CYTOKINE细胞因子
CYTOKINE(英文缩写 CYTOKINE),ISSN 1043-4666,eISSN 1096-0023,中文译名:细胞因子 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：2025-09-27 至 2026-09-27，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 | 3.926 | Q3 |
| 2022 | 3.800 | Q2 |
| 2023 | 3.700 | Q2 |
| 2024 | 3.700 | Q2 |
| 2025 | 3.600 | Q2 |
CYTOKINE 最新收录文献
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1. Patient-derived mesenchymal stromal cells establish an IL-6 axis that marks progression from smouldering to active multiple myeloma.
PMID:日期:2026-11-01IL-6 signalling in the bone marrow (BM) is compartmentalised. Different cell populations within the BM niche contribute distinct components of the IL-6 signalling network, yet how their roles change during myeloma progression has remained unclear. We examined how the respective contributions of mesenchymal stromal cells (MSCs) and primary multiple myeloma (MM) cells to the IL-6 signalling machinery change during disease progression. MSCs were identified as the principal source of IL-6, whereas MM cells secreted minimal IL-6 but were the primary source of soluble IL-6 receptor (sIL-6R). This functional interplay, with MSCs supplying the ligand and MM cells providing the soluble receptor, establishes a paracrine IL-6 trans-signalling axis. The contribution of MM cells to this axis increases significantly with disease stage: cells from patients with active MM secreted substantially greater quantities of sIL-6R than those from patients with smouldering disease, identifying sIL-6R as a marker of biologically active disease. This increase is mirrored by higher basal IL-6 secretion from MSCs in advanced disease, demonstrating augmentation of the IL-6 signalling pathway as disease progresses. Using Hyper-IL-6 and sgp130, we demonstrated that trans-signalling through gp130 is the dominant mechanism by which stromal-derived IL-6 protects MM cells from treatment-induced apoptosis, independent of membrane-bound IL-6R expression. Therefore, targeted inhibition of IL-6 trans-signalling with sgp130 could be used to suppress pathogenic effects in MM while preserving beneficial classical IL-6 signalling, offering a more precise and potentially safer alternative to total IL-6/IL-6R blockade. As disease progression increases trans-signalling through higher sIL-6R expression, early intervention in smouldering myeloma, before pathway amplification, may represent a more effective therapeutic strategy.
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3. A pilot study of a urinary IL-8 and IL-17-based formula for discriminating Hunner-type from non-Hunner-type interstitial cystitis.
PMID:日期:2026-11-01To determine whether urinary or plasma cytokines more effectively differentiate Hunner-type interstitial cystitis (HIC) from non-Hunner-type interstitial cystitis (NHIC), and to develop an interpretable discriminative formula based on the most informative features. Paired urine and plasma samples were collected from 47 patients with IC/BPS (15 HIC, 32 NHIC), and urine samples from 84 healthy controls were analyzed for baseline comparison. Twelve cytokines were quantified in each sample. Classification performance was evaluated using AutoGluon automated machine learning with stratified five-fold cross-validation across three feature sets: urine cytokines, plasma cytokines, and their combination. Symbolic regression with the QLattice algorithm, implemented within a nested cross-validation framework with seed averaging and a complexity constraint to reduce overfitting, was employed to generate a simplified discriminative formula. The urine-based model outperformed both plasma-based and combined models (AUC 0.979 ± 0.028 vs. 0.741 ± 0.271 vs. 0.921 ± 0.087). A clear pathophysiological gradient was observed among healthy controls, NHIC, and HIC, with urinary IL-8 elevated 72-fold in HIC and 5-fold in NHIC compared to healthy controls. The QLattice-derived formula, incorporating uIL-17 and uIL-8, achieved a nested cross-validation accuracy of 90.5% (95% CI: 88.5%-92.4%) and an AUC of 0.948 (95% CI: 0.927-0.966). Urinary cytokines, specifically IL-8 and IL-17, offer a more effective non-invasive approach for IC/BPS subtyping compared to plasma markers. The two-cytokine formula shows promise as an exploratory discriminative tool. However, external validation in larger, independent cohorts is necessary prior to clinical implementation.
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5. The clinical benefit of prostacyclin treatment in mechanically ventilated patients with SARS-CoV-2 infection is not attributed to anti-inflammatory effects.
