Human RANTES (CCL5)
- Known as:
- Human RANTES (CCL5)
- Catalog number:
- GEM-300-180P20
- Product Quantity:
- 20 ug
- Category:
- -
- Supplier:
- SeraLab
- Gene target:
- Human RANTES (CCL5)
Related genes to: Human RANTES (CCL5)
- 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: Human RANTES (CCL5)
Related articles to: Human RANTES (CCL5)
- Although immune checkpoint blockade (ICB) represented by anti-PD-1 therapy has demonstrated significant clinical benefits, its efficacy remains limited by the immunosuppressive tumor microenvironment (TME). Our study revealed that the combination of Cryo-thermal therapy (CTT) and anti-PD-1 therapy suppresses the distal tumor growth compared to either cryoablation or radiofrequency ablation combined with anti-PD-1 therapy. Mechanistically, CTT specifically induces TNF-α production in mature myeloid cells, triggering autocrine CCL5 secretion that recruits peripheral IFN-γ T cells induced by CTT in distal tumors, creating a cytokine loop in which IFN-γ derived from T cells and TNF-α derived from myeloid cells collectively promote CCL5 secretion in myeloid cells to increase effector T-cell recruitment in distal tumors. After CTT, anti-PD-1 treatment amplifies this cascade by enhancing TNF-α production in T cells. The parallel activation of STAT1 by IFN-γ and NF-κB by TNF-α in myeloid cells converges to drive IRF7-dependent CCL5 upregulation to create a local immune enhancing environment via CCL5-mediated recruitment of T cells. Our study demonstrates that CTT establishes an immunologically favorable TME by reprogramming immunosuppressive myeloid cells into mature myeloid cells with high CCL5 production, thereby facilitating effector T-cell recruitment, providing an efficient therapeutic strategy to promote the response to anti-PD-1 therapy. - Source: PubMed
Publication date: 2026/09/30
Hao YuankaiZhang ZeluWang ShichengWang KeLiu XiaohuiLiu Ping - Codonopsis polysaccharides exhibit diverse biological activities, but their antiviral effects against the H1N1 influenza A virus and how these activities change after sulfation modification remains unclear. In this study, crude Codonopsis polysaccharide (COP) was obtained via water extraction and alcohol precipitation, and COP-1 (2.1 × 103 Da, β-D-(2 → 1)-fructan) was isolated and purified. Both COP and COP-1 were modified by sulfation using the sulfur trioxide-pyridine method, yielding derivatives SCOP and SCOP-1 with degrees of substitution of 1.792 and 1.403, respectively. Antiviral activity was evaluated in MDCK cells using MTT and TCID₅₀ assays, revealing that COP, SCOP, and SCOP-1 all inhibited H1N1 replication, with sulfation significantly enhancing antiviral activity. Time-of-addition experiments indicated that inhibition occurred during the early phase of infection (0-4 h). Annexin V-PI staining confirmed that these compounds reduced virus-induced early apoptosis. In H1N1-infected A549 cells, they suppressed NF-κB p65 phosphorylation and downregulated the expression of IL-6, IL-8, MCP-1, CCL-5, TNF-α, and TRAIL. Overall, Codonopsis polysaccharides and their sulfated derivatives exert anti-influenza effects through a triple mechanism involving inhibition of early viral replication, anti-apoptotic activity, and anti-inflammatory action, making them promising candidates for antiflu therapeutics. - Source: PubMed
Publication date: 2026/10/01
Song Ya-HuiMao Fang-QinLiu Meng-FanLiu Zhang-QuanXin Qing-YanYu Lan - Ischemic stroke (IS) triggers neuroinflammation cascades where microglial polarization is a pathological determinant. Mailuoning oral liquid (MLN O) is clinically utilized to prevent thrombosis and treat convalescent IS, but its pharmacological targets in permanent IS remain unclear. - Source: PubMed
Publication date: 2026/09/30
