Relevant bibliographies by topics / CCR5

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Academic literature on the topic 'CCR5'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "CCR5"

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Korbecki, Jan, Klaudyna Kojder, Katarzyna Barczak, Donata Simińska, Izabela Gutowska, Dariusz Chlubek, and Irena Baranowska-Bosiacka. "Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor–A Literature Review." International Journal of Molecular Sciences 21, no. 16 (August 6, 2020): 5647. http://dx.doi.org/10.3390/ijms21165647.

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Hypoxia, i.e., oxygen deficiency condition, is one of the most important factors promoting the growth of tumors. Since its effect on the chemokine system is crucial in understanding the changes in the recruitment of cells to a tumor niche, in this review we have gathered all the available data about the impact of hypoxia on β chemokines. In the introduction, we present the chronic (continuous, non-interrupted) and cycling (intermittent, transient) hypoxia together with the mechanisms of activation of hypoxia inducible factors (HIF-1 and HIF-2) and NF-κB. Then we describe the effect of hypoxia on the expression of chemokines with the CC motif: CCL1, CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL13, CCL15, CCL16, CCL17, CCL18, CCL19, CCL20, CCL21, CCL22, CCL24, CCL25, CCL26, CCL27, CCL28 together with CC chemokine receptors: CCR1, CCR2, CCR3, CCR4, CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10. To better understand the effect of hypoxia on neoplastic processes and changes in the expression of the described proteins, we summarize the available data in a table which shows the effect of individual chemokines on angiogenesis, lymphangiogenesis, and recruitment of eosinophils, myeloid-derived suppressor cells (MDSC), regulatory T cells (Treg), and tumor-associated macrophages (TAM) to a tumor niche.
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Princen, Katrien, Sigrid Hatse, Kurt Vermeire, Stefano Aquaro, Erik De Clercq, Lars-Ole Gerlach, Mette Rosenkilde, et al. "Inhibition of Human Immunodeficiency Virus Replication by a Dual CCR5/CXCR4 Antagonist." Journal of Virology 78, no. 23 (December 1, 2004): 12996–3006. http://dx.doi.org/10.1128/jvi.78.23.12996-13006.2004.

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ABSTRACT Here we report that the N-pyridinylmethyl cyclam analog AMD3451 has antiviral activity against a wide variety of R5, R5/X4, and X4 strains of human immunodeficiency virus type 1 (HIV-1) and HIV-2 (50% inhibitory concentration [IC50] ranging from 1.2 to 26.5 μM) in various T-cell lines, CCR5- or CXCR4-transfected cells, peripheral blood mononuclear cells (PBMCs), and monocytes/macrophages. AMD3451 also inhibited R5, R5/X4, and X4 HIV-1 primary clinical isolates in PBMCs (IC50, 1.8 to 7.3 μM). A PCR-based viral entry assay revealed that AMD3451 blocks R5 and X4 HIV-1 infection at the virus entry stage. AMD3451 dose-dependently inhibited the intracellular Ca2+ signaling induced by the CXCR4 ligand CXCL12 in T-lymphocytic cells and in CXCR4-transfected cells, as well as the Ca2+ flux induced by the CCR5 ligands CCL5, CCL3, and CCL4 in CCR5-transfected cells. The compound did not interfere with chemokine-induced Ca2+ signaling through CCR1, CCR2, CCR3, CCR4, CCR6, CCR9, or CXCR3 and did not induce intracellular Ca2+ signaling by itself at concentrations up to 400 μM. In freshly isolated monocytes, AMD3451 inhibited the Ca2+ flux induced by CXCL12 and CCL4 but not that induced by CCL2, CCL3, CCL5, and CCL7. The CXCL12- and CCL3-induced chemotaxis was also dose-dependently inhibited by AMD3451. Furthermore, AMD3451 inhibited CXCL12- and CCL3L1-induced endocytosis in CXCR4- and CCR5-transfected cells. AMD3451, in contrast to the specific CXCR4 antagonist AMD3100, did not inhibit but enhanced the binding of several anti-CXCR4 monoclonal antibodies (such as clone 12G5) at the cell surface, pointing to a different interaction with CXCR4. AMD3451 is the first low-molecular-weight anti-HIV agent with selective HIV coreceptor, CCR5 and CXCR4, interaction.
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Zhang, Yi-jun, Tatjana Dragic, Yunzhen Cao, Leondios Kostrikis, Douglas S. Kwon, Dan R. Littman, Vineet N. KewalRamani, and John P. Moore. "Use of Coreceptors Other Than CCR5 by Non-Syncytium-Inducing Adult and Pediatric Isolates of Human Immunodeficiency Virus Type 1 Is Rare In Vitro." Journal of Virology 72, no. 11 (November 1, 1998): 9337–44. http://dx.doi.org/10.1128/jvi.72.11.9337-9344.1998.

