IMMUNOBIOLOGY免疫生物学
IMMUNOBIOLOGY(英文缩写 IMMUNOBIOLOGY),ISSN 0171-2985,eISSN 1878-3279,中文译名:免疫生物学 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 | 3.152 | Q4 |
| 2022 | 2.800 | Q4 |
| 2023 | 2.500 | Q3 |
| 2024 | 2.300 | Q3 |
| 2025 | 3.100 | Q3 |
IMMUNOBIOLOGY 最新收录文献
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1. {"_":"Impact of obesity on LAG-3 and CTLA-4 expression in CD4 T cells from lymph nodes of sarcoidosis patients.","sup":["+"]}
PMID:日期:2026-09-25Obesity is increasingly recognized as a metabolic factor influencing immune regulation in sarcoidosis (SA). This study examined whether obesity alters immune-checkpoint expression on lymph-node-resident T cells in newly diagnosed, treatment-naïve SA patients. Sixty-three individuals underwent EBUS-TBNA with flow-cytometric analysis of lymph node (LN) aspirates and peripheral blood (PB), and were stratified into obese (n = 18) and non-obese (n = 45) groups. Obesity was associated with distinct LN-specific immunophenotypic changes, including markedly higher LAG-3 and CTLA-4 expression on CD4 T cells and lower TIM-3 expression on CD8 T cells. Obese patients also showed reduced high-fluorescent cell counts and lower lymphocyte fluorescence intensity, suggesting altered activation states. These differences were absent in PB, underscoring tissue-specific immune modulation. Pulmonary function was lower in obese patients but served mainly as a clinical correlate. Overall, obesity emerges as a relevant modifier of local T-cell regulation in SA, highlighting the value of LN-based immunophenotyping.
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2. Tangeretin ameliorates hypertriglyceridemic acute pancreatitis by restoring Th17/Treg balance via ROS-mediated STAT3 signaling.
2. 桔皮素通过ROS介导的STAT3信号通路恢复Th17/Treg平衡，从而改善高甘油三酯血症性急性胰腺炎PMID:日期:2026-09-23The mechanisms underlying the progression of hypertriglyceridemic acute pancreatitis (HTGP), particularly CD4 T cell-mediated immune dysregulation, remain poorly understood. To address this issue, clinical data and peripheral blood samples from patients with acute pancreatitis (AP) were analyzed to evaluate CD4 T cell subsets and inflammatory markers. Bioinformatics analyses identified key regulatory molecules involved in HTGP progression and were validated using transcriptomic datasets. The underlying mechanisms and therapeutic effects of tangeretin were further investigated in HTGP mice and cultured T cells using histopathological, biochemical, molecular, and flow cytometry analyses. Higher TG levels were associated with a trend toward reduced CD4 T cell proportions in patients with AP. Bioinformatics analyses identified STAT3 as a potential candidate regulator associated with HTGP-related inflammatory signaling. Mechanistically, HTGP induced oxidative stress, promoted Th17 differentiation, reduced Treg proportions, and was associated with enhanced STAT3 activation, accompanied by pancreatic injury and secondary splenic damage. Tangeretin markedly alleviated tissue injury, suppressed oxidative stress and inflammatory responses, inhibited p-STAT3 activation, and restored Th17/Treg immune homeostasis. These findings suggest that oxidative stress and STAT3 activation may contribute to CD4 T cell immune alterations in HTGP. Tangeretin attenuated oxidative stress and STAT3 activation and was associated with improved immune homeostasis, supporting its potential protective effects against HTGP.
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3. Complement dysregulation in lupus nephritis: interplay of hypocomplementemia and complement-directed autoantibodies.
