Ask about this productRelated genes to: CCL5 antibody
- Gene:
- CCL5 NIH gene
- Name:
- C-C motif chemokine ligand 5
- Previous symbol:
- D17S136E, SCYA5
- Synonyms:
- RANTES, SISd, TCP228, MGC17164
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-03-01
Related products to: CCL5 antibody
Related articles to: CCL5 antibody
- This study applied a suite of human-relevant, non-animal cell models to investigate early events associated with respiratory sensitization induced by 4,4'-methylene diphenyl diisocyanate (MDI), a representative low-molecular-weight respiratory sensitizer. Phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 macrophage-like cells (THP-1M) and primary human monocyte-derived macrophages were exposed to MDI (3-300µM, 4h), resulting in a restricted cytokine response characterized primarily by enhanced IL-1α and IL-1β production. In contrast, lipopolysaccharide (LPS, 1 ng/mL-10 µg/mL) induced a pronounced pro-inflammatory response consistent with classical M1-like activation. Flow cytometric analysis of THP-1M indicated a partial M2a-like immunomodulatory phenotype following MDI exposure, characterized by increased CD1a and reduced CD14 expression. This response was accompanied by changes in selected central carbon metabolites, whereas LPS induced changes more consistent with M1-like activation. In human alveolar epithelial type I-like cells (hAELVi), MDI induced changes in selected central carbon metabolites, indicating epithelial metabolic responsiveness. In epithelial-macrophage coculture (hAELVi/THP-1M), metabolic responses to MDI were attenuated while chemokine production (CCL2, CCL5, CXCL8) was enhanced, suggesting macrophage-mediated modulation of epithelial responses and immune cell recruitment potential. In an air-liquid interface coculture model, these early responses were associated with dendritic cell-like activation of THP-1 cells, marked by OX40L upregulation, indicating Th2-skewing potential. Overall, the findings support interacting epithelial-immune key events relevant to respiratory sensitization and highlight the value of incorporating epithelial-immune interactions into new approach methods (NAMs) based hazard assessment. Short summary 4,4'-Methylene diphenyl diisocyanate (MDI) induced epithelial metabolic changes in vitro and promoted a partial M2a-like immunomodulatory macrophage response associated with alterations in central carbon metabolites. In epithelial-macrophage co-culture, macrophages attenuated metabolic responses while enhancing chemokine production, suggesting modulation of epithelial responses and immune cell recruitment potential. In an air-liquid interface co-culture model, these early events were associated with dendritic cell-like activation of THP-1 cells, marked by OX40L upregulation and indicative of Th2-skewing potential. Together, the findings support interacting key events relevant to proposed adverse outcome pathway concepts for respiratory sensitization and highlight candidate biomarkers and mechanistically relevant cellular responses that may support human-relevant NAM development for low-molecular-weight respiratory sensitizers. - Source: PubMed
Publication date: 2026/05/26
Blömeke BrunhildeLichter JuttaWeßendorf AnnaLobes NatalieJax MelinaAruna OsmondRolle-Kampczyk UlrikeEngelmann BeatriceBergen Martin vonBock Udo - BackgroundThird-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have become the first-line treatment for non-small cell lung cancer (NSCLC) with EGFR-sensitive mutations. The optimal treatment strategy after resistance to third-generation EGFR-TKIs still needs further exploration.MethodsThis retrospective study included patients with advanced lung adenocarcinoma who were consecutively enrolled at our hospital between January 2018 and July 2023. All patient data were fully de-identified prior to analysis, and no information that could directly or indirectly identify individual participants was included in this study. We evaluated the objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS), and overall survival (OS) across various treatment strategies. We also explored the tumor microenvironment (TME) in a subset of patients.ResultsA total of 206 patients were included. Chemo-antiangiogenesis (47.6%) achieved longer mPFS than chemo-immunotherapy (8.00 vs. 5.70 months, p=0.033), with higher ORR (34.7% vs. 16.7%, p=0.003). Median OS was shorter in the immunotherapy group (25.83 vs. 32.33 