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ABSTRACT We have tested a panel of pediatric and adult human immunodeficiency virus type 1 (HIV-1) primary isolates for the ability to employ the following proteins as coreceptors during viral entry: CCR1, CCR2b, CCR3, CCR4, CCR5, CCR8, CXCR4, Bonzo, BOB, GPR1, V28, US28, and APJ. Most non-syncytium-inducing isolates could utilize only CCR5. All syncytium-inducing viruses used CXCR4, some also employed V28, and one (DH123) used CCR8 and APJ as well. A longitudinal series of HIV-1 subtype B isolates from an infected infant and its mother utilized Bonzo efficiently, as well as CCR5. The maternal isolates, which were syncytium inducing, also used CXCR4, CCR8, V28, and APJ.
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Taylor, James R., Katherine C. Kimbrell, Robert Scoggins, Marie Delaney, Lijun Wu, and David Camerini. "Expression and Function of Chemokine Receptors on Human Thymocytes: Implications for Infection by Human Immunodeficiency Virus Type 1." Journal of Virology 75, no. 18 (September 15, 2001): 8752–60. http://dx.doi.org/10.1128/jvi.75.18.8752-8760.2001.

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ABSTRACT The presence or absence of the receptor CD4 and the coreceptors CCR5 and CXCR4 restrict the cell tropism of human immunodeficiency virus type 1 (HIV-1). Despite the importance of thymic infection by HIV-1, conflicting reports regarding the expression of HIV-1 coreceptors on human thymocytes have not been resolved. We assayed the expression and function of the major HIV-1 coreceptors, CCR5 and CXCR4, as well as CCR4 and CCR7 as controls, on human thymocytes. We detected CCR5 on 2.5% of thymocytes, CXCR4 on 53% of the cells, and CCR4 on 16% and CCR7 on 11% of human thymocytes. Moreover, infection by R5 HIV-1 did not significantly induce expression of CCR5. We found that two widely used anti-CCR5 monoclonal antibodies cross-reacted with CCR8, which may account for discrepancies among published reports of CCR5 expression on primary cells. This cross-reactivity could be eliminated by deletion of amino acids 2 through 4 of CCR8. Chemotaxis assays showed that SDF-1, which binds CXCR4; MDC, which binds CCR4; and ELC, which binds CCR7, mediated significant chemotaxis of thymocytes. In contrast, MIP-1β, whose receptor is CCR5, did not induce significant chemotaxis. Our results indicate that CXCR4, CCR4, CCR7, and their chemokine ligands may be involved in thymocyte migration during development in the thymus. CCR5 and its ligands, however, are likely not involved in these processes. Furthermore, the pattern of CCR5 and CXCR4 expression that we found may explain the greater susceptibility of human thymocytes to infection by HIV-1 isolates capable of using CXCR4 in cell entry compared to those that use only CCR5.
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Mazur, Grzegorz, Emilia Jaskula, Ilona Kryczek, Dorota Dlubek, Tomasz Wrobel, Aleksandra Butrym, Andrzej Lange, and Kazimierz Kuliczkowski. "Gene Expression for Chemokine Receptors Influences Survival of Non-Hodgkin Lymphoma Patients." Blood 116, no. 21 (November 19, 2010): 3103. http://dx.doi.org/10.1182/blood.v116.21.3103.3103.

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Abstract Abstract 3103 Non-Hodgkin's lymphoma (nHL) represent heterogenous group of lymphoid malignancies derived from B and T lymphocytes, NK cells or histiocytes. Most of lymphomas are B-cell origin. Lymphoma cells can migrate to other organs and their migration could be linked to chemokines and their receptors. Chemokine receptors are expressed by many cell populations, including lymphoid cells, and their main function is lymphocytes. Chemokine receptors guide lymphocytes homing, chemotaxis, adhesion and interplaying between immunologic system response cells. They are also responsible for cancer metastasis, including also dissemination of Hodgkin's and non-Hodgin's lymphomas. The purpose of the study was to determinate expression of genes coding chemokine receptors: CXCR4, CCR1, CCR2a, CCR2b, CCR3, CCR5, CCR7 and CCR8 in lymphoma lymph nodes comparing to their expression in reactive lymph nodes. We also wanted to analyze the influence of chemokine receptor gene expression on lymphoma patient survival. Methods: Chemokine receptor gene expression was evaluated in 63 lymphoma lymph nodes taken from patients (31 women and 32 men, aged 18–81 years; median age 43 years) at the moment of diagnosis. In 25 samples of reactive lymph nodes (taken from 15 women and 10 men; aged 18–59; median age 32 years) expression of chemokine genes was also studied as a control group. Gene expression of chemokine receptors CXCR4, CCR1, CCR2a, CCR2b, CCR3, CCR5, CCR7 and CCR8 was measured by reverse transcription (RT)-polymerase chain reaction method. Gene expression was estimated in arbitrary units (AU) from 0 to 3 AU points scale. PCR was conducted using primer pairs for CXCR4 (sens GAC CGC TAC CTG GCC ATC, antisens GGC AGC CAA CAG GCG AAGg A, 345 bp), CCR2a (sens GTA TCT CTC GGT GTT CTT CC, antisens TCT AGG CTC CTT CTT TGT CCT G, 271 bp), CCR2b (sens GTA TCT CTC GGT GTT CTT CC, antisens ACC AGC CGA GAC TTC CTG CT, 163 bp) CCR3 (sens TCC TTC TCT CTT CCT ATC AAT, antisens GGC AAT TTT CTG CAT CTA, 312 bp), CCR5 (sens AAT CTT CTT CAT CAT CCT CC, antisens TCT CTG TCA CCT GCA TAG C, 506 bp), CCR7 (sens CTG GTG GTG GCT CTC CTT GT, antisens GCC AGG TTG AGC AGG TAG GT, 271 bp), CCR8 (sens GGT TGG TGC TCA TTG TGG TC, antisens AGT CTA CGC TGG AGG AAC GG, 345 bp). Statistical analysis was performed using the CSS Statistica for Windows (version 7.0) software. Probability values <0.05 were considered statistically significant. Results: There was significantly higher expression of CCR1 and CCR8 gene in lymphoma lymph nodes comparing to controls (p<0.05), while CCR5 and CCR7 gene expression was significantly lower in lymphoma lymph nodes (p<0.05) comparing to reactive lymph nodes. CXCR4, CCR2a, CCR2b, CCR3 expression did not differ between lymphoma and control groups. The patients with higher expression of CCR7 gene had significantly longer survival comparing to those with lower expression (p=0.048). Expression of CCR7 was negatively correlated with IPI (p=0.036, coefficient = -0.32). Higher expression of CCR5 gene was positively correlated with Ki-67 (p=0,016, coefficient = 0.34), stage of disease (p=0.048, coefficient = 0.029) and international prognostic index score - IPI (p=0,047, coefficient = 0.298). We also found positive correlation between CCR8 gene expression and IPI (p=0.039, coefficient = 0.32). Conclusions: Lower expression of CCR7 gene is combined with longer survival of nHL patients. As there are positive correlations between CCR5 expression and Ki-67 proliferation marker and IPI as well as CCR8 and IPI in non-Hodgkin's lymphoma, those receptors can promote tumour progression. Disclosures: No relevant conflicts of interest to declare.
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Ren, Han-Yun, Meng Wang, Xiang-Juan Ma, Yu-Jun Dong, Zhi-Xiang Qiu, and Wei Liu. "Differential Regulation Of Chemokine Receptor Expressions On T Lymphocyte Subsets In Healthy Donors After Mobilization With Rhg-CSF and Its Correlation With Acute GvHD." Blood 122, no. 21 (November 15, 2013): 3296. http://dx.doi.org/10.1182/blood.v122.21.3296.3296.

