*  Why CCR2 and CCR5 Blockade Failed and Why CCR1 Blockade Might Still Be Effective in the Treatment of Rheumatoid Arthritis
Background The aim of this study was to provide more insight into the question as to why blockade of CCR1, CCR2, and CCR5 may have failed in clinical trials in rheumatoid arthritis (RA) patients, using an in vitro monocyte migration system model. Methodology/Principal Findings Monocytes from healthy donors (HD; n = 8) or from RA patients (for CCR2 and CCR5 antibody n = 8; for CCR1 blockade n = 13) were isolated from peripheral blood and pre-incubated with different concentrations of either anti-CCR1, anti-CCR2, or anti-CCR5 blocking antibodies (or medium or isotype controls). In addition, a small molecule CCR1 antagonist (BX471) was tested. Chemotaxis was induced by CCL2/MCP-1 (CCR2 ligand), CCL5/RANTES (CCR1 and CCR5 ligand), or by a mix of 5 RA synovial fluids (SFs), and cellular ...
  http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0021772
*  HIV-1 co-receptor CCR5 and CCR2 mutations among Greeks. - MySc...
HIV-1 co-receptor CCR5 and CCR2 mutations among Greeks.: The frequency of CCR5 and CCR2 alleles in human immunodeficiency virus (HIV)-positive and HIV-negative
  https://www.mysciencework.com/publication/show/hiv-1-co-receptor-ccr5-ccr2-mutations-among-greeks-f1cf76b5
*  CCR5 receptor antagonist - Wikipedia
CCR5 receptor antagonists are a class of small molecules that antagonize the CCR5 receptor. The C-C motif chemokine receptor CCR5 is involved in the process by which HIV, the virus that causes AIDS, enters cells. Hence antagonists of this receptor are entry inhibitors and have potential therapeutic applications in the treatment of HIV infections. The life cycle of the HIV presents potential targets for drug therapy, one of them being the viral entry pathway. CCR5 and CXCR4 are the main receptors involved in the HIV entry process. These receptors belong to the seven transmembrane G-protein-coupled receptor (GPCR) family and are predominantly expressed on human T-cells, dendritic cells and macrophages, Langerhans cells. They play an important role as co-receptors that HIV type 1 (HIV-1) uses to attach to cells before viral fusion and entry into host cells. HIV isolates can be divided into R5 ...
  https://en.wikipedia.org/wiki/CCR5_receptor_antagonist
*  mTOR 和CCR7 与乳腺癌侵袭转移的关系 · 临床与病理杂志
目的:探讨乳腺浸润性导管癌组织中哺乳动物雷帕霉素靶蛋白( mammalian target of rapamycin,mTOR) 与趋化因子受体7 (chemokine receptor 7,CCR7) 蛋白的表达,以及二者与乳腺癌侵袭、转移之间的关系。方法:采用免疫组织化学方法检测65 例乳腺浸润性导管癌及32 例正常乳腺组织中mTOR 和CCR7 的表达情况,并分析二者之间的相关性及其与各临床病理特征之间的关系。结果:mTOR 和CCR7 蛋白在乳腺浸润性导管癌中的阳性表达率(mTOR 为68%,CCR7 为74%) 高于癌旁正常乳腺组织中的阳性表达率(mTOR 为25%,CCR7 为28%),差异有统计学意义(P|0.01)。 mTOR 与CCR7 的表达呈正相关 (r=0.485,P|0.05)。mTOR 和CCR7 的高表达均与淋巴结转移、临床恶性肿瘤分期有关( 均P|0.05),而与年龄、雌激素受体、孕激素受体无关( 均P|0.05)。结论:mTOR 和CCR7 ...
  http://lcbl.amegroups.com/articles/69
*  Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal...
