CCL5是一種趨化因子，也稱RANTES（調(diào)節(jié)活化的細(xì)胞產(chǎn)生的趨化因子），它可以引導(dǎo)白細(xì)胞到達(dá)感染或組織損傷的部位，從而參與炎癥反應(yīng)。近年來的研究表明，CCL5不僅參與炎癥反應(yīng)，還與腫瘤發(fā)生和發(fā)展密切相關(guān)。例如，一些研究表明CCL5參與了癌細(xì)胞的侵襲和轉(zhuǎn)移，并且高表達(dá)的CCL5與腫瘤預(yù)后不良有關(guān)。

Chemoattractant for blood monocytes, memory T-helper cells and eosinophils. Causes the release of histamine from basophils and activates eosinophils. May activate several chemokine receptors including CCR1, CCR3, CCR4 and CCR5. One of the major HIV-suppressive factors produced by CD8+ T-cells. Recombinant RANTES protein induces a dose-dependent inhibition of different strains of HIV-1, HIV-2, and simian immunodeficiency virus (SIV). The processed form RANTES(3-68) acts as a natural chemotaxis inhibitor and is a more potent inhibitor of HIV-1-infection. The second processed form RANTES(4-68) exhibits reduced chemotactic and HIV-suppressive activity compared with RANTES(1-68) and RANTES(3-68) and is generated by an unidentified enzyme associated with monocytes and neutrophils. May also be an agonist of the G protein-coupled receptor GPR75, stimulating inositol trisphosphate production and calcium mobilization through its activation. Together with GPR75, may play a role in neuron survival through activation of a downstream signaling pathway involving the PI3, Akt and MAP kinases. By activating GPR75 may also play a role in insulin secretion by islet cells.

