JOURNAL OF IMMUNOLOGY免疫学杂志
JOURNAL OF IMMUNOLOGY(英文缩写 J IMMUNOL),ISSN 0022-1767,eISSN 1550-6606,中文译名:免疫学杂志 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 | 5.430 | Q2 |
| 2022 | 4.400 | Q2 |
| 2023 | 3.600 | Q2 |
| 2024 | 3.400 | Q2 |
| 2025 | 4.000 | Q2 |
JOURNAL OF IMMUNOLOGY 最新收录文献
-
1. Context-dependent regulation of cytotoxic T lymphocytes by nuclear receptors.
1. 核受体对细胞毒性T淋巴细胞的上下文依赖性调控PMID:日期:2026-10-01Cytotoxic CD8⁺ T lymphocytes eliminate pathogen-infected and malignant cells through migration to affected tissues, cytokine production, and cytotoxic activity. A mounting body of evidence indicates that CD8 T cell differentiation into functionally different subsets, such as effector, memory, tissue-resident memory, and exhausted T cells, is controlled by a group of nuclear receptors (NRs). NRs sense signals from various physiological and environmental cues, such as nutritional, endocrine, stress/circadian, and metabolic signals, and translate them into gene-regulatory decisions. NRs act through direct and indirect DNA binding, corepressor-coactivator exchange, and transrepression of effector-associated transcription factors, thereby reshaping chromatin accessibility and metabolic programs during CD8 T cell differentiation. This review highlights major CD8 T cell-regulating pathways involving vitamin A-sensing RAR-α, sterol-responsive LXR-β and ROR-α, orphan NR4A proteins; vitamin D receptor (VDR), glucocorticoid receptor (GR), and androgen receptor (AR). Understanding the shared and separable functions of NRs and their ligands provides insights into therapeutic strategies, such as pharmacologic modulation, checkpoint blockade, and chimeric antigen receptor T cell therapies, to promote durable antitumor and antiviral CD8 T cell activities.
-
2. CTH522/CAF01 vaccination elicits clonally related Th17 subsets that mediate IL-17A-dependent protection against Chlamydia trachomatis.
2. CTH522/CAF01疫苗接种可诱导产生克隆相关的Th17亚群，这些亚群介导IL-17A依赖性的沙眼衣原体保护作用PMID:日期:2026-10-01Chlamydia trachomatis is the leading bacterial sexually transmitted pathogen worldwide and a major cause of reproductive tract disease, highlighting the need for an effective vaccine. Defining the immune mechanisms underlying vaccine-induced protection is therefore critical. We previously demonstrated that in mice vaccinated with CTH522/CAF01, genital tract Th17 cells correlated with protection against both infection and pathology. In this study, we further characterized these vaccine-induced Th17 cells in an infected genital tract. Fate-mapping and single-cell transcriptomic analyses revealed that CTH522/CAF01 vaccination generated multiple Th17-derived subsets, including a large memory-like population as well as effector Th17 and Th17-derived Th1-like subsets. These subsets shared common TCR clonotypes, and RNA velocity analyses predicted a unified differentiation trajectory, with one precursor population seeding both effector lineages. Our findings demonstrate a high degree of plasticity within the Th17 population and reveals previously uncharacterized Th17 subsets present during infection with C. trachomatis. Functional studies demonstrated that the Th17 subset that produced IL-17A was essential for early bacterial control, whereas IFN-γ-producing Th1 cells and Th17-derived Th1-like cells were not. Collectively, our findings provide mechanistic insight into Th17 biology and redefine the importance of IL-17A producing Th17 cells in early vaccine-mediated protection against C. trachomatis.
-
3. Improving peptide vaccine manufacturability without sacrificing immunogenicity: substitution of methionine and cysteine with oxidation-resistant isosteres.
PMID:日期:2026-08-29Vaccines comprising peptide antigens for inducing T cell immunity are being developed for a broad range of therapeutic applications including prevention and treatment of cancer, autoimmunity, and infectious diseases. However, many peptide antigens contain cysteine and/or methionine, which are prone to form oxidation products that can present challenges to manufacturing and reduce biological activity. To address this challenge, we introduced oxidation resistant (OXR) antigens wherein the cysteine and methionine residues of naturally occurring, wild type (WT) peptide antigens are substituted with isosteric residues that are structurally related but omit the oxidation-prone sulfur atom. Using multiple murine epitope models in C57BL/6 mice, we showed that vaccination with OXR antigens substituting cysteine and methionine with isosteres alpha-aminobutyric acid and norleucine, respectively, induced immune responses to the WT antigen that were equivalent or higher than those induced by vaccination with WT antigens. T cell responses were not affected by the position of the amino acid substitutions indicating that the isosteres do not negatively impact major histocompatibility complex (MHC) binding or T cell recognition. The T cells induced were high quality and associated with anti-tumor efficacy in vivo. Interestingly, substitution of cysteine with serine, which replaces the sulfur for an oxygen, did not yield cross-reactive T cell responses, highlighting the high degree of molecular discernment of peptide-MHC processing and presentation. In sum, OXR antigens provide a generalizable strategy for eliminating sulfur oxidation products and improving the manufacturability and shelf-life of peptide-based vaccines without affecting desired biologic activity.
