Ask about this productRelated genes to: CCR5 antibody
- Gene:
- CCR5 NIH gene
- Name:
- C-C motif chemokine receptor 5 (gene/pseudogene)
- Previous symbol:
- CMKBR5
- Synonyms:
- CKR-5, CC-CKR-5, CKR5, CD195, IDDM22
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-15
- Date modifiied:
- 2019-01-10
Related products to: CCR5 antibody
Related articles to: CCR5 antibody
- Invasion and metastasis in multiple solid tumors are promoted by collective invasion which is organized by leader and follower cells. Yet in colorectal cancer (CRC), biomarkers and mechanisms that specify leader cells remain undefined. Here we identify biomarkers of leader cells and elucidate how they drive CRC collective invasion and metastasis. Using a 3D photoconvertible CRC spheroid model, we isolated leader and follower cells. Transcriptomic, functional and in vivo assays show that GLUT1, PLOD2, and CCL5 in leader cells are indispensable for collective invasion. CCL5 activates PI3K/AKT signaling to up-regulate GLUT1 and PLOD2 in leader cells. Moreover, GLUT1 and CCL5 could serve as specific biomarkers for leader cells in CRC collective invasion, and their co-expression correlates with poor prognosis. Pharmacologic inhibition of GLUT1 and CCL5-CCR5 impairs collective invasion. CCL5 and GLUT1 may define the leader cells and are required for CRC collective invasion as potential key regulators of metabolic shifts and collagen deposition. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/08/12
Zhang ZhaowenTan JiayingZeng ZhichengZhu XiaohuiMai LiyaoYin YaoHuang YutingKang WeiJiang HonghuiXu ShaowanDing YanqingPan XinghuaWang FeifeiLiang Li - Few studies have evaluated the impact of organ-specific tumor microenvironments (TMEs) on clinical outcomes in diffuse large B-cell lymphoma (DLBCL). This study investigated potential molecular markers, the immune cell composition within the TME, and their associations with clinical outcomes in patients with primary intestinal DLBCL (PI-DLBCL). We initially analyzed RNA expression in tumor cells from 19 patients with PI-DLBCL in the experimental cohort. Candidate biomarkers were then assessed in lymphoma tissue from a total of 48 patients in the same cohort, including the 19 with RNA-expression data, and validated in an independent cohort of 29 patients with PI-DLBCL. Associations between these markers and clinicopathological features, event-free survival (EFS), and overall survival (OS) in the two cohorts were analyzed. In the RNA expression panel, CCL5 expression was higher in patients with advanced-stage PI-DLBCL and was associated with inferior EFS and OS. Its principal receptor, CCR5, expressed in approximately one-third of patients, was associated with lower complete response rates to first-line immunochemotherapy: 50% in the experimental cohort and 10% in the validation cohort and correlated with the 7-year worse OS rate in both the experimental (49.8% versus 71.4%, p = 0.082) and validation (0% versus 76.2%, p < 0.001) cohorts. In both the experimental and validation cohorts, CCR5-positive tumors exhibited decreased CD86-positive (M1-like) and increased CD206-positive (M2-like) macrophage infiltration, consistent with an immunosuppressive TME. Multivariate analyses revealed that CCR5 expression was independently associated with worse EFS (p < 0.001) and OS (p = 0.004) in patients with PI-DLBCL (combined experimental and validation cohorts). CCR5 expression indicates a biologically aggressive subtype of PI-DLBCL with poor clinical outcomes and M2 macrophage-dominant immunosuppression. - Source: PubMed