PMID:日期:2026-09-17Complement dysregulation is a defining feature of lupus nephritis (LN), traditionally assessed by C3 and C4 levels. Emerging studies suggest that complement-directed autoantibodies may reflect an expanded autoreactive network that remains poorly defined. In this study, complement components and corresponding autoantibodies were assessed in sixty-nine treatment naïve renal biopsy-proven (2003 ISN/RPS) LN patients and fifty healthy controls using nephelometry, commercially available ELISA and in-house standardized ELISA. LN patients exhibited widespread hypocomplementemia, with reduced C3 (94.2%), C4 (84.1%), C1q (79.7%), complement factor H (CFH; 34.8%), complement factor B (CFB; 18.8%) and complement factor P/properdin (CFP; 65.2%) levels. Anti-C1q (62.3%) and anti-C3 (21.7%) autoantibodies predominated in LN patients. At the nominal significance level, hypocomplementemia and complement-directed autoantibodies significantly associated with disease activity, renal dysfunction, cytopenias, and nuclear autoantibodies (p < 0.05). Following Benjamini-Hochberg FDR correction, significant associations were retained among complement proteins, complement-directed autoantibodies, and nuclear autoantibodies (q < 0.05). These findings demonstrated that complement dysregulation in LN encompasses both hypocomplementemia and complement-directed autoantibodies, reflecting a systemic autoreactive immune network. Comprehensive complement profiling may provide additional clinical-serological information for LN assessment and improve disease monitoring.
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4. Ketone ester alleviates sepsis-associated liver injury through β-hydroxybutyrylation of STAT1.
4. 酮酯通过STAT1的β-羟基丁酰化减轻脓毒症相关肝损伤PMID:日期:2026-09-11Sepsis-associated liver injury is characterized by excessive inflammation and macrophage activation. β-Hydroxybutyrate (β-OHB) has anti-inflammatory effects and induces lysine β-hydroxybutyrylation (Kbhb), but the role of site-specific Kbhb in septic liver injury remains unclear. This study examined the role of STAT1 K679 Kbhb in the protective effect of ketone ester (KE) against LPS-induced liver injury. STAT1 knock-in mice were generated, and liver injury was induced by lipopolysaccharide (LPS). KE pretreatment alleviated hepatic histopathological injury, reduced serum alanine aminotransferase and aspartate aminotransferase levels, and decreased the Bax/Bcl-2 ratio in wild-type mice. These effects were significantly attenuated in STAT1 mice. KE increased hepatic STAT1 Kbhb, whereas the K679R mutation markedly reduced this modification. In RAW264.7 macrophages, K679R reduced β-OHB-induced STAT1 Kbhb, while no significant effect was observed in AML12 hepatocytes. KE also reduced hepatic M1 macrophage markers, IL-6 and IL-12 expression, and STAT1 Ser727 phosphorylation in LPS-treated wild-type mice, whereas these effects were attenuated by K679R. These results show that STAT1 K679 Kbhb contributes to the inhibition of macrophage M1 polarization by KE and is involved in its protective effect against LPS-induced liver injury.
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6. The anti-leukemia drug ponatinib attenuates NLRP3 inflammasome activation in macrophages.
PMID:日期:2026-09-04The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is an established driver of inflammation in diseases such as diabetes, Alzheimer's disease, and gout. Previously, we screened 875 FDA-approved drugs for NLRP3 inhibitors and identified ponatinib as one of the five candidates that reduced NLRP3 inflammasome activation without causing cytotoxic effects in bone marrow-derived macrophages (BMDMs). Therefore, we hypothesize that ponatinib may be an effective NLRP3 inflammasome inhibitor. We performed dose curves and cytotoxicity assays to determine an effective in vitro concentration of ponatinib in BMDMs (1 μM) and primary microglia (0.5 μM) that reduced IL-1β secretion without inducing cytotoxicity. In BMDMs, ponatinib inhibited Nlrp3- and Caspase-1-dependent IL-1β and IL-18 secretion and significantly reduced caspase-1 processing. Ponatinib also reduced IL-1β secretion by microglia, indicating possible NLRP3 inflammasome inhibition in this cell type, but further testing is required. Although ponatinib has previously been demonstrated to drive cardiotoxicity-mediated inflammation, these data suggest that at specific doses, in vitro ponatinib can be non-cytotoxic and effective in attenuating NLRP3 inflammasome activation in macrophages and microglia.