-
4. Mechanism of SGLT2 inhibitors in improving immune imbalance in diabetic mice with sepsis via regulating macrophage M2 polarization through the APOC1/HMGB1/TLR4 axis.
4. SGLT2抑制剂通过APOC1/HMGB1/TLR4轴调控巨噬细胞M2极化改善糖尿病脓毒症小鼠免疫失衡的机制PMID:日期:2026-08-29This study aimed to investigate the mechanism by which the sodium-glucose cotransporter-2 (SGLT2) inhibitor dapagliflozin improves immune imbalance in sepsis with diabetes, focusing on its regulation of macrophage M2 polarization through the APOC1/HMGB1/TLR4 axis. A mouse model of type 2 diabetes was established through intraperitoneal injection of streptozotocin, after which sepsis was induced by cecal ligation and puncture. For in vitro studies, RAW264.7 macrophages and bone marrow-derived macrophages were exposed to high glucose and lipopolysaccharide. Molecular docking was employed to examine potential binding between dapagliflozin and APOC1. Organ pathology in lung, liver, and kidney was evaluated using hematoxylin and eosin staining and biochemical assay kits. Expression levels of APOC1, HMGB1, TLR4, and macrophage M1/M2 markers were analyzed via immunohistochemistry and immunofluorescence. Inflammatory cytokine levels were quantified with enzyme-linked immunosorbent assay. The SGLT2 inhibitor dapagliflozin effectively alleviated lung, liver, kidney injury and dysfunction and reduced inflammatory responses in diabetic mice with sepsis. The treatment also decreased inflammatory cytokine levels in the high glucose/lipopolysaccharide-stimulated cellular model. Furthermore, dapagliflozin treatment significantly increased the levels of M2 macrophage markers in both in vivo and in vitro models. Mechanistically, dapagliflozin was found to target, bind to, and downregulate APOC1 expression. Further investigations revealed that APOC1 promotes macrophage M1 polarization via the APOC1/HMGB1/TLR4 axis, an effect reversed by dapagliflozin. The SGLT2 inhibitor dapagliflozin ameliorates organ damage and inflammation in sepsis with diabetes by promoting macrophage M2 polarization through inhibition of the APOC1/HMGB1/TLR4 axis.
-
5. Distinct effects of two different human interferon-alpha subtypes on indicators of T-cell proliferation, activation and inhibition.
PMID:日期:2026-08-29Humans produce 12 distinct interferon alpha (IFN-α) subtypes that were previously thought to be functionally redundant. Recent studies have revealed that IFN-α subtypes differ in their ability to control different viral infections. However, little is known about how IFN-α subtypes differentially modulate immune cells to mediate these effects. This study compared the effects of IFN-α2 and IFN-α14, subtypes identified to differentially control viral infection, on T cells both in vivo in humanized TKO-BLT mice and in vitro using human peripheral blood mononuclear cells (PBMC). Treatment of humanized mice with the 2 IFN-α subtypes resulted in the differential modulation of genes associated with T-cell immunity, such as proliferation, activation and inhibition. Therefore, we assessed whether stimulation of PBMC in the presence of IFN-α2 or IFN-α14 resulted in subtype-specific effects on T cells in vitro. IFN-α14 decreased the proliferation of human CD4+ and CD8+ T cells significantly more than IFN-α2. Additionally, IFN-α14 increased expression of T-cell activation markers and the frequency of IL-2 producing T cells to a significantly greater extent compared to IFN-α2. However, the co-culture of CD8+ T cells with IFN-α-treated, autologous CD4+ T cells or IFN-α-matured monocyte-derived dendritic cells (mo-DC) only increased the expression of CD38 compared to no IFN-α treatment in a non-subtype specific manner. Overall, we identified IFN-α subtype-specific effects on the proliferation and activation of T cells. However, there were no significant differences detected directly between the IFN-α subtypes when the effects on CD8+ T cells arose through IFN-α pre-treatment of CD4+ T cells or mo-DC.
-
6. A circular RNA modulates IL-6 transcription via HuR-dependent stabilization of C/EBPβ mRNA.
6. 一种环状RNA通过HuR依赖的C/EBPβ mRNA稳定性调节IL-6转录PMID:日期:2026-08-29Inflammatory responses require precise posttranscriptional control of gene expression, yet the contribution of circular RNAs (circRNAs) to this process remains poorly understood. Here, we performed circRNA sequencing in murine macrophages stimulated with lipopolysaccharide (LPS) and identified dynamic and stimulus-dependent changes in circRNA expression. Among 1,298 high-confidence circRNAs, 54 showed significant expression changes upon LPS stimulation. We focused on circNav1, which was downregulated upon LPS stimulation. Functional analyses revealed that circNav1 enhances LPS-induced Il6 expression in macrophages. Transcriptomic and mechanistic studies identified C/EBPβ as a key downstream effector of circNav1. CircNav1 interacts with the RNA-binding protein HuR (ELAVL1) and promotes HuR-dependent stabilization of Cebpb mRNA, thereby reinforcing Il6 transcription. Consistent with these findings, circNav1 expression was markedly reduced in murine models of colitis and septic shock. Together, these results uncover a circNav1-HuR-C/EBPβ regulatory axis that fine-tunes Il6 expression during inflammatory responses and highlight circRNAs as dynamic posttranscriptional regulators in innate immunity.
