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
- Pregnancy elicits extensive remodeling of the mammary gland to establish the alveolar network required for lactation, yet the cellular programs underlying this transition in pigs remain poorly resolved. Here, we generated a single-cell transcriptomic atlas of the porcine mammary gland across gilt, late pregnancy, and post-lactational stages. Differential expression analyses identified epithelial, fibroblast and endothelial compartments as the most dynamic during pregnancy, motivating higher-resolution analyses of these lineages. Epithelial trajectories toward alveolar fate exhibited induction of fibrillar collagen programs, including , and , implicating epithelial contributions to extracellular matrix assembly. Fibroblast analysis revealed a PGLYRP1 fibroblast subtype enriched for the chemokines , and , suggesting a role in immune cell recruitment. Endothelial cells undergo stage-specific metabolic reprogramming, with late pregnancy characterized by increased expression of glycolysis-associated genes, including , and , as well as lipid metabolism-related genes such as , and . Cross-species comparison revealed conserved cellular identities and key molecular features ( , , ) across human, pig, and mouse mammary glands. Together, this atlas delineates the cellular logic underlying pregnancy-associated remodeling and serves as a resource for elucidating transcriptomic changes in the porcine mammary gland. - Source: PubMed
Yang Si-YuYao Tian-XiongHuang Lu-Sheng - Insufficient T-cell infiltration is a major barrier to the efficacy of immune checkpoint inhibitors (ICIs) in lung adenocarcinoma (LUAD). We aimed to investigate how the tumor-intrinsic mC methyltransferase NSUN2 shapes the immune landscape of LUAD. - Source: PubMed
Publication date: 2026/09/07
Meng WangyangLu TongDu MingyuanDai XinHan YichaoLi YingyiXu HaiminYang BiaolongWang ZeyuDu HaileiLiao KemanLiu XinnanSun YidanYang CuiDong DongYan YanGuo WeiLi BinLi Hecheng - Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) affects millions of men, yet the immune circuits that sustain sterile prostatic inflammation and pain remain poorly defined. Here we identify a T cell-macrophage metabolic signaling axis that drives chronic prostatitis. Integrated analysis of mouse experimental autoimmune prostatitis, chronically inflamed human prostate tissue, single-cell transcriptomes and spatial profiles revealed a population of glycolytic, HIF-1α-activated inflammatory macrophages enriched in diseased prostate niches. T cell-derived CCL5 was markedly induced and spatially positioned adjacent to CCR5 macrophages, where it licensed M1-like polarization, glycolytic remodeling and inflammatory transcription. Using T cell-specific Ccl5 knockout mice, we established CCL5 as a genetic driver of macrophage inflammation, prostate tissue injury and pelvic pain hypersensitivity, and these pathogenic features were further suppressed by CCL5 neutralization or pharmacological CCR5 blockade. Mechanistically, rmCCL5 stimulation promoted CCR5-sensitive ERK1/2 activation, PKM2 Ser37 phosphorylation and nuclear accumulation, enhanced the PKM2-HIF-1α interaction, and increased HIF-1α occupancy at the Il1b and Nos2 promoters. Targeting ERK1/2, PKM2 remodeling or HIF-1α collapsed this program and protected against prostatitis pathology. Together, these findings show how T cell-derived chemokine signals are translated into macrophage metabolic reprogramming and persistent inflammatory activation, nominating the CCL5-CCR5-ERK-PKM2/HIF-1α pathway as a genetically validated and pharmacologically tractable therapeutic axis in CP/CPPS. - Source: PubMed
Publication date: 2026/09/03
Liu XianhongLi BoyangDou XianchaoJu WenyueLiu WeihaoZhang FeiJin ChenLu YifengWang RonghaoChen XianguoLiang ChaozhaoZhang Meng - Oxidative stress induced by inhaled oxidants, particularly cigarette smoke, contributes to the development of several acute and chronic respiratory diseases through oxidative damage and epigenetic alterations. Curcumin (CUR), a well-characterized natural polyphenol with potent antioxidant and anti-inflammatory properties, is considered a promising agent for modulating oxidative stress-related signaling pathways and epigenetic mechanisms; however, its poor aqueous solubility and bioavailability limit its clinical application. Therefore, in the present study, PEGylated curcumin (PEG-CUR) was investigated as a modified CUR formulation for subsequent incorporation into a dissolving microneedle-based intranasal delivery system. Exposure to cigarette smoke resulted in significant alterations in the expression of oxidative stress-related genes (SEPP1, NCF2, SFTPD, CCL5, and PTGS1) in nasal epithelial cells. However, pretreatment with curcumin (CUR) and polyethylene glycol-curcumin (PEG-CUR) mitigated these gene expression changes. Both treatments also reduced global DNA methylation, with PEG-CUR showing a more pronounced effect than CUR. Following the demonstration of the beneficial effects of PEG-CUR, we developed PEG-CUR-loaded dissolving microneedle patches (PEG-CUR-DMNPs) as a localized intranasal delivery platform designed to facilitate PEG-CUR delivery through rapid dissolution of the microneedle tips. The mechanical robustness and penetration capability of the patches were initially evaluated using Parafilm® and ex vivo rat dorsal skin models. To further confirm their appropriateness for intranasal use, PEG-CUR-DMNPs were subsequently tested on ex vivo sheep nasal mucosa to evaluate microneedle penetration and dissolution kinetics. Overall, these results indicate that PEG-CUR-DMNPs represent a promising approach for localized intranasal drug delivery targeting oxidative stress-related respiratory diseases. - Source: PubMed
Publication date: 2026/09/05
Kilic BusraBilgic Hayriye AkelUnal Bugra KaganMerdivenli OnurUzun CengizCakmak SonerAydin Halil MuratKaraaslan Cagatay - Small extracellular vesicles (sEVs) derived from tubular epithelial cells (TECs) are important mediators of tubular-immune cell communication in diabetic nephropathy (DN). However, the RNA cargo involved in TEC-macrophage inflammatory communication remains incompletely understood. This study investigated whether sEV-associated CCL5 mRNA contributes to inflammatory communication between TECs and macrophages in DN. - Source: PubMed
Publication date: 2026/09/05
Xie LuyangYe JianHe ShanYang LanChen QinkaiHuang JiayanZhao QingWang Yu