With our interest in Th17 cell-specific cell-surface molecules, we analyzed CCR6 expressed by Th17 cells in young (2-mo-old) or aged (10-mo-old) SKG mice, or BALB/c Th17 cells induced via homeostatic proliferation (Fig. 1 B). The majority of Th17 cells in SKG mice expressed CCR6 whether the mice were young or aged, whereas SKG Th1 cells did not (Fig. 1 F). After cell transfer to RAG2−/− mice, the majority of IL-17+CD4+ T cells that had differentiated from IFN-γ−/− or WT T cells were CCR6+, whereas IFN-γ+ CD4+ T cells derived from WT CD4+ T cells were CCR6− (Fig. 1 G). Furthermore, IL-6−/−CD4+ T cells not only failed to give rise to IL-17+CCR6+ cells but also preferentially differentiated to IFN-γ+CCR6− cells (Fig. 1 G).. It was also noted that CCR6+ cells, either IL-17+ or IL-17−, increased in number among CD4+ T cells in aged SKG mice compared with aged BALB/c or young SKG mice (Fig. 1 F ...
  http://jem.rupress.org/content/204/12/2803
*  Mouse Inflammatory Response & Autoimmunity PCR Array
Chemokine Receptors: Ccr1, Ccr2, Ccr3, Ccr4, Ccr7, Cxcr4, Cxcr1 (Il8ra), Cxcr2 (Il8rb).. Cytokine Metabolism: Il10, Il18, Tlr1, Tlr3, Tlr4, Tlr6.. Cytokine-Mediated Signaling Pathway: Ccl2 (Mcp-1), Ccl5 (Rantes), Ccr1, Ccr2, Ccr3, Ccr4, Ccr7, Cxcr2, Cxcr4, Il10rb, Il1a, Il1b, Il1r1, Il1rap, Il1rn, Il23r, Il5, Il6, Il6ra, Myd88, Ripk2, Tirap, Tnf.. Acute-Phase Response: Ccl5 (Rantes), Ccr1, Il1a, Il1b, Il1rn, Il6, Ptgs2 (Cox2), Tnf.. Chronic Inflammatory Response:Ccl11 (Eotaxin), Ccl5 (Rantes), Il1b, Lta (Tnfb), Tnf.. Regulation of Inflammatory Response: Bcl6, C3, C3ar1, C4b, Ccl1, Ccl12, Ccl17 (Tarc), Ccl19, Ccl2 (Mcp-1), Ccl20, Ccl22 (Mdc), Ccl24 (Eotaxin-2), Ccl25, Ccl3 (Mip-1a), Ccl4 (Mip-1b), Ccl7 (Mcp-3), Ccl8 (Mcp-2), Ccr2, Ccr3, Ccr4, ...
  http://www.sabiosciences.com/rt_pcr_product/HTML/PAMM-077Z.html
*  Blocking HIV‐1 infection via CCR5 and CXCR4 receptors by acting in trans on the CCR2 chemokine receptor | The EMBO Journal
Several models have been postulated by which chemokines inhibit HIV‐1 infection (Doranz et al, 1997; Berger et al, 1999). The steric hindrance model sustains that chemokine binding to its receptor blocks interaction of the HIV‐1‐env/CD4 complex with the receptor (Doranz et al, 1997; Murakami et al, 1997; Schols et al, 1997). Another model attributes this effect to a signaling mechanism, and a third suggests that chemokines induce receptor desensitization and internalization, preventing the virus from interacting with and infecting the target cell (Mack et al, 1998). In accordance with our previous results, we show that HIV‐1 infection can also be prevented in the absence of chemokine signaling, steric hindrance or receptor internalization. The fact that HIV‐1 infection through CCR5 could be blocked by induction of receptor dimerization (Vila‐Coro et al, 2000), and that CCR2 can form heterodimers with CCR5 points to CCR2 as a potential target ...
  http://emboj.embopress.org/content/23/1/66
*  Safety/Effectiveness of Oral Chemokine Coreceptor 5 (CCR5) Antagonist INCB009471 in R5-tropic HIV Infected Patients - Full Text...