1. These CCL5 derivatives may now be tested against several inflammation-related pathologies where the CCL5:CCR5 axis plays a relevant role. PMID: 29382912
2. The CCL5 In1.1T/C polymorphism may modulate pulmonary early-onset tuberculosis risk. PMID: 29608337
3. We use CPRC prostate cancer model and demonstrate that endothelial cells secrete large amount of CCL5 and induces autophagy by suppressing AR expression in prostate cancer cell lines. Consequently, elevated autophagy accelerates focal adhesions proteins disassembly and promoted prostate cancer invasion. Inhibition of both CCL5/CCR5 signaling and autophagy significantly reduces metastasis in vivo PMID: 30200999
4. CCL5, from endothelial cells, acts in a paracrine fashion on triple-negative breast cancer (TNBC) cells to enhance their migration, invasion, and metastasis. CCL5, in turn, accelerates TNBC cell secretion of PAI-1 and promotes TNBC cell metastasis, thus forming a positive feedback loop. Moreover, this enhanced metastatic ability is reversible and dependent on CCL5 signaling via the chemokine receptor, CCR5. PMID: 28899878
5. high concentration of plasma CCL5 may promote EMT of breast cancer cells. Plasma CCL5 could be a promised candidate to predict chemotherapy response in NCT of LABC. PMID: 29758926
6. The polymorphism of CCR1 rs3733096 and CCL5 rs3817656 are associated with spontaneous clearance of hepatitis C virus in Chinese Han population. PMID: 29703961
7. Our results suggested that the CCL5 level was influenced collectively not only by the genotypes of -403G>A SNP and bacillary load but also by the treatment. Thus, CCL5 may be considered for the development of a diagnostic marker and also as an indicator of recovery. PMID: 29664036
8. serum levels in active vitiligo significantly elevated compared to those in stable vitiligo patients PMID: 29115683
9. these findings collectively indicate that TGF-beta regulates CCL5 expression in a stage-dependent manner during breast cancer progression PMID: 29107385
10. KLF5-regulating cancer-associated fibroblasts affect gastric cancer cells progression by CCL5 secretion and activation of CCR5. PMID: 28934010
11. Data show that plasminogen activator inhibitor-1 (PAI-1) and chemokine CCL5 (CCL5) overexpression promoted cell proliferation and migration in breast cancer cells. PMID: 29601121
12. Among infants with lower CCL5 levels, the Haemophilus-dominant microbiota profile was associated with a higher risk of intensive care use and hospital length-of-stay >/=3 days compared to the Moraxella-dominant profile. Conversely, among those with higher CCL5 levels, there were no significant associations between the microbiota profiles and these severity outcomes PMID: 28306146
13. The current study suggests that TLR3 signaling induces CCL5 expression via NF-kappaB and IRF3 in bile duct cells, and this pathway may be involved in the pathogenesis of BA. PMID: 29070776
14. Study demonstrates that increased CCL5 expression was restricted to human mesenchymal glioblastoma (GBM) and suggests that CCL5 functions in an autocrine growth-promoting circuit, and establish a new receptor responsible for CCL5 function in mesenchymal glioblastoma cells. PMID: 28380429
15. Study showed that bone stromal cells promoted prostate cancer progression through the secretion of CCL5. In vitro co-culture of bone stromal cells with prostate cancer cells induced the expression of CCL5, which promoted prostate cancer cell migration. CCL5 was found to have a key role in the progression of prostate cancer in the bone metastasis microenvironment. PMID: 29288523
16. identifies the essential role of the chemoattractive cytokine CCL5 for liver disease progression and especially hepatocellular carcinoma development PMID: 28011329
17. Breast cancer cell CCL5 mediates bone marrow independent angiogenesis via paracrine signaling. PMID: 27863423
18. the present study has demonstrated a novel pathway involving CCl5/CCR1/beta-catenin/Slug, via which human Mesenchymal stem cells promotes colorectal cancer development. PMID: 28542126
19. The present study suggest that TT genotype of CCL5 In1.1T/C (rs2280789) polymorphism play an important role to increased CCL5 expression in T cell which may enhanced Th1 immunity and help in protection against tuberculosis PMID: 28336310
20. CSF levels of RANTES were remarkably high only in active multiple sclerosis patients. RANTES levels were associated with transcranial magnetic stimulation measures of cortical synaptic excitability, but not with long-term potentiation (LTP)-like plasticity. PMID: 26733422
21. we document for the first time that CCL5 induces tumor lymphangiogenesis by the induction of VEGF-C in human cancer cells PMID: 27166194
22. Our findings indicate that the -403 G/A RANTES (CCL5) promoter gene polymorphism is connected with psoriasis vulgaris disease severity. PMID: 27859608
23. Baseline serum CCL5 levels and decrease of the serum VEGF-A levels may serve as potential predictive markers for survival or treatment-specific toxicities in metastatic colorectal cancer patients receiving regorafenib. PMID: 27166185
24. This meta-analysis suggests that RANTES -403G/A and -28C/G polymorphisms confer possible protection against HIV-1 infection, whereas In1.1T/C polymorphism may increase risk of HIV-1 infection, especially in Asians. PMID: 26690919