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Abstract Introduction This study is aimed to investigate chemokine receptors (CCR5, CCR6, CCR7, CCR9, CXCR3 and CCR2) expression on T cell subsets in healthy donors after mobilization with recombinant human granulocyte colony-stimulating factor (rhG-CSF) and analyze its correlation with acute graft-versus-host disease (aGVHD) and to understand the possible mechanisms underlying rhG-CSF-induced immune tolerance. Methods Sixty-eight healthy donor and their recipient pairs of family donor allogeneic hematopoietic stem cell transplantation (allo-HSCT) were included in this study. The expressions of chemokine receptors on CD4+ and CD8+ T cells in the peripheral blood (PB) before and after mobilization was detected using flow cytometry (FCM) respectively. Six chemokine receptors (CCR2, CCR5, CCR6, CCR7, CCR9 and CXCR3) were detected on T cell subsets in all the donors, and CCR5 and CCR7 were detected only in eighteen of all the donors. The expressions of chemokine receptor before and after mobilization was compared and its correlation with II-IV aGVHD were analyzed. Results After rhG-CSF mobilization, the expression of CCR9 on CD4+ T cells and CCR7 on CD8+ T cells were significantly upregulated compared with that before mobilization (p<0.05). However, the mean value of CCR5, CCR6 and CXCR3 expression on CD4+ and CD8+ T cell subsets in PB after mobilization didn’t differ significantly compared with that before mobilization(p>0.10). However, different individuals showed apparent inconsistencies. According to the changes of chemokine receptor expression on CD4+ and CD8+ T cell subsets, the evaluable donors and their relevant recipients were divided into the down-regulated group and the non-down-regulated (unchanged or up-regulated ) group. The incidence of grade II to IV aGVHD in the two groups were compared in their corresponding recipients. In the univariate analysis, mismatched HLA (p=0.046), down-regulation of CCR7 expression on donor CD4+ T cell subsets (p=0.010), unchangeableness or up-regulation of CCR5 expression on donor CD4+ T cell subsets (p=0.032) and CCR6 down-regulation on donor CD8+ T cells (p=0.045) were risk factors for recipients to develop II-IV aGVHD. In the multivariate analysis, down-regulation of CCR7 expression on donor CD4+ T cells after rhG-CSF was independent risk factor for II-IV aGVHD [RR=3.5, 95% CI (1.3-9.4), p=0.012], while CCR5 down-regulation on CD4+ T cells could reduce the incidence of II-IV aGVHD [RR=0.3, 95% CI (0.1-0.8), p=0.031]. Conclusions rhG-CSF mobilization could lead to differential regulation of chemokine receptors expression on T cell subsets, which might cause different effects on the migration of T cells in vivo, and decrease T cells trafficking towards GVHD target organs, and thus reduce the incidence of aGVHD after transplantation. Disclosures: No relevant conflicts of interest to declare.
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Kim, Chang H., Jeeho Lee, and Seung G. Kang. "Developmental and antigen-driven switches in the trafficking receptors of FoxP3+ regulatory T cells (99.2)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S194. http://dx.doi.org/10.4049/jimmunol.178.supp.99.2.

