JOURNAL OF EXPERIMENTAL MEDICINE实验医学杂志
JOURNAL OF EXPERIMENTAL MEDICINE(英文缩写 J EXP MED),ISSN 0022-1007,eISSN 1540-9538,中文译名:实验医学杂志 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 | 17.579 | Q1 |
| 2022 | 15.300 | Q1 |
| 2023 | 12.600 | Q1 |
| 2024 | 10.600 | Q1 |
| 2025 | 11.600 | Q1 |
JOURNAL OF EXPERIMENTAL MEDICINE 最新收录文献
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1. Natural microbiota-based mouse models: A platform to fast-track translation of fundamental discoveries into the clinic.
1. 基于天然微生物群的小鼠模型：加速将基础发现转化为临床应用的平台PMID:日期:2026-10-05Conventional laboratory mice are invaluable tools in biomedical research, but their restricted microbial complexity limits their translational relevance. Several streams of evidence now indicate that (re)colonizing laboratory mice with a naturally evolved microbiota more faithfully recapitulates key features of the human physiological response. Here, we outline where natural microbiota-based models can improve the investigation of human disease, and how findings in such models bear on several aspects of translational biomedical research.
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2. The IKKε-GABPA axis regulates STING transcription to orchestrate antiviral immunity and inflammation.
PMID:日期:2026-10-01The cGAS-STING pathway plays a critical role in antiviral defense and inflammatory homeostasis. While posttranslational regulation of STING is well characterized, the transcriptional networks directly governing Sting1 expression remain unclear. Here, we identify the transcription factor GA-binding protein alpha (GABPA) as a critical regulator of STING-dependent type I IFN (IFN-I) responses in macrophages. Mechanistically, GABPA directly binds to the Sting1 promoter, thereby transcriptionally sustaining basal STING expression. Upon viral infection, activated IκB kinase epsilon (IKKε) phosphorylates GABPA at S447, which further enhances its transcriptional activity and amplifies the STING-IFN-I signaling cascade. Notably, Gabpa deficiency protects mice from DSS-induced colitis, and this protective effect is abolished upon Sting1 deletion. Strikingly, patients with inflammatory bowel disease (IBD) or systemic lupus erythematosus (SLE) exhibit elevated GABPA expression that positively correlates with STING hyperactivation and enhanced inflammatory signatures. Moreover, a GABPA-blocking peptide effectively suppresses aberrant IFN-β production in peripheral blood mononuclear cells (PBMCs) from SLE patients, highlighting its therapeutic potential for interferonopathies.
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3. Helios is critical for Treg effector differentiation in adipose autoimmunity.
3. Helios对脂肪组织自身免疫中Treg效应分化至关重要PMID:日期:2026-10-01The deletion of the transcription factor Helios in regulatory T cells (Tregs) in mice leads to systemic Th1 immune activation, decreased T follicular regulatory cells, and enhanced germinal center formation. We report here these mice also exhibit acquired lipodystrophy, hepatic steatosis, and insulin resistance. Adipose tissue exhibited lymphocytic infiltration followed by CD8+ T cell-mediated destruction of adipocytes. Helios-deficient Tregs were more frequent in adipose tissue and showed an enhanced effector Treg (eTreg) phenotype (CD62Llo Tcf1lo). The Helios-deficient eTregs in adipose tissue, but not spleen, failed to develop into terminally differentiated eTregs, which express ST2+, CXCR3+, IRF4, or Klrg1+. ChIP-seq studies demonstrated that Helios bound to regulatory elements in multiple genes (Tcf7, Lef1, Bach2, and Id3) known to restrict eTreg generation. Thus, Helios not only directly restricts eTreg generation but also indirectly enforces functional eTreg differentiation. In the absence of Helios, the process of eTreg differentiation proceeds unchecked, resulting in enhanced but dysfunctional eTregs, which fail to control adipose tissue homeostasis.
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4. Autoantibodies neutralizing type I IFNs underlie ~5% of herpes simplex encephalitis in adults.
PMID:日期:2026-09-28Inborn errors of type I interferon (IFN-I) immunity account for ∼7-8% of herpes simplex encephalitis (HSE) cases in young children, but the pathogenesis of HSE in adults is largely unknown. We report that IFN-I autoantibodies (auto-Abs) in serum/plasma samples drawn before, during, or after HSE in 16/339 Danish adults neutralized 0.1-10 ng/ml of IFN-I. Neutralization was IgG-mediated and was also detected in cerebrospinal fluid in several patients. Patients' serum impaired the ability of exogenous IFN-I to protect fibroblasts against herpes simplex virus (HSV)-1 infection in vitro. Among patients with neutralizing IFN-I auto-Abs, a larger fraction were HSV-1 IgG seronegative, suggesting that these auto-Abs confer a greater risk of HSE during primary HSV-1 infection. Neutralization was mainly driven by auto-Abs to IFN-ω, and the risk of HSE in adults with auto-Abs was significantly elevated (odds ratio [OR] = 3.1 for IFN-ω and OR = 2.0 for any IFN-I) compared with the general population. Overall, auto-Abs neutralizing IFN-I accounted for ∼5% of adult HSE cases.
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5. CAMKV kinase drives neuroblastoma growth and acts as a novel therapeutic target.