months, p=0.012). TME analysis (n=27) revealed an immunosuppressive profile (low PD-L1, CCL5, CD8, granzyme B; high Foxp3). In EGFR exon 21 L858R patients, EGFR-TKI continuation was inferior to chemotherapy (mPFS: 3.53 vs. 8.00 months, p=0.001; ORR: 10.5% vs. 40.3%, p=0.015; DCR: 27.4% vs. 69.2%, p=0.009). In oligoprogressive disease, EGFR-TKIs plus radiotherapy improved OS (37.23 vs. 27.77 vs. 25.83 months, p=0.045). Platelet count, LDH, D-dimer, and smoking history were independent predictors of poor prognosis.ConclusionsChemo-antiangiogenesis remains a key treatment option after resistance. For oligoprogressive disease, continuing EGFR-TKIs with local radiotherapy may provide superior survival benefit. Chemo-immunotherapy appears less effective, potentially due to an immunosuppressive TME. Prospective validation is warranted. - Source: PubMed
Publication date: 2026/05/27
Li XinyueDing KaiboLiu DujiangSong RuiqiPeng ZhongshengXu YanjunLu Yi - Extracellular vesicles (EVs) are naturally occurring nanoparticles secreted by diverse cell types and are increasingly explored as delivery vehicles and immunomodulatory platforms. Rigorous preclinical safety and immunotoxicological evaluation is therefore essential prior to clinical translation. Here, using a modified OECD 423 acute toxicity class method, we assessed the toxicity of EVs loaded with glucose oxidase (GOX) along with T-dependent antibody response (TDAR) analyses in repeated-dose toxicity studies. - Source: PubMed
Publication date: 2026/05/11
Grudzinski Ireneusz PBamburowicz-Klimkowska MagdalenaSochanowicz BarbaraBrzoska KamilProchorec-Sobieszek MonikaCabaj MarzenaTargonska AlicjaStawarska AgnieszkaKruszewski Marcin - Head and neck squamous cell carcinoma (HNSCC) frequently resists PD-1 blockade due to an immunologically "cold" tumor microenvironment (TME). Here, we identify Z-DNA binding protein 1 (ZBP1) as a key immunoregulator that reprograms immune-suppressive TMEs. Integrated TCGA/SangerBox analyses revealed ZBP1 as a hub gene strongly correlated with cytotoxic CD8+ T cells (r = 0.48, p < 0.0001) and M1 macrophages (r = 0.39, p < 0.0001). Multi-model validation in 92 HNSCC specimens revealed elevated ZBP1 expression versus normal tissues (p < 0.01), co-localized with infiltrating CD8+/CD4+ T cells and CD68+ macrophages through multiplex immunofluorescence. Clinically, high ZBP1 predicted improved survival (HR = 0.61 for overall survival; HR = 0.45 for disease specific survival; p < 0.0001) and early-stage presentation (p = 0.004). Mechanistically, ZBP1 overexpression in SCC-7/MOC2 models suppressed tumor growth while enhancing IFN-γ+ CD8+ T cell activation and reducing M2 polarization (CD206+: 16.91% vs 38.19% in ZBP1-high vs control, p < 0.001). Single-cell transcriptomics uncovered ZBP1-driven TME remodeling through chemokine signaling networks and expanded effector T cell compartments, validated by 1.49-fold increased CD8+ T cell infiltration via flow cytometry. Spatial analysis revealed ZBP1 overexpression amplified immune cell crosstalk (1.65-fold interaction increase, p < 0.001), upregulating CD8+ T cell chemotaxis (CXCR3/CCR5-CCL5 axis) and effector functions (p < 0.0001). Concurrently, it suppressed immunosuppressive pathways (ARG1 ↓ /IDO1↓) through metabolic reprogramming, establishing ZBP1 as a dual regulator synchronizing lymphocyte recruitment and myeloid suppression. Our integrative approach bridges computational biology with functional validation, demonstrating ZBP1's capacity to convert "cold" tumors into immunologically active niches. This work positions ZBP1 as both a stratification biomarker for checkpoint inhibitor response and a therapeutic target for TME reprogramming in HNSCC. - Source: PubMed
Publication date: 2026/05/26
Min YuSong GeYang LianlianHe LingXu ShihongGao KunLiu ZheranPeng XingchenDai Lei - Trigeminal neuralgia (TN) is a debilitating neuropathic pain disorder traditionally attributed to neurovascular compression; however, this mechanism does not fully explain the marked clinical heterogeneity or persistent pain observed in a subset of patients. Increasing evidence suggests that central neuroinflammatory processes contribute to neuropathic pain, but immune profiles in the cerebrospinal fluid (CSF) and serum of patients with TN remain poorly characterized. - Source: PubMed
Publication date: 2026/05/08
Liu HongLiu Zi-WeiZhang Jiang-TaoWang Xue-LongChen Li-HuaJin Xiao-HongLiu TongJi Fu-Hai