This study will evaluate the safety, pharmacokinetics and efficacy of the CCR5 antagonist INCB009471 in HIV-1 infected patients who are antiretroviral therapy naïve, or who are not currently on a HAART regimen and have not received any antiretroviral agents for 3 months prior to the Screening visit. Subjects will receive study medication (INCB009471) admnistered orally or placebo once daily with food for 14 days. Clinical safety laboratories, 12-lead electrocardiograms, physical examinations and virologic assessments, including viral load, viral tropism and CD4+ cell count determinations will be performed at the Screening visit and at regularly scheduled visits throughout the study. A blood sample will also be obtained and stored to potentially determine the genotype of the CCR5 receptor.. The primary objectives are:. ...
  https://clinicaltrials.gov/ct2/show/study/NCT00393120?view=results
*  CCR5 Inhibitor Treatment Intensification on CD4+ T-cell Recovery - Full Text View - ClinicalTrials.gov
Blunted CD4+ T-cell responses during viral control may be a consequence of on-going T-cell destruction in the regenerative phase of CD4 recovery from activation-induced apoptosis and/or reduced production from decreased thymic output. Maraviroc, a CCR5 inhibitor, may improve the clinical status of HIV-infected by two distinct mechanisms. First, by blocking HIV entry into CD4+ T-cells, CCR5 inhibitors have direct antiviral activity. Second, as the pro-inflammatory state of HIV infection up-regulates CCR5 ligands and receptors, this CCR5 receptor antagonist may abrogate immune activation and resultant T-cell apoptosis. Importantly, MVC binds CCR5 receptors without inducing intracellular signaling or altering cell-surface expression. Potentially, MVC intensification during viral suppression with ART may further decrease persistent activation-induced apoptosis and improve repair and remodeling ...
  https://clinicaltrials.gov/show/NCT00925756?order=37
*  CCR5 Inhibitor Treatment Intensification on CD4+ T-cell Recovery - Full Text View - ClinicalTrials.gov
Blunted CD4+ T-cell responses during viral control may be a consequence of on-going T-cell destruction in the regenerative phase of CD4 recovery from activation-induced apoptosis and/or reduced production from decreased thymic output. Maraviroc, a CCR5 inhibitor, may improve the clinical status of HIV-infected by two distinct mechanisms. First, by blocking HIV entry into CD4+ T-cells, CCR5 inhibitors have direct antiviral activity. Second, as the pro-inflammatory state of HIV infection up-regulates CCR5 ligands and receptors, this CCR5 receptor antagonist may abrogate immune activation and resultant T-cell apoptosis. Importantly, MVC binds CCR5 receptors without inducing intracellular signaling or altering cell-surface expression. Potentially, MVC intensification during viral suppression with ART may further decrease persistent activation-induced apoptosis and improve repair and remodeling ...
  https://clinicaltrials.gov/show/NCT00925756?order=427
*  CCR5 Inhibitor Treatment Intensification on CD4+ T-cell Recovery - Full Text View - ClinicalTrials.gov
Blunted CD4+ T-cell responses during viral control may be a consequence of on-going T-cell destruction in the regenerative phase of CD4 recovery from activation-induced apoptosis and/or reduced production from decreased thymic output. Maraviroc, a CCR5 inhibitor, may improve the clinical status of HIV-infected by two distinct mechanisms. First, by blocking HIV entry into CD4+ T-cells, CCR5 inhibitors have direct antiviral activity. Second, as the pro-inflammatory state of HIV infection up-regulates CCR5 ligands and receptors, this CCR5 receptor antagonist may abrogate immune activation and resultant T-cell apoptosis. Importantly, MVC binds CCR5 receptors without inducing intracellular signaling or altering cell-surface expression. Potentially, MVC intensification during viral suppression with ART may further decrease persistent activation-induced apoptosis and improve repair and remodeling ...
  https://clinicaltrials.gov/show/NCT00925756?order=432
*  AID 52699 - Inhibitory activity against human CCR5 chemokine receptor (CCR5) expressed in CHO cells - PubChem
BioAssay record AID 52699 submitted by ChEMBL: Inhibitory activity against human CCR5 chemokine receptor (CCR5) expressed in CHO cells.