Ma Wei-LiChen Tsai-YunFu Pei-AnChen Jo-PaiYao MingWang Hsiu-PoLin Been-RenLin Chung-WuHsu Chia-LangHuang Chung-YuCheng Ann-LiiKuo Sung-Hsin - Lack of access to antiretroviral therapy (ART) leads to the transmission of human immunodeficiency virus in ~120,000 children annually, emphasizing the need for new strategies to prevent lifelong infection. Here in an infant rhesus macaque model of peripartum oral infection, we show that broadly neutralizing antibodies directed to the viral envelope protein were insufficient to prevent latent reservoir establishment, independent of daily ART. Blockade of the human immunodeficiency virus co-receptor CCR5 via the antibody leronlimab also failed to prevent reservoir establishment, but it significantly reduced reservoir seeding in lymphoid and gastrointestinal tissues. Following the treatment of infants with viraemia at 72 h post-infection with the combination of broadly neutralizing antibodies, ART and leronlimab, no subsequent evidence of replicating or latent virus and antiviral immunity was observed 1 year after treatment interruption. These findings suggest a synergy between broadly neutralizing antibodies, ART and CCR5 blockade for preventing viral reservoir establishment and offer potential improvements over current therapies for newborns exposed to human immunodeficiency virus. - Source: PubMed
Publication date: 2026/08/10
Sacha Jonah BOrdonez TracyPandey ShilpiWebb GabrielaBarnette PhilipPessoa CleitonHumkey Matthew CReed JasonMorehead AndenWatanabe Jennifer KUsachenko Jodie LVijayan ShrivaasFazio AltairSidener HeatherLewis Anne DPastenkos GabrielleOjha SohitaBarber-Axthelm AaronSwan BellaBochart RacheleMascola John RPegu AmarendraFray Emily JWolters Rachael MSiliciano Janet DSiliciano Robert FHansen Scott GVan Rompay Koen K AHessell Ann JHaigwood Nancy L - Dyslipidemia, inflammation and angiogenesis pathways contribute to the genetic susceptibility to diabetic nephropathy (DN) in type 2 diabetes mellitus (T2DM). This study investigated the association of common genetic variants; Apolipoprotein C1 (APOC1) rs4420638, C-C chemokine receptor type 5 (CCR5) rs1799987, C-X-C motif chemokine ligand 8 (CXCL8) rs4073, Matrix metallopeptidase 9 (MMP9) rs17576, Erythropoietin (EPO) rs1617640 and Vascular Endothelial Growth Factor A (VEGFA) (rs833061 and rs3025039) with DN susceptibility in Tunisian T2DM patients. - Source: PubMed
Publication date: 2026/08/10
Moussa AmiraMethnani JabeurHassine RefkaAbbes HouwaidaAmmar MariemBjaoui WidedTriki SoniaKoubaa AfifaAmor DorraRejeb Nabila BenNeffati FadouaNajjar Med-FadhelBouslama AliOmezzine Asma - Traumatic brain injury (TBI) involves both primary and secondary pathological processes, including hemorrhage, ischemia, edema, and neuroinflammation. Although tissue-derived exosomes have emerged as important mediators of intercellular communication within local tissue microenvironments, their role in TBI-associated inflammatory responses remains incompletely understood. This study integrated brain tissue-derived exosomal proteomics with publicly available hippocampal transcriptomic data to investigate the potential association between tissue-derived exosomes and chemotaxis-related inflammatory responses after TBI. Brain tissue-derived exosomes were isolated, characterized, and subjected to label-free proteomic analysis. Public hippocampal transcriptomic data from GSE173975 were analyzed, and differentially expressed proteins (DEPs) and genes (DEGs) were identified from the exosomal proteomic and transcriptomic datasets, respectively. Functional enrichment, co-enrichment, and protein-protein interaction network analyses were performed, followed by quantitative real-time PCR, exosomal western blotting, and Transwell migration assays for validation and functional assessment. In total, 190 DEPs and 465 DEGs were identified. Co-enrichment analyses highlighted immune- and inflammation-related processes, particularly chemotaxis-related processes and chemokine signaling. LGALS3 and ITGB2 were increased at the exosomal protein level in brain tissue-derived exosomes from TBI rats and also showed increased hippocampal mRNA expression, whereas CCL2, CCL3, and CCR5 were upregulated at the hippocampal mRNA level. Functionally, TBI-derived exosomes enhanced BV2 microglial migration in vitro. Overall, these findings suggest that injury-associated brain tissue-derived exosomes may be associated with chemotaxis-related inflammatory and pro-migratory responses after TBI. - Source: PubMed
Publication date: 2026/08/10
Chen Wei-CanChen Xin-LiLin Cheng-YeHuang Yang-ZiHe He-FanZhou Yi-LinLiu Yi-Bin