/NAGG, by screening inhibitory plasma from P. vivax-infected individuals. The epitopes were located in the N- and C-terminal regions of PvCSP, respectively, and were distinct from the canonical central repeat region epitope. We isolated a monoclonal antibody, GRAM-4, that recognized the PvCSP-B/NAGG epitope and mediated potent inhibition of traversal, hepatocyte invasion, and liver-stage development in vitro, confirming PvCSP-B/NAGG as a genuine neutralization target. Structural resolution of the GRAM-4:PvCSP-B/NAGG interaction at 2.65 Å revealed the molecular basis of epitope recognition, providing a blueprint for PvCSP vaccine development.
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6. Germinal center interleukin-4 microniches drive tissue divergence of IgE memory B cell responses.
6. 生发中心白细胞介素-4微环境驱动IgE记忆B细胞反应的组织分化PMID:日期:2026-09-23Immunoglobulin E (IgE) drives allergy, yet how memory B cells (MBCs) reactivate to produce IgE, and how tissue localization shapes recall responses, remains unclear. Using mouse models of airborne exposure to house dust mites and Alternaria, we found that allergen sensitization generated lymph node (LN)- and lung-resident MBCs. Upon allergen re-exposure, MBCs follow two differentiation trajectories: a germinal center (GC)-dependent pathway, generating IgG1 and IgE plasma cells (PCs) and occurring predominantly in LNs, and a GC-independent pathway, generating mainly IgG1 PCs and present in both organs. GC re-entry granted MBCs access to an interleukin (IL)-4-rich microniche formed by T follicular helper (Tfh) cells, which was essential for IgE production. Disrupting GC re-entry, IL-4 signaling, or Tfh cell-derived IL-4 during recall markedly reduced allergen-specific IgE. These findings reveal a spatially and cytokine-restricted mechanism that confines IgE memory to lymphoid organs, positioning GC IL-4 microniches as anatomical safeguards against IgE production at barrier sites frequently exposed to environmental antigens.
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7. Sensory neuronal mTORC1 kinase signaling establishes neuroimmune memory that initiates allergic immunity.
7. 感觉神经元mTORC1激酶信号建立神经免疫记忆，从而启动过敏性免疫PMID:日期:2026-09-22Environmental allergens are enriched in protease activity, which activates cutaneous sensory neurons, triggering itch and substance P release to promote migration of T helper (Th)2 cell-skewing CD301b dendritic cells and initiate allergic immunity. However, allergens are typically encountered through repeated subthreshold exposures, and how these cumulatively induce sensitization is unknown. We identified a sensory neuron-intrinsic mechanism of neuroimmune memory. Protease allergen exposure induced sustained mechanistic target of rapamycin complex 1 (mTORC1) kinase signaling and transcriptional activator peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α)-associated mitochondrial remodeling in sensory neurons, establishing a metabolically primed state with enhanced neuronal responsiveness. Upon allergen re-exposure, this state drove enhanced itch, CD301b dendritic cell migration, and Th2 cell differentiation. Disrupting neuronal mTORC1 signaling or mitochondrial stability abrogated this amplification while sparing primary responses. This mechanism generalized across distinct protease allergens, revealing mTORC1-driven metabolic reprogramming in sensory neurons as a form of innate neuroimmune memory underlying allergen cross-sensitization and polysensitization.
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8. Cancers modulate processing and presentation of p53 neoantigens to evade T cell detection.
8. 癌症通过调节p53新抗原的加工和呈递，逃避T细胞的检测PMID:日期:2026-09-17TP53 mutations occur early in malignant transformation as truncal events in tumor evolution and are therefore generally present in all descendant tumor cells, creating an immunological vulnerability. Here, we examined the immunogenicity and antigenicity of p53 neoantigens emerging from these truncal mutations. Comprehensive immunopeptidomics revealed that hotspot mutations in human tumors preferentially localize to p53 regions resistant to antigen processing, thereby avoiding display altogether. Moreover, for neoantigens presentable by HLA-A02:01 or HLA-B07:02 and structurally divergent from corresponding wild-type p53 peptide-HLA complexes, clinical tumors commonly lacked the relevant presenting HLA allele. Tumor cells further resisted T cell killing through increased activity of the aminopeptidase ERAP1, preventing display of high-affinity HLA-A02:01 complexes containing an immunogenic p53-derived 11-mer, or by expressing low-affinity HLA-A02:01 complexes containing a p53-derived 9-mer with poor antigenicity despite high-quality human TCRs. These findings define mechanisms by which tumors restrict targetable truncal neoantigen display and suggest immunopeptidome shift strategies to circumvent immune escape.
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9. Effector differentiation by stem-like intraepithelial γδ T cells is required for host defense against infection.
9. 干细胞样上皮内γδ T细胞介导的效应分化是宿主抵御感染所必需的PMID:日期:2026-09-09该文献暂无摘要。
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10. A pulmonary innate lymphoid cell-driven serotonergic neuroimmune axis orchestrates airway hyperreactivity and cough hypersensitivity.
10. 肺固有淋巴细胞驱动的5-羟色胺能神经免疫轴协调气道高反应性和咳嗽超敏反应PMID:日期:2026-09-07Asthma is a heterogeneous disease characterized by airway hyperreactivity (AHR) and chronic cough, exacerbated by respiratory viruses or allergen exposure. Yet, the immune pathway-mediated serotonergic circuits underlying these responses remain poorly defined. Here, we identified a serotonergic neuroimmune axis in which pulmonary group 2 innate lymphoid cells (ILC2s) expressed tryptophan hydroxylase-1 (Tph1) and released serotonin via CCAAT/enhancer-binding protein beta (C/EBPβ)-dependent transcription following interleukin (IL)-33 stimulation. Tph1 deficiency in ILC2s and adoptive transfer experiments demonstrated that ILC2-derived serotonin amplified type 2 cytokine production via 5-hydroxytryptamine (5-HT)-NF-κB activation, resulting in exacerbated AHR in respiratory syncytial virus-driven asthmatic models. Using engineered viral tools, we showed that ILC2-derived serotonin sensitized vagal sensory neurons through 5-HT to promote cough hypersensitivity. Clinically, asthma patients exhibited elevated TPH1 and plasma serotonin levels, both of which correlated with type 2 cytokines. Together, these findings reveal that an ILC2-driven serotonergic circuit contributes to asthma pathophysiology and highlight serotonergic signaling as a therapeutic target.