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Abstract FoxP3+ regulatory T cells play important roles in immune regulation and tolerance. There is an increasing body of evidence that the migration ability of FoxP3+ T cells is important for their regulatory functions at effector tissue sites. We investigated the two different trafficking receptor switches of FoxP3+ T cells occurring in the thymus and secondary lymphoid tissues. The first trafficking receptor switch in the thymus is developmentally programmed: Precursors of FoxP3+ cells undergo the first trafficking receptor switch from CCR8/CCR9 to CXCR4 and then finally to CCR7, generating mostly homogeneous CD62L+CCR7+ FoxP3+ T cells. The recent thymic emigrant CD62L+CCR7+ FoxP3+ T cells are programmed to migrate to secondary lymphoid tissues. The CD62L+CCR7+ FoxP3+ T cells undergo the second switch in trafficking receptors in an antigen-dependent manner. This second switch involves down-regulation of CCR7 and CXCR4 but up-regulation of a number of memory/effector type homing receptors, resulting in generation of heterogeneous FoxP3+ T cell subsets expressing various combinations of trafficking receptors including CCR2, CCR4, CCR5, CCR6, CCR7, CCR8, CCR9 and CXCR5. FoxP3+ cells undergo the second switch to selected non-lymphoid tissue homing receptors at highly accelerated rates. This results in generation of FoxP3+ T cells with unconventionally efficient migratory capacity to major non-lymphoid tissues such as intestinal lamina propria and bone marrow. Importantly, this accelerated switch of FoxP3+ T cells is conserved in both men and mice. The two switches in homing receptors are though to be important for effective distribution and differentiation-dependent effector functions of FoxP3+ regulatory T cells.
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Paula Costa, Guilherme de, Laís Roquete Lopes, Maria Cláudia da Silva, Aline Luciano Horta, Washington Martins Pontes, Cristiane M. Milanezi, Paulo Marcos da Mata Guedes, et al. "Doxycycline and Benznidazole Reduce the Profile of Th1, Th2, and Th17 Chemokines and Chemokine Receptors in Cardiac Tissue from ChronicTrypanosoma cruzi-Infected Dogs." Mediators of Inflammation 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/3694714.

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Chemokines (CKs) and chemokine receptors (CKR) promote leukocyte recruitment into cardiac tissue infected by theTrypanosoma cruzi. This study investigated the long-term treatment with subantimicrobial doses of doxycycline (Dox) in association, or not, with benznidazole (Bz) on the expression of CK and CKR in cardiac tissue. Thirty mongrel dogs were infected, or not, with the Berenice-78 strain ofT. cruziand grouped according their treatments: (i) two months after infection, Dox (50 mg/kg) 2x/day for 12 months; (ii) nine months after infection, Bz (3,5 mg/kg) 2x/day for 60 days; (iii) Dox + Bz; and (iv) vehicle. After 14 months of infection, hearts were excised and processed for qPCR analysis of Th1 (CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL11), Th2 (CCL1, CCL17, CCL24, and CCL26), Th17 (CCL20) CKs, Th1 (CCR5, CCR6, and CXCR3), and Th2/Th17 (CCR3, CCR4, and CCR8) CKR, as well as IL-17.T. cruziinfection increases CCL1, CCL2, CCL4, CCL5, CCL17, CXCL10, and CCR5 expression in the heart. Dox, Bz, or Dox + Bz treatments cause a reversal of CK and CKR and reduce the expression of CCL20, IL-17, CCR6, and CXCR3. Our data reveal an immune modulatory effect of Dox with Bz, during the chronic phase of infection suggesting a promising therapy for cardiac protection.
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Zvejniece, Laura, Svetlana Kozireva, Zanna Rudevica, Ainars Leonciks, Barbro Ehlin-Henriksson, Elena Kashuba, and Irina Kholodnyuk. "Expression of the Chemokine Receptor CCR1 in Burkitt Lymphoma Cell Lines Is Linked to the CD10-Negative Cell Phenotype and Co-Expression of the EBV Latent Genes EBNA2, LMP1, and LMP2." International Journal of Molecular Sciences 23, no. 7 (March 22, 2022): 3434. http://dx.doi.org/10.3390/ijms23073434.

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Chemokines and their receptors regulate the migration of immune cells and the dissemination of cancer cells. CCR1, CCR2, CCR3, and CCR5 all belong to a single protein homology cluster and respond to the same inflammatory chemokines. We previously reported that CCR1 and CCR2B are induced upon Epstein-Barr virus (EBV) infection of B cells in vitro. EBV is present in almost all cases of endemic Burkitt lymphoma (BL); however, the contribution of EBV in the pathogenesis of the disease is not fully understood. Here, we analyzed the relation of the expression of CCR1, CCR2, CCR3, and CCR5, the EBV DNA load and expression of EBV latent genes in nine EBV-carrying and four EBV-negative BL cell lines. We revealed that CCR1 is expressed at high mRNA and protein levels in two CD10-negative BL cell lines with co-expression of the EBV latent genes EBNA2, LMP1, and LMP2. Low levels of CCR2 transcripts were found in three BL cell lines. CCR3 and CCR5 transcripts were hardly detectable. Our data suggest that in vivo, CCR1 may be involved in the dissemination of BL cells and in the selection of BL cells with restricted EBV gene expression programs.
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Catusse, Julie, Chris M. Parry, David R. Dewin, and Ursula A. Gompels. "Inhibition of HIV-1 infection by viral chemokine U83A via high-affinity CCR5 interactions that block human chemokine-induced leukocyte chemotaxis and receptor internalization." Blood 109, no. 9 (January 5, 2007): 3633–39. http://dx.doi.org/10.1182/blood-2006-08-042622.

