Journal of Immunology Research免疫学研究杂志
Journal of Immunology Research(英文缩写 J IMMUNOL RES),ISSN 2314-8861,eISSN 2314-7156,中文译名:免疫学研究杂志 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：2025-09-28 至 2026-09-28，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 | 4.493 | Q3 |
| 2022 | 4.100 | Q3 |
| 2023 | 3.500 | Q2 |
| 2024 | 3.600 | Q2 |
| 2025 | 3.200 | Q3 |
Journal of Immunology Research 最新收录文献
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1. Research Progress on Mechanisms of Immune Tolerance Induced by Hepatitis B Surface Antigen in Chronic HBV Infection.
PMID:日期:2026-01-01The sustained elevation of hepatitis B surface antigen (HBsAg) facilitates the progression of chronic hepatitis B virus (HBV) pathogenesis, and initiates and sustains host immune tolerance. Immune tolerance is a major factor contributing to viral persistence and viral clearance failure. HBsAg exerts regulatory effects on innate defenses and adaptive responses, limiting the activity of dendritic cells (DCs), natural killer (NK) cells, monocytes/macrophages, T lymphocytes, and B cells. Furthermore, it fosters a tolerogenic environment via interconnected regulatory cell networks, immune checkpoint molecules, and anti-inflammatory cytokines. HBsAg can enhance the intrahepatic immune-tolerant (IT) microenvironment by downregulating costimulatory molecules and promoting the secretion of immunosuppressive cytokines by intrahepatic nonparenchymal cells. This review systematically summarizes how HBsAg interferes with immune cell function and signaling pathways to establish a tolerogenic environment. We also cover recent progress in treatments that target HBsAg-induced immune tolerance. This review establishes a solid theoretical foundation and identifies new therapeutic approaches that can break tolerance to achieve a functional cure for chronic hepatitis B (CHB).
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2. Harmine Derivative H-2-104 Alleviates Echinococcus granulosus-Induced Pulmonary Fibrosis in Mice by Inhibiting Fibroblast Activation and Inducing DNA Damage.
PMID:日期:2026-01-01Pulmonary fibrosis (PF) secondary to Echinococcus granulosus infection is a severe complication with limited therapeutic options. Harmine (HM) exhibits antifibrotic potential but is restricted by significant neurotoxicity. This study aimed to evaluate the therapeutic efficacy and underlying mechanism of HM derivative H-2-104 in a clinically relevant E. granulosus-induced PF mouse model, and to clarify its advantages over parent compound HM. A mouse model of E. granulosus-induced PF was established, and treated with H-2-104 (25 or 50 mg/kg) or nintedanib for 21 days. Lung function, histopathology, hydroxyproline (HYP), inflammatory cytokines, and fibrosis-related protein expression were assessed. In vitro, human embryonic lung fibroblasts (MRC-5) were activated with TGF-β1 and treated with H-2-104. Cell viability, migration, apoptosis, differentiation, DNA damage, and related gene expression were evaluated. H-2-104 significantly improved lung function, alleviated pathological damage, and collagen deposition, decreased HYP, TGF-β1, TNF-α, IL-6, and IL-1β, elevated IL-10, and downregulated α-smooth muscle actin (α-SMA), collagen I, and fibronectin. Importantly, H-2-104 showed no obvious neurotoxicity and exhibited better safety than HM. In vitro, H-2-104 inhibited TGF-β1-induced MRC-5 cell viability (IC = 13.49 µg/mL), migration, and fibroblast-to-myofibroblast differentiation, while promoting apoptosis along with increased DNA damage in a dose-dependent manner. Additionally, H-2-104 downregulated the expression of fibrosis-related genes and upregulated DNA damage-related genes (H2AX, ATR, and RAD51) in TGF-β1-induced MRC-5 cells. This study establishes H-2-104 as a promising antifibrotic candidate for E. granulosus-induced PF, using a clinically meaningful parasitic infection-associated fibrosis model. H-2-104 retains strong antifibrotic efficacy while overcoming the neurotoxicity limitation of HM. Mechanistically, the activation of DNA damage response is correlated with the antifibrotic activities of H-2-104, providing a new perspective for targeting fibroblast activation in PF therapy.