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7. m6A writer METTL14 restricts Mycobacterium tuberculosis infection by promoting TAX1BP1-mediated autophagy in macrophages.
7. m6A写入蛋白METTL14通过促进TAX1BP1介导的巨噬细胞自噬来限制结核分枝杆菌感染PMID:日期:2026-09-01N6-methyladenosine (m6A) modification plays a crucial role in regulating immune responses against Mycobacterium tuberculosis (Mtb) infection, but the underlying mechanisms remain unclear. Here, we analyzed m6A regulatory gene expression in GEO dataset GSE139825 and validated the finding in THP-1-derived macrophages. Bioinformatics analysis showed that METTL14, ALKBH5, and YTHDC1 were significantly downregulated, while METTL3 was upregulated in Mtb-infected alveolar macrophages compared to controls. In vitro experiments confirmed METTL14 expression was dose-dependently reduced with Mtb infection in macrophages, and METTL14 overexpression reversed Mtb-induced decreases in cell viability, reduced LDH release, and diminished intracellular Mtb burden. Mechanistically, METTL14 overexpression restored Mtb-suppressed autophagy, evidenced by increased LC3II/I ratio and Beclin1 expression as well as decreased p62 levels, which was abrogated by the autophagy inhibitor 3-MA. Further, as validated by bioinformatic prediction, RIP assay and actinomycin D experiment, METTL14 directly bound to TAX1BP1 mRNA and enhanced its m6A modification, thereby stabilizing TAX1BP1 mRNA and upregulating its expression. TAX1BP1 knockdown abolished the protective effects of METTL14 overexpression on macrophage viability, autophagy, and anti-Mtb capacity. Collectively, our findings demonstrate that METTL14, downregulated by Mtb infection, promotes macrophage autophagy and antibacterial activity via m6A-mediated stabilization of TAX1BP1. This METTL14-TAX1BP1-m6A pathway provides a novel therapeutic target for tuberculosis treatment.
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8. ECMO-assisted whole lung lavage combined with GM-CSF inhalation for severe pulmonary alveolar proteinosis: a comparative cohort study.
8. ECMO辅助全肺灌洗联合GM-CSF吸入治疗重度肺泡蛋白沉积症：一项比较队列研究PMID:日期:2026-08-31This study evaluated the association of combining veno-venous extracorporeal membrane oxygenation (ECMO) with whole-lung lavage (WLL) and granulocyte-macrophage colony-stimulating factor (GM-CSF) nebulization in pulmonary alveolar proteinosis (PAP), focusing on pulmonary function, oxygenation, lipid metabolism, and inflammatory modulation. This retrospective cohort study included 40 PAP patients, categorized into WLL + GM-CSF (n = 20) and ECMO + WLL + GM-CSF (n = 20) groups according to the treatment they received. Outcomes included pulmonary function [diffusing capacity for carbon monoxide (DLCO%), forced vital capacity (FVC%)], arterial blood gas parameters [partial pressure of oxygen (PaO), carbon dioxide (PaCO), oxygen saturation (SaO)], lipid profiles [total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C)], inflammatory cytokines such as interleukin-6 (IL-6) and C-reactive protein, and functional assessments (Barthel Index score, 6-min walk distance). Correlations between lipids profiles, arterial blood gas parameters, pulmonary functional indicators, and inflammatory cytokines were evaluated using Pearson's or Spearman's correlation coefficients. The ECMO + WLL + GM-CSF group showed greater improvements in DLCO% and FVC%, significant increases in PaO and SaO, and greater reductions in PaCO, pro-inflammatory markers (IL-6, CRP), and lipid levels (TC, TG, LDL-C) compared to the WLL + GM-CSF group. In the ECMO + WLL + GM-CSF group, negative correlations were observed between serum TG and PaO, DLCO%, and FVC%, and IL-6 inversely correlated with FVC%. The ECMO + WLL + GM-CSF group also achieved higher functional recovery based on the higher Barthel index scores and longer 6-min walk distance. ECMO-assisted WLL combined with GM-CSF was associated with greater improvements in pulmonary function and oxygenation, as well as greater reductions in serum lipid levels and inflammatory markers.