-
7. High-mobility group N proteins are required for regulation of antigen-presentation genes in macrophages.
7. 高迁移率族N蛋白是巨噬细胞中抗原呈递基因调控所必需的PMID:日期:2026-08-29The expression, localization, and secretion of certain chromatin proteins are tightly regulated in response to inflammatory challenges or tissue damage. High mobility group (HMG) nucleosome-binding proteins can translocate out of the nucleus to act as alarmins in immune cell communications. The consequences of nuclear depletion of HMGs in genome organization and gene regulation are not understood in the context of innate immunity. Here, we report alterations of tissue-specific macrophage transcriptome using a genetic knockout (KO) of HMGN1 and HMGN2, an HMGN double knockout mouse line. Lack of both HMGN proteins disrupted the expression of key macrophage genes, including those encoding MHCs, M-CSF, and ApoE, as well as acute responses to LPS, in a sex-dependent manner. These transcriptional effects were associated with concomitant changes in chromatin accessibility, as profiled by an assay for transposase accessible chromatin by sequencing, in regulatory sites distal and proximal to the corresponding genes. These findings highlight the importance of macrophage HMGNs in maintaining tissue-specific gene expression and supporting inflammatory responses.
-
8. Prostaglandin D2 production in obese mice is associated with reduced lung inflammation and improved control of Francisella tularensis and Bordetella pertussis infection.
PMID:日期:2026-08-29Obesity is a risk factor for severe respiratory viral infections, but its impact on bacterial respiratory diseases remains unclear and is sometimes paradoxical. Herein, we demonstrate that diet-induced obese, male C57BL/6J mice exhibited increased resistance to pulmonary infection with Francisella tularensis and Bordetella pertussis compared with lean controls. This enhanced protection in obese mice was associated with early production of the lipid mediator prostaglandin D2 (PGD2), reduced prostaglandin E2 levels, attenuated pulmonary inflammation and decreased lung cell death. Using in vitro models, we found that PGD2 and its metabolites, PGJ2 and 15-deoxy-PGJ2, suppressed macrophage inflammatory responses and limited replication of both F. tularensis and B. pertussis. In studies using the highly virulent F. tularensis SchuS4 strain, antagonism of the PGD2 receptor DP2 increased bacterial burden in macrophages in vitro, and activation of both PGD2 receptors (DP1 and DP2) in lean mice reduced bacterial loads and lung inflammation in vivo. Together, these data indicate that PGD2 signaling promotes bacterial control and limits inflammation during these bacterial infections. The association between early PGD2 production and enhanced resistance to F. tularensis and B. pertussis in obese mice suggests that modulation of PGD2 signaling may contribute to obesity-associated protection and represents a potential host-directed therapeutic strategy to improve protection of these infections.
-
9. Correction to: Metabolic adaptations of inflammatory macrophages govern ferroptosis susceptibility via the GCH1-BH4-iNOS axis.
9. 更正：炎症巨噬细胞的代谢适应通过GCH1-BH4-iNOS轴调控铁死亡易感性PMID:日期:2026-08-29该文献暂无摘要。
-
10. A gavage-fomite based method to generate mouse models with natural microbiota.
10. 一种基于灌胃-污染物方法生成具有自然微生物群的小鼠模型PMID:日期:2026-08-29Laboratory-raised specific pathogen-free (SPF) mice have been indispensable for fundamental immunology research, yet their reliability in predicting human clinical outcomes has been questionable. A major factor contributing to this disconnect is the sanitized housing environment, which deprives laboratory mice of physiological microbial exposure critical for immune maturation. Various approaches have been developed to introduce microbes to SPF mice, aiming to mimic human-like microbial experiences and engender adult human-like immune traits. However, some of these methods, specifically the pet store mice cohousing approach suffer from significant variability in pathogen exposure driven by the uncontrolled nature of microbial exchange and is associated with heightened mortality. Here we present an alternative gavage-fomite (GaF) method that exposes mice to a similarly diverse array of pathogens and commensal as the pet store cohousing method while limiting mortality. GaF-treated mice exhibited consistent gut microbial composition, robust immune maturation characterized by mucosal T cell distribution, elevated serum inflammatory cytokines, and a splenic immune transcriptional signature closely aligned with that of adult humans. Furthermore, these mice demonstrated enhanced protection against a virulent bacterial challenge. The simplicity and effectiveness of the GaF method for generating "mice with natural microbiota," may support broader use of these models in basic and translational immunological research across institutions.