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3. {"_":"Mesenchymal Stem Cells Ameliorate Acute-on-Chronic Liver Failure Associated With Expansion of Immunoregulatory Hepatic NKp46DX5 NK Cells.","sup":["+","-"]}
PMID:日期:2026-01-01Hepatitis B virus (HBV)-related acute-on-chronic liver failure (HBV-ACLF) is a life-threatening syndrome characterized by rapid hepatic decompensation and immune dysregulation, with limited treatment options. Mesenchymal stem cells (MSCs) have shown therapeutic potential, but their precise mechanisms-particularly regarding their interaction with hepatic NKp46DX5 natural killer (NK) cells-remain unexplored. We investigated whether MSC treatment alleviates ACLF, which is associated with the modulation of NK cell populations, and sought to identify key factors driving this immunoregulatory effect. Peripheral NK cells were analyzed in ACLF patients receiving MSC infusion or standard therapy. Flow cytometry assessed NK frequency, phenotype, and correlations with survival. Murine ACLF was induced by carbon tetrachloride (CCL), followed by MSC treatment. Flow cytometry characterized NK subsets (DX5). In vitro cocultures evaluated MSC-NK interactions, proliferation, and cytokine secretion. NK-MSC conjugation was quantified via live imaging. Frequency of peripheral blood NK cells from ACLF patients was upregulated after MSCs infusion, which correlated with liver function recovery. Phenotypic changes included upregulation of NKG2A and downregulation of NKp30 and FasL. MSC infusion effectively rescued ACLF mice and increased NK cell frequency in both blood and liver. Strikingly, NKp46 DX5, instead of NKp46 DX5 hepatic NK cells, responded well to MSCs. In vitro, MSCs promoted proliferation, granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion, and adhesion of NKp46 DX5 liver NK cells. MSC infusion holds significant clinical promise for ACLF patients. In addition to promoting liver regeneration, the immunomodulatory effect of MSCs on hepatic NKp46DX5 NK cells may provide a novel rationale for refining future therapeutic regimens.
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4. Imbalance of Circulating B-Cell Subsets Was Associated With Higher Risk of Relapses in RRMS Patients.
PMID:日期:2026-01-01B-cell aggregates below the meninges have been associated with progression of neurodegeneration in multiple sclerosis (MS). We aimed to investigate the frequency of different B-cell subsets and their relationship with MS severity. Also, we quantified the CXCL13 and neurofilament (NfL) plasma levels. According to the differential expression of IgD, CD38, CD27, HLA-DR, CD138, IL-10, and IL-17, the frequency of different circulating B-cell (CD19) subsets was evaluated using flow cytometry. Plasma levels of CXCL13 and NfL were quantified using ELISA. Here, the severity of neurological impairment positively correlated with the percentage of plasmablast (CD138, IL-17IL-10, HLA-DRIgD) and memory CD27CD38B-cell subsets (IL-17IL-10 and HLA-DRIgD), but negatively correlated with the proportion of HLA-DRIgD and IL-17IL-10 among transitional and plasmablasts. The occurrence of new clinical relapses was mainly observed among patients who showed an elevated proportion of CD138 and HLA-DRIgD plasmablast and HLA-DRIgD memory and CD27CD38B-cell subsets. Further, relapsed patients showed a higher percentage of IL-17IL-10 cells among transitional, naïve and different memory B cells at baseline. By contrast, elevated frequency of HLA-DRIgD memory B cells and IL-17IL-10 among transitional and plasmablasts was observed in nonrelapsed patients over time. CXCL13 levels were higher in relapsed patients, and positively correlated with CD138 plasmablasts and memory B-cell subsets. Finally, plasma levels of NfL correlated positively with both CD138 and HLA-DRIgD plasmablasts, but negatively with transitional and naïve B cells with HLA-DRIgD phenotype. In summary, our findings suggest that increased circulating anergic or immunogenic B-cell subsets could be candidate biomarkers for low- and high-risk of disease activity, respectively.
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5. Therapeutic Potential of Thiosemicarbazone Derivative in LPS-Induced Mastitis: Dual Modulation of Inflammatory Response and Blood-Milk Barrier Integrity.