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AbstractHIV-1 strains use C-C-chemokine receptor 5, CCR5, as a coreceptor for host transmission. Human CCR5 chemokine ligands inhibit binding and infection, whereas CCR5 mutations also inhibit infection by preventing surface expression, resulting in delayed progression to AIDS. Here, we describe a human herpesvirus 6 (HHV-6A) chemokine, U83A, which binds CCR5 with higher affinity than human chemokines, displacing their binding and leading to inhibition of chemotaxis of human leukocytes. Similarly, U83A inhibits infection by HIV-1 strains which use CCR5, but not the CXCR4, coreceptor. Unlike human CCR5 chemokine ligands which induce rapid CCR5 internalization mediated via clathrin, treatment with U83A prevents internalization. A spliced truncated U83A isoform, U83A-N, also binds CCR5 albeit with lower affinity, and this correlates with lower HIV-1 infection inhibition, whereas further truncation abolishes binding and any inhibition. Confocal microscopy confirms CCR5 internalization inhibition by U83A treatment, whereas labeled transferrin uptake shows that endocytosis via clathrin is unaltered. Previous results show that, although U83A-N is an antagonist, U83A is an agonist for CCR1, CCR4, CCR6, and CCR8 present on immune effector and antigen-presenting cells and here also shown for CCR5. Thus, U83A could act as a novel inhibitor of HIV-1 infection while also stimulating local immunity to the virus.
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Dissertations / Theses on the topic "CCR5"

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Schauren, Juliana da Silveira. "Estudo dos polimorfismos CCR2-64I, CCR5-59353, CCR5-59356, CCR5-59402 e CCR5-59653 em pacientes com lúpus eritematoso sistêmico do sul do Brasil." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/78127.

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O Lúpus Eritematoso Sistêmico (LES) é uma doença autoimune inflamatória crônica que possui uma etiopatogênese complexa. Diversos fatores participam da patogênese da doença, dentre eles alterações no balanço de citocinas e quimiocinas. As quimiocinas e seus receptores são fundamentais na regulação da migração de leucócitos durante a inflamação e acredita-se que elas possam ter um papel importante na patogênese de doenças autoimunes, inclusive no LES. Diversos estudos abordaram o papel de quimiocinas e seus receptores no LES, porém, principalmente se tratando dos receptores de quimiocinas CCR5 e CCR2, não existe um consenso. Devido à falta de consenso em relação ao papel dos receptores de quimiocinas na patogênese do LES e considerando a necessidade de mais estudos nesta área, o presente trabalho tem por objetivo investigar o possível papel de polimorfismos na região promotora do CCR5 no desenvolvimento do LES, comparando as frequências dos genótipos e haplótipos entre pacientes e controles, e analisar o possível envolvimento destes polimorfismos nas manifestações clínicas/laboratoriais da doença. O estudo incluiu 382 pacientes com LES (289 Euro-descendentes e 93 Afro-descendentes) e 375 controles (243 Euro-descendentes e 132 Afro-descendentes) genotipados para os polimorfismos CCR2-64I G>A (rs1799864), CCR5-59353 C>T (rs1799988), CCR5-59356 C>T (rs41469351), CCR5-59402 A>G (rs1800023) e CCR5-59653 C>T (rs1800024) através de PCR-RFLP e sequenciamento, respectivamente. Dados prévios de nosso grupo em relação ao CCR5delta32 foram incluídos no estudo para a inferência dos haplótipos e como um possível fator de confusão na regressão binária logística. Os resultados obtidos indicam que, em pacientes Euro-descendentes, as frequências reduzidas o polimorfismo CCR5delta32 e o haplótipo HHG*2 observadas em pacientes quando comparados com controles foram associadas com a doença (p=0,001; OR 3,5; 95%CI 1,6-7,5 e 2,0% vs. 7,2%; presidual=2,9E-5; respectivamente). Em pacientes Afrodescendentes, as frequências dos haplótipos HHA/HHB, HHC e HHG*2 foram diferentes em pacientes e controles (10% vs. 20,5%, presidual = 0,003; 29,4% vs. 17,4%; presidual=0,003 e 3,9% vs. 0,8%; presidual=0,023; respectivamente). Em relação às manifestações clínicas da doença, a presença do CCR5delta32 foi confirmada como um fator de susceptibilidade para nefrite classe IV em pacientes Afro-descendentes e no grupo de pacientes como um todo (pcorrigido=0,012; OR 3,0; 95%CI 3,0-333,3 e pcorrigido=0,0006; OR 6,8; 95%CI 1,9-2,48; respectivamente). Em conclusão, o presente estudo indica que polimorfismos na região promotora do CCR5 podem atuar como modificadores no LES. Os resultados observados reforçam o papel do polimorfismo CCR5delta32 como um fator de proteção para o desenvolvimento do LES em Euro-descendentes e como um fator de susceptibilidade à nefrite classe IV em pacientes Afro-descendentes. Além disto, também foram descritos a redução da frequência dos haplótipos HHA/HHB e o aumento da frequência dos haplótipos HHC e HHG*2 em pacientes Afro-descendentes, que possivelmente podem estar associados com uma maior expressão do CCR5 em subtipos específicos celulares e com uma menor expressão deste receptor de maneira geral.
Systemic Lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease, characterized by a complex etiopathogenesis. Many factors are known to participate in the pathogenesis of SLE, including alterations in the cytokines or chemokines balance. Chemokines and their receptors are central players in the regulation of leucocytes chemotaxis in inflammation and they are thought to have an important role in the pathogenesis of autoimmune diseases, including SLE. Several studies have addressed the role of chemokines and their receptors in SLE, however there is no consensus regarding their involvement on the pathogenesis of the disease. Given the lack of consensus considering the role of chemokine receptors in SLE pathogenesis and the need for more studies in this area, the present work aims to investigate a possible role of the CCR5 promoter region polymorphisms in the development of SLE comparing the frequencies of the genotypes and haplotypes with ethnically matched controls and analyze if there is a possible involvement of the polymorphisms in the clinical outcome of the disease. This study included 388 SLE patients (289 classified as Europeanderived and 93 as African-derived) and 375 controls (243 European-derived and 132 African-derived) genotyped for the CCR2-64I G>A (rs1799864), CCR5-59353 C>T (rs1799988), CCR5-59356 C>T (rs41469351), CCR5-59402 A>G (rs1800023) and CCR5-59653 C>T (rs1800024) polymorphisms though PCRRFLP and direct sequencing, respectively. Previous data from CCR5delta32 were included in the study to infer the haplotypes and also as a possible confounding factor in the binary logistic regression. Our results indicated that, in Europeanderived patients, CCR5delta32 and the HHG*2 haplotype reduced frequencies in patients when compared to controls were associated with the disease (p=0.001; OR 3.5; 95%CI 1.6-7.5 and 2.0%, vs. 7.2% residual p= 2.9E-5, respectively). In African-derived patients, the HHA/HHB, HHC and HHG*2 haplotype frequencies differed between patients and controls (10% vs. 20.5%, residual p= 0.003; 29.4% vs. 17.4%, residual p=0.003 and 3.9% vs. 0.8%, residual p=0.023; respectively). Considering the clinical manifestations of the disease, CCR5delta32 presence was confirmed as a susceptibility factor to class IV nephritis in the African-derived group and when patients were considered together (pcorrected=0.012; OR 3.0; 95%CI 3.0-333.3 and pcorrected= 0.0006; OR 6.8; 95%CI 1.9-2.48, respectively). In conclusion, this study indicates that CCR5 promoter polymorphisms are important disease modifiers in SLE. Present data reinforces CCR5delta32 polymorphism as a protective factor for the development of the disease in European-derived patients and as a susceptibility factor for class IV nephritis in African-derived patients. Furthermore, we also describe a reduced frequency of HHA/HHB and an enhanced frequency of HHC and HHG*2 haplotypes in our African-derived patients, which potentially could reflect in a higher expression of CCR5 in specific cell subsets and in a lower expression of CCR5 overall.
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Sax, Michael John. "The CCL5-CCR5 Axis in Breast Cancer." Thesis, Griffith University, 2015. http://hdl.handle.net/10072/365646.