25. CCL5 and CXCL11 expression were also induced in response to the activation of the PKC pathway, and gene silencing experiments indicated that their inducible expression was dependent on RIPK4 and IRF6. Moreover, gene reporter assays suggested that RIPK4 induces CCL5 and CXCL11 expression by stimulating the transactivation of their promoters by IRF6. PMID: 27014863
26. Data suggest that inhibition of CCL5 in adipose microenvironment may represent an approach for the therapy of highly malignant Triple Negative Breast Cancer (TNBC). PMID: 27027351
27. RNA-binding protein HuR (HuR) expression negatively correlated with chemokine (CC motif) ligand 5 (CCL5) expression and macrophage appearance in a cohort of breast tumors. PMID: 28731284
28. we have utilized a broad-scaled affinity proteomics approach to identify three proteins (CCL5, HPGDS, and NPSR1) with altered plasma levels in asthmatic children compared to healthy controls, representing the first evaluation of HPGDS and NPSR1 in plasma. PMID: 27145233
29. Data provide evidence that CCL5 enhances the proliferation and the invasive capacity of human breast cancer cell lines mediated by CCR5 activation. PMID: 27335323
30. Cancer-FOXP3 serves as a prognostic biomarker and a crucial determinant of immunosuppressive microenvironment via recruiting Treg cells by directly trans-activating CCL5. Therefore, cancer-FOXP3 could be used to select patients with better response to CCL5/CCR5 blockade immunotherapy. PMID: 27991933
31. data suggest that STAT2 plays a role in the psoriasis pathogenesis by regulating the expression of CXCL11 and CCL5, and thereby attracting IFNgamma-producing immune cells to the skin PMID: 28472186
32. Mean RANTES concentrations in nasal fluid in patients with perennial allergic rhinitis and nonallergic and allergic chronic rhinosinusitis with nasal polyps patients were significantly higher in comparison to control subjects. PMID: 28587510
33. All fatty necrotic and osteolytic jawbone (FDOJ) samples showed high expression of RANTES and fibroblast growth factor (FGF)-2. PMID: 28685531
34. This study showed that RANTES is important in the regulation of vascular dysfunction through modulation of perivascular inflammation. PMID: 26873938
35. These data indicate that ECFCs, not SPCs, are the major players in MMD pathogenesis and that the chemokine CCL5 mediates the interactions. It can be hypothesized that in MMD patients, defective ECFCs direct aberrant SPC recruitment to critical vascular locations through the action of CCL5. PMID: 28072843
36. miR-200c represses IL-6, IL-8 and CCL-5 and improves osteogenic differentiation PMID: 27529418
37. this study shows that melanoma peptides vaccination and intratumoral administration of IFNgamma increases production of CCL5 in patient tumors PMID: 27522581
38. Findings indicate the importance of chemokine (CC motif) ligand 5 (CCL5) genetic variability and CCL5-CCR5 (CC chemokine receptor 5) axis on the susceptibility to HCV. PMID: 27304910
39. combined experimentally determined binding affinities (KD) of several orthologs of CCL5 with HNP1 with in silico studies to identify the most likely heterodimeric CCL5-HNP1 complex which was subsequently used as a starting structure to rationally design peptidic inhibitors PMID: 26871718
40. CCL5 plays a pivotal regulatory role in hepatic fibrosis during nonalcoholic fatty liver disease. PMID: 27639593
41. Intermolecular interactions of RANTES with its receptor CCR5 have been reported based on NMR spectroscopy measurements. PMID: 28052516
42. our findings proposed that CCL5 -403G>A polymorphism may be a risk factor for susceptibility TO pulmonary tuberculosis PMID: 27668525
43. IL-17A could enhance the expression of RANTES, but not IL-16, in cultured primary OFs in cooperation with CD40L. PMID: 27832278
44. We also found that the activation of H4R caused the release of IL-13 and RANTES on human mast cells.these data demonstrate that the H4R activates divergent signaling pathways to induce cytokine and chemokine production in human mast cells PMID: 27400655
45. The chemokine RANTES level could become a useful marker of severity of coronary artery disease PMID: 27226191
46. Findings show the significant upregulated expression of chemokine CCL5 (RANTES) in plasma, compared to CSF and contused brain tissue following severe traumatic brain injury (TBI). PMID: 28340601
47. There were no associations of CCL5 gene promoter polymorphism with the risk of diabetic microvascular complications (DMI); However, the 59029A polymorphism in CCR5 might affect individual susceptibility for DMI [Meta-Analysis] PMID: 27042273
48. RANTES Gene Polymorphisms are Associated with HIV-1 Infections. PMID: 27821902
49. Through the self-production of CCL5, ovarian cancer stem-like cells are induced to differentiate into endothelial cells and participate in tumor angiogenesis. PMID: 27033454
50. monocytes and lymphocytes cooperate to enhance migration towards CXCR3 chemokines and CCL5 in COPD PMID: 26965295

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Secreted.

Intercrine beta (chemokine CC) family

Expressed in the follicular fluid (at protein level). T-cell and macrophage specific.

HGNC: 10632

OMIM: 187011

KEGG: hsa:6352

STRING: 9606.ENSP00000293272

UniGene: Hs.514821