PMID:日期:2026-01-01Mastitis is a prevalent inflammatory disorder in women, this condition exhibits a particularly elevated prevalence among breastfeeding women, which significantly compromises mammary health and lactation function. This research explored the anti-inflammatory properties of YWJ-6 in lipopolysaccharide (LPS)-induced mastitis, its protective role on the blood-milk barrier (BMB), and the underlying mechanisms. An LPS-induced mastitis rat model was established. H&E staining assessed mammary tissue damage, and myeloperoxidase (MPO) activity was measured. RT-qPCR and IHC were used to demonstrate interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNFα) expression. These data indicated that inflammatory injury was alleviated. Following drug treatment, MPO expression and the mRNA/protein expression of these inflammatory factors were suppressed. Immunofluorescence staining analyzed the distribution of Zonula Occludens-1 (ZO-1), Occludin, and Claudin-3. WB quantitatively detected ZO-1 and Occludin expression, confirming that YWJ-6 promoted tight junction (TJ) protein expression restoration and distribution integrity, repairing the damaged BMB. Consistently, Evans blue extravasation assay demonstrated that YWJ-6 reduced mammary vascular permeability, providing direct functional evidence for BMB protection. mIHC detected the colocalization of CD68, MPO, and nuclear factor-kappa B (NF-κB) p65 subunit (NF-κB p65), showing that YWJ-6 modulated inflammatory cell infiltration and p65 activation. RT-qPCR, WB, and ELISA assays in HC11 and RAW264.7 cells confirmed that YWJ-6 downregulated inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and IL-1β, IL-6 and TNF-α expression in HC11 cells, and suppressed agent responsible for inflammation secretion in RAW264.7 cells. WB and immunofluorescence showed that YWJ-6 inhibited inhibitor of NF-κB alpha (IκBα) and NF-κB p65 phosphorylation in both HC11 and RAW264.7 cells. In conclusion, YWJ-6 exerts dual protective effects by targeting NF-κB signaling pathway activation, providing experimental evidence for mastitis treatment in future.
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6. Macrophage TMEM175-Mediated Transcriptional Regulation of Cathepsins Drives Bacterial Killing in Sepsis.
PMID:日期:2026-01-01Sepsis is a life-threatening condition characterized by a dysregulated host response to infection, in which lysosomal acidification and hydrolytic activity are crucial for effective pathogen clearance by macrophages. Transmembrane Protein 175 (TMEM175) is a key regulator of lysosomal pH, and its deficiency is reported to cause lysosomal over-acidification and impaired cathepsin D (CTSD) activity. However, the role of TMEM175 in sepsis remains uncertain. We hypothesize that TMEM175 deficiency exacerbates sepsis by impairing CTSD activity. TMEM175 mRNA expression levels were measured in peripheral blood mononuclear cells (PBMCs) from septic patients and healthy controls (HCs). Using a cecal ligation and puncture (CLP) mouse model, we evaluated the effects of the TMEM175 inhibitor 2-phenylcyclopentylamine (2-PPA) on mortality and bacterial load in target organs. In vitro, TMEM175-knockdown in macrophages was performed to assess its impact on bacterial clearance, phagocytosis, lysosomal acidification, and cathepsin maturation. Results showed that TMEM175 expression was significantly downregulated in PBMCs from septic patients. Pharmacological inhibition of TMEM175 in CLP mice exacerbated bacterial burden and increased mortality. Mechanistically, TMEM175 deficiency impaired macrophage-mediated bacterial clearance, despite having no effect on the initial phagocytic uptake. This dysfunction was attributed to TMEM175, which directly regulates cathepsin transcription. Additionally, TMEM175 deficiency suppressed PI3K-Akt signaling, reducing inflammatory cytokine production.
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7. Cancer-Testis Antigens in Immuno Oncology Mechanisms Therapeutic Strategies and Clinical Perspectives.
PMID:日期:2026-01-01Cancer-testis antigens (CTAs) represent a unique class of tumor-associated antigens (TAAs) with highly restricted expression in immune-privileged tissues and widespread aberrant activation in various malignancies. Their potent immunogenicity and tumor specificity make CTAs promising targets for cancer immunotherapy. This review provides a comprehensive overview of the molecular regulation, biological functions, and therapeutic applications of CTAs. We detail the genetic and epigenetic mechanisms that drive CTA expression in cancer, their roles in tumor progression, and their capacity to elicit robust CD8 T cell responses. Recent clinical advances in peptide- and dendritic cell-based vaccines, T-cell receptor (TCR)-engineered adoptive cell therapies, and combination strategies with immune checkpoint inhibitors (ICIs) are highlighted, emphasizing NY-ESO-1 and MAGE family antigens as leading candidates. We further discuss the major challenges limiting clinical translation, emphasizing that despite promising immunogenicity, most CTA-directed modalities remain in early clinical evaluation with heterogeneous response rates, intratumoral heterogeneity, antigen loss, and risks of off-target toxicity. The review also explores emerging approaches-such as epigenetic modulators, multiantigen targeting, and CRISPR-based gene editing-that aim to enhance the precision and efficacy of CTA-based immunotherapies. Together, these insights underscore the strategic potential of CTAs in next-generation immunotherapy and outline the future directions required to bring these promising agents from bench to bedside.