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Cancer is one of the leading underlying causes of death worldwide. Despite decades of research, cancer is predicted to be the leading cause of death by the year 2020. Anti angiogenic therapies that target the key signalling molecule, vascular endothelial growth factor (VEGF) have shown promise in the treatment of some solid tumours, resulting in increased progression-free survival times in patients. However, there are several significant problems with current anti-angiogenic therapies, such as the phenomenon of resistance. Tumours can be divided into those that are intrinsically nonresponsive to therapy, and those that do respond. However, for those tumours that do respond to therapy, an initial positive response (tumour regression) is followed by tumour re-vascularisation and rapid relapse. Secondly, anti-angiogenic therapies target normal physiological processes, including vascular homeostasis, wound healing and the immune system, leading to a range of potentially negative side effects, including death. Thus unravelling the biology of angiogenesis and developing new drug targets is a priority of current research. The C-C chemokine receptor 5 (CCR5) has been the subject of extensive research in the last few years. This is primarily because of its association with the pathology of disease, viral infection, and the immune response. However, while the main ligand for CCR5, C C chemokine ligand 5 (CCL5) is known to be upregulated in malignant breast cancer, little has been done to unravel the CCL5-CCR5 axis in breast cancer and its potential role as a driver of malignancy. Furthermore, while experimental evidence, including data from CCR5 knockout mouse, suggests a role for CCL5-CCR5 in neovascularisation, little has been done to study the potential role of CCL5-CCR5 in tumour angiogenesis, as well as implications CCL5-CCR5 signalling may have on clinical course in breast cancer.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Sato, Wakiro. "Human Th17 Cells Are Identified as Bearing CCR2+CCR5- Phenotype." Kyoto University, 2008. http://hdl.handle.net/2433/124335.

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John, Bangan. "Association Among CCR5 Genotypes, CCR5 Expression, And In Vitro HIV Infection." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1365888090.

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Sohy, Denis. "Etude de la dimérisation des récepteurs aux chimiokines CCR2, CCR5 et CXCR4." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210282.