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9. Transcriptomic profiling reveals complement activation in chronic pancreatitis adjacent to pancreatic ductal adenocarcinoma.
9. 转录组学分析揭示胰腺导管腺癌邻近慢性胰腺炎中的补体激活PMID:日期:2026-08-28Chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) frequently coexist, yet distinguishing inflammatory changes secondary to malignancy from primary pancreatitis remains challenging. Here, we present an integrated multi-omics analysis of spatially distinct pancreatic tissue compartments obtained from a single patient undergoing pancreaticoduodenectomy for PDAC, combining histopathology, transcriptomics, immunofluorescence, and meta-transcriptomic microbial profiling. Morphological assessment identified tumor tissue, adjacent CP, and normal pancreas. Transcriptomic profiling of macro-dissected samples revealed differential gene expression and enrichment of the classical complement pathway in the CP compartment, which was qualitatively supported by immunofluorescent detection of C1q and C3 along the ductal epithelium. Meta-transcriptomic analysis detected a limited number of bacterial taxa and no viral RNA; these findings were interpreted conservatively given the constraints of low-biomass tissue profiling and the single-patient design. Although causal inference and generalizability are limited by the single-patient design, this study demonstrates the feasibility of integrating pathology with transcriptomic and microbial analyses to generate a hypothesis-generating, multi-omics framework for exploring inflammatory-malignant interactions in pancreatic disease.
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10. The Sesn2/Nrf2 axis suppresses oxidative stress and pyroptosis-associated signaling in LPS/nigericin-challenged alveolar macrophages.
10. Sesn2/Nrf2轴抑制LPS/黑曲霉素攻击的肺泡巨噬细胞中的氧化应激和焦亡相关信号传导PMID:日期:2026-08-27Pyroptosis is a key mechanism driving immune imbalance in sepsis, while the stress-induced protein Sestrin 2 (Sesn2) and Nuclear factor E2-related factor 2 (Nrf2) are core regulators of antioxidant defense. No existing studies have clarified the interactive regulatory effect of the Sesn2/Nrf2 axis on pyroptosis in alveolar macrophages. Therefore, this study aims to investigate the regulatory mechanism of the Sesn2/Nrf2 axis on pyroptosis and oxidative stress in LPS/nigericin-challenged alveolar macrophages, providing a theoretical basis for further understanding of sepsis. Bioinformatics analysis involved screening differentially expressed genes in sepsis from the Gene Expression Omnibus dataset GSE185263, intersecting them with genes related to pyroptosis and ferroptosis, constructing a protein-protein interaction network, and identifying core genes. An inflammatory injury model was established in the mouse alveolar macrophage cell line MH-S by stimulating cells with LPS and nigericin. Interventions were performed using siRNA to knock down Sesn2 and plasmids to overexpress Nrf2. Cell viability, oxidative stress markers, expression of pyroptosis-related molecules, and secretion of inflammatory cytokines were measured. SESN2 as a key gene common to sepsis, pyroptosis, and ferroptosis. The Sesn2/Nrf2 signaling axis significantly enhanced the cell viability of MH-S cells after inflammatory injury, increased Superoxide Dismutase activity and Glutathione levels, and reduced reactive oxygen species and Lactate Dehydrogenase levels. Simultaneously, this axis suppressed the expression of pyroptosis-related inflammasomes (NOD-like receptor thermal protein domain associated protein 3, Absent in melanoma 2) and key execution proteins (Gasdermin D, Cleaved Caspase-1, Caspase-4), and reduced the secretion of inflammatory cytokines IL-1β, IL-18, and TNF-α. Sesn2 and Nrf2 exhibited mutual positive regulation in macrophages following inflammatory injury. In vitro cell model studies indicate that the Sesn2/Nrf2 axis synergistically suppresses oxidative stress and pyroptosis-associated signaling in LPS/nigericin-challenged alveolar macrophages, suggesting that this axis may represent a potential target warranting further investigation in in vivo models.