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8. Associations Between Short-Term Changes in Disease Activity and Long-Term Clinical Outcomes in Activated Phosphoinositide 3-Kinase Delta Syndrome.
PMID:日期:2026-01-01Clinical trials in activated phosphoinositide 3-kinase delta (PI3Kδ) syndrome (APDS), an ultra-rare disease, have evaluated treatment response to the PI3Kδ inhibitor leniolisib using disease activity endpoints, including those measuring immunodeficiency and immune dysregulation. However, the relationship between disease activity endpoints and long-term clinical outcomes has not been quantified. Data from a randomised controlled trial and its open-label extension (OLE) investigating leniolisib were used to evaluate associations between short-term disease activity endpoints and longer-term clinical outcomes. Both single time point and repeated measures analyses were conducted using linear regression modelling and random effects multilevel regression modelling, respectively. In total, 39 patients were included (≤6 years of follow-up). Improvements in multiple immunodeficiency and dysregulation disease activity endpoints were significantly associated with increases in the patient global assessment (PtGA) and the 36-item short form survey (SF-36) physical component score and mental component score (PCS/MCS). Increasing proportion of naïve B cells was associated with reduction in infection rates (2.3% fewer infections per 1% increase in naïve B cells). In this clinical trial setting, short-term improvements in immunodeficiency and dysregulation following treatment with leniolisib were associated with longer-term improvements in clinical outcomes, including infection rates and quality of life, for patients with APDS.
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9. Running on Empty Signals: What Human MALT1 Deficiency Reveals About Immune Control.
PMID:日期:2026-01-01Human genetic disorders affecting intracellular signaling pathways provide an unparalleled opportunity to understand how immune responses are regulated in vivo. Among these conditions, MALT1 deficiency has emerged as a particularly informative model because it reveals how subtle quantitative changes in antigen receptor signaling can translate into profound clinical consequences. As a central component of the CARD11-BCL10-MALT1 (CBM) signalosome, MALT1 integrates receptor-derived signals and determines whether downstream nuclear factor kappa B (NF-kB) activation reaches thresholds required for effective immune responses. Rather than representing a single, uniform loss-of-function condition, MALT1 deficiency is genetically and functionally heterogeneous: different pathogenic variants affect MALT1 protein expression, paracaspase/protease activity, or its scaffolding role within the CBM complex to varying degrees, and these differences determine whether the predominant phenotype reflects impaired immune activation, immune dysregulation, or a combination of both. This functional diversity helps explain why patients with MALT1 deficiency may present with recurrent infections, inflammatory features, regulatory T-cell defects, and progressive impairment of B-cell immunity, either alone or in combination. In this review, we discuss how insights from human disease, experimental models, and therapeutic studies converge to position MALT1 as a critical regulator of immune homeostasis and explore broader implications for translational immunology. Due to the rarity of MALT1 deficiency, we carefully compiled and contextualized the few reported cases of hematopoietic stem cell transplantation (HSCT), highlighting emerging translational patterns.
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10. Impact of Transport Media on IL-33 Levels in Samples From Patients With Viral Respiratory Infections.
PMID:日期:2026-01-01Interleukin-33 (IL-33) is an IL-1 family cytokine that activates various immune cells and induces both systemic and localized Th2 responses during infection. An association between IL-33 and its suppresion of tumorigenicity 2 (ST2) receptor with inflammation during respiratory tract infection has been previously reported. Furthermore, some data suggest that during respiratory infections, IL-33 may serve as an indicator of disease severity, as high levels of this cytokine have been found in nasopharyngeal swab (NPS) samples of infants with lower respiratory tract disease caused by respiratory syncytial virus (RSV). As viral diagnosis is mostly compartmentalized in NPS, in this report, we aimed at detecting IL-33 in NPS from patients with respiratory tract infections that were collected in two different transport media (universal transport medium [UTM], and phosphate-buffered saline [PBS]). IL-33 levels were evaluated in 230 NPS samples, 121 obtained in PBS, and 109 in UTM. The samples were tested for RSV, metapneumovirus, adenovirus (ADV), influenza, and parainfluenza. In this cohort, higher levels of IL-33 were detected in virus-positive samples collected in PBS compared to virus-negative samples collected in the same transport medium. In addition, RSV- and FLU-positive samples collected in PBS showed higher measured IL-33 levels than those collected in UTM. No significant differences were found for the other viruses included in this study. These findings highlight the importance of considering sample collection and transport conditions when interpreting IL-33 measurements in NPS, particularly in future studies evaluating IL-33 as a potential severity-associated biomarker during RSV or influenza infection.