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La dimérisation des récepteurs couplés aux protéines G est un nouveau concept apparu dans la littérature au cours des quelques années qui ont précédé le début de notre travail. Bien qu’il soit clairement établi que les récepteurs sont capables de former des homo et des hétérodimères, les conséquences fonctionnelles de telles interactions demeurent souvent peu claires. Dans une étude précédente, le laboratoire d’accueil a montré que les récepteurs aux chimiokines CCR2 et CCR5 forment des homo et des hétérodimères de manière constitutive et identifié une coopérativité négative de liaison de nature allostérique entre les deux sites de liaison de CCR2 et CCR5 dans des cellules co-exprimant les deux récepteurs. Dans ce travail, nous avons étendu cette étude au récepteur CXCR4, structurellement plus éloigné que CCR2 et CCR5 entre eux. Nous montrons par une méthode biophysique se basant sur le transfert d’énergie de bioluminescence (le BRET) que CCR2, CCR5 et CXCR4 forment des homodimères et des hétérodimères de manière constitutive. De plus nous démontrons une coopérativité négative de liaison de nature allostérique des deux sites de liaisons pour les hétérodimères CCR2/CXCR4 et CCR5/CXCR4. lorsque CXCR4 est co-exprimé avec CCR2 ou CCR5, la chimiokine spécifique de CXCR4 (SDF-1α) inhibe la liaison du traceur spécifique de CCR2 (MCP-1) ou du traceur spécifique de CCR5 (MIP-1β), et vice-versa. La nature allostérique de ces interactions est démontrée par des expériences mesurant la dissociation de traceurs en présence ou non de compétiteurs. La coopérativité négative de liaison de nature allostérique des deux sites de liaisons est montrée également dans des cellules primaires, excluant tout effet indésirable dû à la surexpression de récepteurs. Nous montrons également que l’antagoniste spécifique de CXCR4 (AMD3100) inhibe la liaison du traceur spécifique de CCR2 (MCP-1) ou du traceur spécifique de CCR5 (MIP-1β), et vice-versa (TAK-779 vs SDF-1α), uniquement quand CXCR4 est co-exprimé respectivement avec CCR2 ou CCR5. Il s’agit là de la première preuve montrant que les interactions allostériques au sein d’hétérodimères de récepteurs aux chimiokines impliquent aussi des antagonistes, et qu’un antagoniste de récepteur aux chimiokines influence la réponse fonctionnelle d’un autre récepteur aux chimiokines auquel il ne se lie pas. De tels effets fonctionnels ont été montré dans des expériences de mobilisation de Ca++, de chimiotactisme sur lymphoblastes et dans des expériences d’air pouch in vivo.
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished
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6

Longden, James. "Quantitative approaches to the study of the trafficking of CCR1 and CCR5." Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437076.

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Zambra, Francis Maria Báo. "Influência dos genes CCR2 e CCR5 em hiperplasia e câncer de próstata." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/69706.

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A hiperplasia prostática benigna (HPB) e o câncer de próstata (CaP) são duas condições crônicas muito comuns em homens com idade avançada e têm sido relacionadas a processos inflamatórios. As quimiocinas são reconhecidas como mediadores críticos da resposta inflamatória por regular a migração das células imunológicas através da ativação de receptores de quimiocinas na superfície destas células. As quimiocinas estão relacionadas à patogênese tumoral, embora não seja claro de que modo afetam a progressão tumoral humana. O objetivo desse estudo foi investigar a associação de dois polimorfismos de receptores de quimiocinas, CCR2-64I e CCR5-delta32, com HPB e CaP. Neste trabalho foram genotipadas 385 amostras de DNA genômico de homens do sul do Brasil, predominantemente euro-descendentes, incluindo 130 casos de HPB, 136 casos de CaP e 119 indivíduos controle saudáveis. Para o polimorfismo CCR2-64I a genotipagem foi realizada por PCR-RFLP e para o CCR5-delta32 foi por PCR convencional. As frequências alélicas do CCR2-64I foram 14,0%; 15,8% e 11,1% nos grupos controle, HPB e CaP, respectivamente; enquanto as do CCR5-delta32 foram 5,1%; 7,1% e 6,2%, respectivamente. A mediana referente aos níveis de PSA foi de 0,79; 1,45 e 6,91 ng/mL nos grupos controle, HPB e CaP, respectivamente; diferindo significativamente entre estes (todos p<0,001). A mediana do volume da próstata foi 20,00 cm3 no grupo controle, portanto, menor que dos grupos HPB (35,35 cm3) e CaP (35,80 cm3) (ambos p<0,001); no entanto, não foi observada diferença entre pacientes com HPB e CaP (p=0,172). Algo interessante observado foi CCR2-64I como um fator protetor para CaP quando comparado com HPB (OR=0,550; IC95%=0,311–0,975), mas não quando comparado com o grupo controle (p=0,448). Não foi observada associação do CCR2-64I com os estados clinicopatológicos do CaP (estadiamento tumoral e escore de Gleason) (todos p≥0,308). Não foi observada associação significativa da variante CCR5-delta32 com HPB ou CaP (todos p≥0,072), ou com os estados clinicopatológicos do CaP (todos p≥0,253). Assim, nossos dados sugerem a influência da variante CCR2-64I, observada como fator protetor para CaP quando comparada com HPB, no desenvolvimento do câncer de próstata.
Benign prostatic hyperplasia (BPH) and prostate cancer (PCa) are two chronic conditions very common in aged men and have been related to inflammatory process. Chemokines are recognized as critical mediators of inflammatory responses by regulating the migration of immune cells through the activation of chemokine receptors on the surface of these cells. Chemokines are implicated in tumor pathogenesis, although it is not clear how it affects human tumor progression. The aim of this study was to investigate the association of two chemokine receptor gene polymorphisms, CCR2-64I and CCR5-delta32, with BPH and PCa. In this study were genotyped 385 genomic DNA samples from southernmost Brazilian men, predominantly euro-descendants, including 130 BPH, 136 PCa and 119 healthy control subjects. To CCR2-64I polymorphism the genotyping was performed by PCR-RFLP and to CCR5-delta32 by conventional PCR. The allele frequencies of CCR2-64I were 14.0%, 15.8% and 11.1% in control, BPH and PCa, respectively; while of CCR5-delta32 were 5.1%, 7.1% and 6.2%, respectively. Median of serum PSA levels were 0.79, 1.45 and 6.91 ng/mL in control, BPH and PCa group, respectively (all p<0.001). The prostate volume median was 20.00 cm3 in the control group, thus, lower than BPH (35.35 cm3) and PCa (35.80 cm3) group (both p<0.001), nevertheless no difference was observed between BPH and PCa patients (p=0.172). Interestingly, CCR2-64I was detected as a protective factor to PCa when compared with BPH (OR=0.550; 95%CI=0.311–0.975), but not when compared with control group (p=0.448). No significant associations of the CCR2-64I were observed with PCa clinicopathologic states (tumor stage and Gleason score) (all p≥0.308). No significant associations of the CCR5-delta32 variant were observed with BPH or PCa (all p≥0.072), or with PCa clinicopathologic status (all p≥0.253). Thus, our data suggest a influence of the CCR2-64I variant, that was observed as a protective factor in PCa when compared with BPH, in prostate cancer development.
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Fish, Richard James. "RANTES derivatives and CCR5." Thesis, University of York, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369362.