  https://pubchem.ncbi.nlm.nih.gov/bioassay/52699
*  CCR10 / GPR2 antibody | acris-antibodies.com
CCR10, C-C chemokine receptor type 10 is a protein that in humans is encoded by the CCR10 gene. CCR10 is constitutively expressed in skin melanocytes,…
  https://www.acris-antibodies.com/target/ccr10-antibody-gpr2-antibody.htm
*  Human CCR1/Galpha15 Stable Cell Line-Chem-1 CSC-RG0627 - Creative BioMart
This human CCR1-expressing cell line is made in the Chem-1 host, which supports high levels of recombinant CCR1 expression on the cell surface and contains high levels of the promiscuous G protein Galpha15 to couple the receptor to the calcium signaling pathway. Thus, the cell line is an ideal tool for screening for antagonists of interactions between CCR1 and its ligands.
  https://www.creativebiomart.net/description_146276_185.htm
*  Interleukin-4 promotes human CD8 T cell expression of CCR7. - Radcliffe Department of Medicine
Despite strong evidence supporting a pathway of human T cell differentiation characterized by changes in the expression of CCR7, CD28, CD27 and CD62L, few studies have addressed the mechanisms of pathway regulation. Cutaneous lymphocyte-associated antigen (CLA)-positive skin-homing CD8(+) T cells expressed significantly elevated levels of activation markers compared with CLA(-) CD8(+) T cells in individuals (n = 27) with cutaneous atopic disease. Despite such an activated phenotype, CLA(+) T cells expressed significantly higher levels of CCR7 than a CLA(-) T cell subset. Interleukin (IL)-4 was found to dramatically promote CCR7 expression by antigen-specific CD8(+) cells. Furthermore, skin-homing CD8(+) T cells from individuals with severe disease produced significantly less IL-10 than those derived from mildly affected atopic subjects. Thus in a T-helper 2 dominated disease, tissue-specific CD8(+) T cells show altered CCR7 expression and ...
  https://www.rdm.ox.ac.uk/publications/17503
*  Ccr2 - C-C chemokine receptor type 2 - Rattus norvegicus (Rat) - Ccr2 gene & protein
Receptor for the CCL2, CCL7 and CCL13 chemokines. Receptor for the beta-defensin DEFB106A/DEFB106B (By similarity). Transduces a signal by increasing intracellular calcium ion levels (By similarity). Upon CCL2 ligation, mediates chemotaxis and migration induction through the activation of the PI3K cascade, the small G protein Rac and lamellipodium protrusion (By similarity).
  http://www.uniprot.org/uniprot/O55193
*  Targeted disruption of the mouse ccr2 gene. (a) The wil | Open-i
Targeted disruption of the mouse ccr2 gene. (a) The wild-type ccr2 genomic DNA locus is depicted in the middle. Relevant restriction endonuclease sites are indi
  https://openi.nlm.nih.gov/detailedresult.php?img=PMC2199145_JEM.971437f1&req=4
*  The obesity and inflammatory marker haptoglobin attracts monocytes via interaction with chemokine (C-C motif) receptor 2 (CCR2)...
The results described herein demonstrate that Hp is a novel chemotactic factor and that its capacity to recruit monocytes is mediated (at least in part) by an interaction with the chemokine receptor CCR2. Evidence for this interaction is based on the capacity of Hp to induce CCR2 internalization, the capacity of Hp to bind (albeit with low affinity) CCR2 in vitro, Hp induced intracellular calcium flux and Hp activation of the ERK 1/2 pathway. The two latter properties reveal two additional novel roles/functions for Hp. These concepts will be extensively discussed in the following paragraphs.. The in vitro evidence reported herein demonstrate that the inflammation/adiposity marker Hp possesses chemotactic potential at doses well within its human physiological concentrations or less [3, 15]. Further, our findings highlight differences in the two Hp isoforms 1-1 and 2-2, with the latter being a more potent monocyte chemoattractant. This result should be ...