PMID:日期:2026-09-25High-risk (HR) neuroblastoma (NB) remains a leading cause of pediatric cancer mortality, frequently driven by MYCN amplification or MYC overexpression. Despite their central role, direct pharmacological targeting of these transcription factors remains clinically challenging. Here, we identify CaM kinase-like vesicle-associated protein (CAMKV) as a MYCN/MYC-regulated effector of NB pathogenesis. Although previously classified as a nonfunctional pseudokinase, we demonstrate that CAMKV possesses intrinsic kinase activity that is essential for tumor growth. Analysis of patient datasets and primary tumors shows that elevated CAMKV expression correlates with advanced disease stage and poor overall survival. Through integrated transcriptomics, ChIP-seq, and phosphoproteomics, we establish CAMKV as a central signaling hub that coordinates metabolic and proliferative pathways. Both genetic depletion and small-molecule inhibition of CAMKV significantly impair NB cell proliferation in vitro and suppress tumor growth in vivo. Collectively, our findings establish CAMKV as a unifying therapeutic vulnerability and highlight this functional kinase as a promising target for translational development in HR NB.
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6. Slow-cooked naive T cells make better effectors.
6. 缓慢培育的初始T细胞能产生更有效的效应细胞PMID:日期:2026-09-25While the TCR diversity of naive T cells is well established, the extent of their functional heterogeneity remains largely uncharted. In this issue of JEM, Sajiki et al. (https://doi.org/10.1084/jem.20252076) demonstrate that long-lived naive CD8 T cells accrue tonic TCR signaling during homeostasis, driving their differentiation into functionally superior effectors.
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7. Vagal neuroimmune circuits in inflammation and immunity.
PMID:日期:2026-09-25The peripheral nervous system serves as a critical interface between the brain and the immune system, orchestrating bidirectional communication that maintains homeostasis and coordinates host defense responses. Peripheral neuroimmune crosstalk occurs through multiple anatomical pathways, including autonomic efferents, sympathetic circuits, and sensory afferents that detect tissue perturbation. Among these pathways, the vagus nerve has emerged as a prominent conduit for neuroimmune communication, integrating homeostatic and inflammatory cues to shape both local and systemic immune responses. In this review, we examine the structural and functional organization of vagal neuroimmune circuits, highlighting how vagal sensory neurons detect and encode inflammatory cues and how defined vagal pathways modulate immune responses in health and disease. We also discuss recent advances in bioelectronic medicine for treating chronic inflammatory disorders, emphasizing both therapeutic promise and current challenges that remain for clinical translation. Defining the cellular specificity and physiology of vagal neuroimmune circuits will be essential for developing precise neuromodulation strategies to treat inflammatory and autoimmune disorders.
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9. Alox15 restrains glycolysis to support M2 macrophage effector function during helminth immunity.
9. 在蠕虫免疫过程中，Alox15通过抑制糖酵解来支持M2巨噬细胞的效应功能PMID:日期:2026-09-18Macrophage polarization by type-2 cytokines is central to anti-helminth immunity and tissue repair. While some hallmark changes in macrophages are well-characterized and associated with protection against helminths, it is still unclear how macrophages exert their anti-helminth effects. In this context, we investigated arachidonate 15-lipoxygenase (LOX) (Alox15), a LOX well known for its role in macrophage polarization in the context of metabolic diseases, and a hallmark of type-2 macrophage (M2) human polarization. We show that in the absence of Alox15, M2 cannot trap and kill helminths. Surprisingly, expression of M2 markers was normal despite a loss of function. Instead, we found a concomitant increase in pro-inflammatory responses due to an uncontrolled activation of glycolysis. We further show that activation of Peroxisome proliferator-activated receptor-delta (PPAR-δ) by lipids downstream of docosapentaenoic acid (DPA) can restore normal glycolysis control, highlighting a novel role of lipids in the fine-tuning of the metabolic support required for optimal macrophage polarization.
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10. UA-30 mitigates systemic aging and motor decline by inhibiting RalA signaling in naturally aged mice.
10. UA-30通过抑制自然衰老小鼠体内的RalA信号通路，减轻系统性衰老和运动功能衰退PMID:日期:2026-09-16Aging, characterized by progressive physiological decline and systemic dysfunction, represents a major risk factor for age-related diseases such as sarcopenia, which involves fibrosis that disrupts muscle regeneration and function. Effective therapeutic strategies remain limited. Here we report UA-30, a novel compound with a favorable pharmacokinetic and safety profile, that delayed systemic aging in naturally aged mice, as indicated by reduced frailty, slowed epigenetic age, extended lifespan, and improved muscle function. 10-wk UA-30 treatment reduced fibrosis and muscle atrophy in 18.5-mo-old mice. Thermal proteome profiling, surface plasmon resonance, and functional analyses identified Ras-related protein Ral-A (RalA) as a direct molecular target of UA-30. UA-30 suppressed RalA activity, thereby inhibiting the pro-fibrotic JNK-Smad signaling axis and enhancing mitochondrial functions. Overexpression of constitutively active RalA largely abolished the anti-aging and anti-fibrotic effects of UA-30. These findings support UA-30 as a promising therapeutic candidate for aging and sarcopenia, and indicate RalA is a potential target for age-related muscle degeneration.