PMID:日期:2026-11-01Treatment with the synthetic prostacyclin analog iloprost has been shown to attenuate endothelial glycocalyx shedding and organ failure in patients with critical Covid-19. The treatment is currently being investigated in a broader setting of patients with acute respiratory failure. We here investigated the effect on inflammatory and T-cell-derived cytokine and growth-factor responses in patients with critical Covid-19. Post-hoc analysis of a randomized controlled trial (n = 80) in mechanically ventilated patients with SARS-CoV-2 infection and concomitant endotheliopathy, defined as soluble thrombomodulin plasma-levels ≥4 ng/mL. Patients received 72 h iloprost infusion (1 ng/kg/min) or placebo. Blood samples were collected at baseline and 24 h after inclusion. Fifty-four cytokines and growth factors, distributed into six biomarker classes, were measured using the Meso Scale Discovery V-PLEX platform. Iloprost treatment, compared with placebo, did not result in statistically significant changes of any of the fifty-four measured biomarkers at 24 h, when adjusting for multiple testing. Likewise, linear mixed-effects models did not identify significant effects of iloprost on any of the six predefined biomarker classes at 24 h. In mechanically ventilated patients with SARS-CoV-2 infection and endotheliopathy, iloprost treatment had no detectable effect on inflammatory and T-cell-derived cytokine and growth-factor responses. The findings corroborate that the clinical benefit of iloprost is not attributed to anti-inflammatory effects. We suggest that future studies focus on patient selection for targeted treatment, and on combined treatment with anti-inflammatory and endothelium-stabilizing interventions, in patients with respiratory failure, hyperinflammation, and endotheliopathy.
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6. Obesity exacerbates cardiac oxidative stress and fibrosis upon coronavirus infection.
PMID:日期:2026-11-01Coronavirus diseases, particularly COVID-19, been associated with cardiac injury. Given that obesity is a well-known risk factor for severe cases with poorer outcomes, we hypothesized that cardiac involvement in a murine betacoronavirus infection would be exacerbated in pre-obese mice. To test this hypothesis, we fed mice a short-term (4-week) cafeteria diet (Caf), which resulted in increased body fat and mild cardiac histological damage, myocyte hypertrophy and fibrosis. Following the diet, we performed intranasal infection with MHV-A59 and evaluated the lungs and hearts eight days post-infection. In the lungs, infection was acute, caused moderate lung injury and was self-limited in both Chow-fed and Caf-fed mice with similar low viral loads recovered from this tissue. Meanwhile, cardiac fibrosis was significantly exacerbated in the Caf diet mice infected with MHV-A59. We also observed elevated levels of circulating cytokines, TNF and IL-10, as well as increased cardiac oxidative stress, solely in the obese infected mice. In contrast, isolated hearts from lean infected mice showed an increased response to β-adrenergic stimulation, which was damped in the Caf diet infected group. These findings indicate that obesity is a significant risk factor for cardiac issues caused by coronavirus infection by modulating local oxidative stress and systemic inflammation.
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7. Combinatorial therapy of LL-37 and ADSCs accelerates diabetic wound repair by orchestrating NRROS-mediated crosstalk between TGF-β/SMAD and hippo/TEAD1 axes.
PMID:日期:2026-11-01Diabetic wounds pose a significant therapeutic challenge. While the antimicrobial peptide LL-37 and adipose-derived stem cells (ADSCs) individually show potential for wound repair, the efficacy and mechanism of their combined treatment remain unclear. This study aimed to investigate the therapeutic effect of LL-37 combined with ADSCs on diabetic wound healing. Clinical samples from diabetic and non-diabetic patients were analyzed, combined with bioinformatics analysis of public datasets (GSE144441 and GSE182906) to identify key genes. A diabetic mouse wound model was established to validate the healing effects of individual and combined LL-37 and ADSCs treatments. In vitro assays, co-culture models were employed to explore the mechanisms involving ADSCs and fibroblasts. Analysis of human diabetic wounds revealed impaired healing associated with deficiency in cathelicidin antimicrobial peptide (CAMP), the precursor of LL-37. In diabetic mice, the combination of LL-37 and ADSCs promoted wound healing more effectively than either treatment alone. LL-37 enhanced ADSC viability in a dose-dependent manner. Mechanistically, LL-37 treatment significantly upregulated the expression of negative regulator of reactive oxygen species (NRROS) in ADSCs. Exosomes derived from these LL-37-primed ADSCs were taken up by fibroblasts, leading to increased NRROS expression in the recipient fibroblasts. Upregulated NRROS subsequently activated both the TGF-β/SMAD and Hippo/TEAD1 signaling pathways. Further experiments confirmed crosstalk between these two pathways, which collectively enhanced fibroblast proliferation and migration. In conclusion, the combination of LL-37 and ADSCs promotes diabetic wound healing by enhancing fibroblast activity. This effect is mediated through exosomal transfer of NRROS from ADSCs to fibroblasts, leading to the activation of the interconnected TGF-β/SMAD and Hippo/TEAD1 signaling pathways.