  https://bmcbiol.biomedcentral.com/articles/10.1186/1741-7007-7-87
*  Applications filed at Jun 01 2017 | TAL-EFFECTOR NUCLEASE FOR TARGETED KNOCKOUT OF THE HIV CO-RECEPTOR CCR5 | Patents.com
Lipase Variants and Polynucleotides Encoding Same | Fusion Polymerase and Method for Using the Same | Fusion Polymerase and Method for Using the Same | POLYMERASES FOR NUCLEOTIDE ANALOGUE INCORPORATION | T7 EXPRESSION SYSTEM, METHOD FOR ITS PRODUCTION AND USE THEREOF FOR PRODUCING RECOMBINANT PROTEINS |
  http://www.patents.com/ap-20170601-p63.html
*  CCR6, CD196 or CC chemokine receptor type 6 Antibody
Research proven mouse monoclonal CCR6 antibody. Useful for studying immune and inflammatory response. Designed for immunohistochemistry, immunofluorescence and related applications. IHC image available.
  http://www.neuromics.com/ittrium/visit/A1x66x1y1x85b1x1x9cy1x6217x1x96y1x581x1x82y1x343dx1x7f
*  ZK-756326 dihydrochloride | CAS# 1780259-94-0 | 874911-96-3 | CCR8 chemokine receptor agonis | MedKoo
ZK-756326 is a potent, selective and non-peptide CCR8 chemokine receptor agonist. ZK 756326 inhibited the binding of the CCR8 ligand I-309 (CCL1), with an IC(50) value of 1.8 muM. ZK 756326 was a full agonist of CCR8, dose-responsively eliciting an increase in intracellular calcium and cross-desensitizing the response of the receptor to CCL1.
  http://www.medkoo.com/products/11661
*  Human CCR9-FLAG Stable Cell Line-HEK293T CSC-RG0212 - Creative Biomart
HEK293T-HuCCR9-FLAG cell line is a hypotriploid human cell line, which has been transfected with a Human chemokine (C-C motif) receptor 9 (CCR9) tagged in the N-terminus with FLAG to allow stably express of the human CCR9 tagged in the N-terminus with FLAG protein. It is an example of a cell line transfected using our proprietary CBTGS gene screening and amplification system.
  http://www.creativebiomart.net/description_145626_185.htm
*  Journal of Alzheimer's Disease - Volume 14, issue 2 - Journals - IOS Press
Authors: Reale, Marcella , Iarlori, Carla , Feliciani, Claudio , Gambi, Domenico Article Type: Research Article Abstract: Cerebral inflammation as well as systemic immunological alterations has been reported in Alzheimer's disease (AD). We aimed to determine whether spontaneous and mitogen stimulated production of peripheral blood mononuclear cell (PBMC) cytokines, chemokines and chemokine receptors in clinically diagnosed patients with AD were unregulated. PBMC were purified from AD patients and from healthy controls. Supernatants were analyzed for cytokine levels by ELISA methods. mRNA expression was determined by RT-PCR. Expression of chemokine receptors CCR2 and CCR5 was determined by cytofluorimetric analysis. Both CCR5 and CCR2 expression were increased in AD patients respect to control subjects and the expression of CCR2 …and CCR5 was more frequent on CD4+ and less ...
  https://content.iospress.com/journals/journal-of-alzheimers-disease/14/2
*  AID 611988 - Antagonist activity against human CCR5 receptor assessed as inhibition of HIV1 gp120-induced cell-cell fusion...
BioAssay record AID 611988 submitted by ChEMBL: Antagonist activity against human CCR5 receptor assessed as inhibition of HIV1 gp120-induced cell-cell fusion between viral envolop protein expressing human HEK293 cells to human CD4/CCR5 receptor expressing HOS cells after 24 hrs by luciferase reporter gene assay.
  https://pubchem.ncbi.nlm.nih.gov/bioassay/611988
*  OriGene - Ccr6 (NM 001190333) cDNA Clone
Ccr6 - Ccr6 (untagged) - Mouse chemokine (C-C motif) receptor 6 (Ccr6), transcript variant 2, (10ug) available for purchase from OriGene - Your Gene Company.
  http://www.origene.com/Mouse_cDNA/MC208239.aspx