Liu XiaoqiongLin YandanLi JianJiang HongSui YihangLi YueyuanFan LinglingChen HaiTan Ninghua - Despite a myriad of medicinal breakthroughs in lipid-lowering and antithrombotic therapies, cardiovascular diseases (CVDs) are still the main killers worldwide. According to the consolidated scientific evidence, atherosclerosis, ischemic heart disease, and other vascular pathologies are attributed to endothelial dysfunction and vascular inflammation. The standard treatments' failure to adequately control the inflammatory and endothelial pathways has led researchers to biologics that are molecularly specific. Nanobodies (Nbs) are single-domain antibody fragments obtained from camelid heavy-chain antibodies. Due to their small size, good tissue penetration, and stability, they are regarded as therapeutic agents and diagnostic tools. This paper is focused on the current and potential future uses of nanobodies in the treatment of endothelial activation, the blockade of adhesion molecule expression, and the management of cytokine-induced vascular inflammation. The literature shows that diagnostic nanobody tracers achieve high accuracy for vascular inflammation imaging, yet therapeutic Nbs exist only in preclinical stages. PANX1-blocking Nbs show promise for treating ischemia-reperfusion injury, and IL-1β-targeted Nbs demonstrate effectiveness in reducing hypoxia-induced damage to endothelial cells. The therapeutic potential of Nbs has been proven by caplacizumab, which functions as an anti-vWF nanobody, but its approved medical use exists only for hematologic disorders. The therapeutic potential of Nbs remains unexplored for ROS, ox-LDL, AT1R, and chemokines CCL2 and CCL5 because researchers have not developed corresponding nanobody-based interventions. The review demonstrates how nanobody engineering advances combined with current molecular knowledge create a promising yet underdeveloped therapeutic area for cardiovascular medicine, which could use precise biologic treatments to restore vascular equilibrium and fight inflammation, thus transforming future CVD treatment approaches. - Source: PubMed
Publication date: 2026/09/15
Aljaezi Ibrahim - Natural compounds with anti-inflammatory properties are increasingly explored as therapeutic agents due to their lower risk of side effects compared with conventional drugs. Fisetin, a dietary bioflavonol abundant in fruits and vegetables, exhibits anti-inflammatory activity in several cell types, including murine macrophages. However, its effects on human macrophages remain unclear. In this study, human pro-inflammatory M1 macrophages were generated from THP-1 monocytes using PMA, LPS, and IFN-γ. The effects of fisetin on cytokine and chemokine secretion, reactive oxygen species (ROS) production, apoptosis, and phagocytic activity were evaluated. In addition, the NF-κB, MAPK, and NLRP3 inflammasome pathways were analyzed. This study shows that fisetin pre-treatment significantly suppressed LPS/IFN-γ-induced secretion of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IL-8) and chemokines (MCP-1, CCL5, CXCL9, CXCL10). It also reduced ROS generation, NLRP3 inflammasome activation, and phagocytic activity. Mechanistically, fisetin inhibited NF-κB activation as well as JNK/MAPK and p38/MAPK signaling, indicating that its anti-inflammatory actions are mediated through multiple pathways. Importantly, fisetin did not affect the viability or proliferation of THP-1-derived macrophages, suggesting that reduced cytokine release was primarily due to attenuation of macrophage polarization rather than cytotoxicity. Fisetin attenuates inflammatory responses in human M1 macrophages through suppression of NF-κB, MAPK, and NLRP3 inflammasome signaling. By limiting cytokine release, ROS production, and phagocytic activity without impairing cell survival, fisetin emerges as a promising natural candidate for managing chronic inflammatory disorders, including atherosclerosis, neurodegenerative diseases, and inflammatory bowel disease. - Source: PubMed
Onpan NattayaLorthongpanich ChanchaoKheolamai PakpoomChingsuwanrote PimjaiRodboon NapachaiLuanpitpong SudjitSaisawang ChontichaIssaragrisil Surapol