CCR5 Antibody
- Known as:
- CCR5 Antibody
- Catalog number:
- 1112
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CCR5 Antibody
Related 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
- CCL5, abbreviated from C-C motif chemokine ligand 5, exerts diverse regulatory effects on both the initiation and progression of breast cancer (BC), making it a focal point of extensive research within the field. By enhancing the growth, invasive ability, and metastatic potential of BC cells, simultaneously recruiting and polarizing immunosuppressive cell populations, CCL5 actively reshapes the tumor immune microenvironment. Furthermore, elevated CCL5 levels are strongly linked to particular clinicopathological parameters, worse clinical outcomes, and a higher likelihood of recurrence in BC, suggesting its value in early diagnosis and prognosis. Current preclinical studies targeting the CCL5/CCR5 axis have demonstrated notable efficacy in inhibiting the progression of BC. This article explores how CCL5 contributes to BC progression and elucidates its regulatory mechanisms, providing theoretical support and potential targets for innovative therapeutic approaches. - Source: PubMed
Publication date: 2026/08/06
Mu JiaYingZhang MeiZhiChen QianLiu WeiDongFeng WeiKeZhang YaNan - Neonatal and adult platelets are functionally different, with neonatal platelets being comparatively hypo-reactive to multiple platelet agonists. When transfused, neonates receive platelets from adult donors, resulting in a cellular developmental mismatch. Platelets are key regulators of the monocyte inflammatory response, yet how the developmental stage of the platelet affects this response is unknown. In this study, we modeled this developmental mismatch to investigate the neonatal (cord blood) monocyte inflammatory response and migratory phenotype after exposure to either neonatal (cord blood) or adult platelets. Adult platelets expressed more P-selectin on the surface and released more beta-2-microglobulin (B2M) after activation compared to neonatal platelets. While exposure to platelets of either developmental stage increased the release of IL-8 and MCP-1 from neonatal monocytes to a similar degree, exposure to adult platelets induced significantly greater monocyte CCR2 and CCR5 surface expression, consistent with a pro-migratory monocyte phenotype. Blocking P-selectin/PSGL-1 interactions had no effect on platelet induced monocyte cytokine release but completely abrogated monocyte CCR2 and CCR5 surface upregulation. These findings suggest that the monocyte pro-migratory phenotype is regulated by P-selectin exposure, which is influenced by the platelet developmental stage, while monocyte cytokine release is independent of platelet P-selectin expression or developmental stage. - Source: PubMed
Publication date: 2026/09/22
Soule-Albridge ErinFlahardy EmilyFeldman Henry AKane NatalieBanfield KimberleyEl Nems AmaliaRomero Escobar JesselinSola-Visner MarthaDavenport Patricia - To evaluate whether high-intensity interval training (HIIT) modulates NLRP3 inflammasome expression, monocyte subtypes and chemokine receptor profiles in adults with obesity. Prospective randomised controlled trial. Sedentary adults with obesity (n = 109, 82.6% women), aged 18-60 years, were randomised to an 8-week HIIT programme (three sessions/week) or to a nontrained control group. Expression of the NLRP3 inflammasome, characterisation of monocyte subset distribution and chemokine receptor expression (CCR2, CCR5 and CX3CR1) were assessed at baseline and after 8 weeks by flow cytometry. Intermediate monocytes increased within the control group (p = 0.006) but remained unchanged after HIIT and were significantly higher in the control than in the trained group at T1 (p = 0.014). Nonclassical monocytes increased within the trained group (p = 0.016) and decreased within the control group (p = 0.018). NLRP3 expression in circulating monocytes increased within the control group after 8 weeks (p = 0.028), with no significant change within the trained group; however, the between-group comparison at T1 was not significant (p = 0.857). Expression of CCR2 in intermediate monocytes increased within the control group, with no significant changes after HIIT. HIIT was associated with prevention of the shift toward a pro-inflammatory monocyte profile-most robustly, a between-group difference in intermediate monocytes. These findings suggest a modulatory role of exercise on monocyte-driven inflammatory responses, independent of changes in body composition, in a predominantly female cohort. Trial Registration: Brazilian Registry of Clinical Trials-ReBEC number RBR-8vfxfqd. - Source: PubMed
Publication date: 2026/09/21
Abreu Daniela A deSilveira Ana Luíza P AVieira Stella de SFonseca Francisco A HIzar Maria CristinaAmaral Jônatas B doFrança Carolina N - The programmed death-ligand 1 (PD-L1) antibody, while revolutionizing oncology through immune checkpoint blockade, is increasingly associated with clinically significant cardiac immune-related adverse events (irAEs). This study systematically investigates the early cardiotoxic effects of PD-L1 inhibition using murine models, revealing through integrated cardiac functional assessments (systolic performance, myocardial deformation, and electromechanical synchronicity) and spatial transcriptomics that PD-L1 antibody treatment acutely disrupts cardiac synchronicity and contractile function. Mechanistic profiling identified monocyte-derived C-C motif chemokine receptor 5-positive (CCR5) macrophage proliferation driven by PD-L1-induced C-C motif chemokine ligand 5 (CCL5) chemokine signaling, with flow cytometry/immunofluorescence confirming CD45CD11bF4/80CCR5 macrophage infiltration in treated myocardium. Therapeutic intervention with the CCR5 antagonist maraviroc demonstrated multi-modal cardiac protection: attenuating cardiac dysfunction, reducing CCR5 macrophage recruitment, suppressing CCL5 overproduction, and modulating redox/apoptosis pathways through hypoxia-inducible factor 1α (HIF-1α)/pyruvate kinase isozyme type M2 (PKM2) Y105 phosphorylation regulation and apoptosis inhibition. Notably, although maraviroc failed to potentiate the anti-tumor effect of PD-L1 therapy, it effectively attenuated the PD-L1-associated myocardial toxicity without diminishing the anti-tumor response in melanoma-bearing mice. These findings delineate a CCL5/CCR5 axis as the central mechanism underlying early PD-L1-induced cardiotoxicity, while establishing CCR5 blockade as a translatable strategy for preventing immunotherapy-associated cardiac complications, with maraviroc demonstrating pleiotropic protective effects spanning immune modulation, metabolic reprogramming, and apoptosis control. - Source: PubMed
Publication date: 2026/09/19
Lin JialeSong FeiYuan QianLi Yun-DaChen RuolanTang JianWang YutianWu Wei-YinCai BinniLi Gang - Diabetic gastroparesis (DGP) is characterized by delayed gastric emptying and limited mechanism-based therapies. Pyloric dysfunction has been associated with loss of interstitial cells of Cajal (ICC) and altered muscularis macrophage polarization. This study examined whether early growth response 1 (EGR1) links macrophage polarization to ICC integrity in DGP. - Source: PubMed
Xie NiSu GuanhaoWu YingPeng KuiMei ZhuChen WeiXu KaiLi Baiwen