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9. A STAT3-dominant signalling signature associated with immune suppression in human visceral leishmaniasis is reversed by checkpoint blockade and STAT3 inhibition.
PMID:日期:2026-11-01Visceral leishmaniasis (VL) is associated with impaired Th1 responses, yet the intracellular signalling events linking immunosuppressive pathways to effector dysfunction remain poorly defined. We studied 150 adults in endemic northern Nigeria (50 active VL, 50 healed VL, 50 endemic controls) using flow cytometry, cytokine profiling, targeted RT-qPCR of 13 JAK-STAT pathway genes with dual reference gene normalisation, ex vivo checkpoint blockade, and phospho-flow cytometry for STAT1/STAT3 in both CD4+ T cells and CD14+ macrophages. Active VL was associated with reduced antigen-specific IFN-γ (220 versus 940 pg/mL in healed VL; P < 0.001), elevated IL-10, expanded regulatory T cells, transcriptional upregulation of STAT3 (2.66-fold, adjusted P < 0.001), and downregulation of its negative regulator SOCS3 (0.56-fold, adjusted P = 0.001). A STAT3-dominant phosphorylation profile was present in both CD4+ T cells (pSTAT1/pSTAT3 ratio 1.33) and, more prominently, CD14+ macrophages (ratio 0.51; Kruskal-Wallis P < 0.001 across disease groups). CD14+ pSTAT3 correlated with macrophage infection index (Spearman ρ = 0.52, P < 0.001), linking signalling state to effector function. Combined IL-10 and PD-1 blockade reversed the signalling imbalance in both compartments, restored IFN-γ production up to 4.8-fold, and reduced macrophage infection index by 42%. Pharmacological STAT3 inhibition with Stattic confirmed pSTAT3 reduction by phospho-flow cytometry (-33%, P < 0.001), reproduced transcriptional reprogramming comparable to checkpoint blockade for 9 of 13 genes, and enhanced macrophage parasite clearance (infection index -36%, P < 0.001). These findings across phosphoprotein, transcript, and functional levels identify a STAT3-dominant signalling signature spanning T-cell and macrophage compartments as a consistent feature of immune suppression in human VL and a candidate therapeutic target warranting investigation.
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10. Stage-resolved cytokine profiling nominates IL-17 as a prognostic node in relapsed/refractory B-cell lymphoma.
PMID:日期:2026-11-01B-cell non-Hodgkin lymphoma (B-NHL) and B-cell acute lymphoblastic leukemia (B-ALL) are highly heterogeneous malignancies. While immunochemotherapy and CD19 chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized the treatment of newly diagnosed (ND) and relapsed or refractory (R/R) disease, clinical outcomes remain inconsistent. This study aims to evaluate a baseline levels of 12-cytokine panel across the ND, R/R, and CAR-T cohorts to identify robust biomarkers predictive of treatment response and long-term prognosis. We enrolled 120 patients (ND B-NHL: n = 42; R/R B-NHL: n = 52; ND B-ALL: n = 10; R/R B-ALL: n = 21) and a separate cohort of 23 patients receiving CD19 CAR-T therapy. Plasma levels of 12 cytokines were quantified and analyzed using ROC curves, Kaplan-Meier survival analysis, and regression analyses to determine independent prognostic factors. Baseline cytokine profiling revealed that IL-17 was one of the four markers exhibiting significant inter-group differences (P = 0.034). In the R/R B-NHL cohort, high baseline IL-17 was significantly associated with inferior OS (log-rank P < 0.0001) and shorter progression-free survival (PFS) (P = 0.003). Univariate and multivariate Cox regression confirmed IL-17 as a significant risk factor for poor OS (HR = 1.802, P < 0.001) and PFS (HR = 1.279, P = 0.048) in R/R B-NHL. In CAR-T cohort, IL-17 levels also provided substantial discrimination for PFS (AUC 0.725). Our findings indicate that IL-17 may be a potential biomarker with stage-specific clinical associations in B-NHL. Its relevance may vary across disease stages, but overall, it warrants further investigation for risk stratification and individualized treatment monitoring.