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Simonis, Christopher. "Molekulare Klonierung, stabile Transfektion und funktionelle Expression der murinen Chemokinrezeptoren Ccr2 und Ccr5." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-99950.

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Manin, Graziele Zenaro. "Identificação dos componentes do Sistema Imune que participam na resistência de camundongos em modelo de infecção letal por Legionella longbeachae." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-21052014-153321/.

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A doença dos legionários consiste em uma broncopneumonia severa e atípica, que acomete de 2 a 7% das pessoas infectadas com Legionella spp e que apresenta taxa de mortalidade que varia de 5 a 30%, sendo considerada uma importante causa de morbidade e mortalidade mundial. A patologia causada pela espécie L. pneumophila tem sido amplamente estudada em modelos experimentais e suas características clínicas foram extensivamente descritas. No entanto, este modelo não representa adequadamente a doença que acomete seres humanos, pois L. pneumophila não é letal aos camundongos como é para humanos. Recentemente, uma nova espécie de bactéria do gênero Legionella, denominada Legionella longbeachae, foi descrita como importante agente de doença dos legionários em países do hemisfério sul. A pneumonia induzida por L. longbeachae em humanos não difere da induzida por L. pneumophila. No entanto, L. longbeachae é letal para camundongos em doses baixas, o que torna esse modelo murino de doença dos legionários mais fidedigno ao que ocorre com humanos. Com a acentuada mudança dos hábitos de nossa sociedade, há o aumento do número de pessoas com fatores que predispõe a doença, como idade elevada ou tratamento imunossupressor. Assim, entender melhor a relação patógeno-hospedeiro no curso da doença dos legionários por meio da utilização de um modelo experimental adequado é importante para a descoberta de novos meios de combater este patógeno. Neste trabalho, geramos uma cepa de L. longbeachae mutante para rpsL, que se torna resistente à estreptomicina. Essa cepa pode ser utilizada para infecções in vivo nas quais a quantificação da CFU foi estimada em placas contendo antibiótico, o que culmina em maior eficiência experimental e menor quantidade de contaminações. Essa cepa foi utilizada em experimentos in vivo para avaliar os componentes do sistema imune que operam na resistência diante de uma dose letal bacteriana administrada pela via intranasal. Demonstramos que camundongos deficientes para as citocinas IFN ou TNF e para o receptor de quimiocinas CCR2 são mais susceptíveis à infecção do que os camundongos selvagens. No entanto, camundongos deficientes para o receptor de quimiocinas CCR5, para o receptor de IL-17, para a citocina IL-6 ou para o receptor citoplasmático NOD2 são mais resistentes à infecção quando comparados com animais selvagens. A descoberta destas moléculas em um modelo de infecção letal in vivo ressalta a importância de alguns componentes da imunidade para a resistência durante a doença dos legionários experimental e possíveis alvos terapêuticos para essa doença.
Legionnaires disease is a severe and atypical bronchopneumonia, which affects 2-7% people infected with Legionella spp and has a mortality rate of 5 to 30%, therefore it is considered an important cause of mortality and morbidity worldwide. Disease caused by Legionella pneumophila has been largely studied in experimental models and its clinical characteristics was extensively described. However this model does not adequately represent the disease that affects humans, because L. pneumophila is not lethal to mice, as it is to humans. Recently, a new species of bacterium from Legionella genus, called Legionella longbeachae, was described as an important agent of Legionnaires disease in the southern hemisphere. The pneumonia induced by L. longbeachae in humans is not different from pneumonia induced by L. pneumophila. However, a low dose of L. longbeachae is lethal to mice, which makes this murine infection model of Legionnaires disease more reliable than that which occurs in humans. Because our society is changing, there is an increase in the number of persons with predisposing factors, like higher age or immunosuppressive treatment. So, a better understanding of host-pathogen relationship by using a suitable experimental model is important to find new ways to fight this pathogen. Here, we generated a strain of rpsL mutant L. longbeachae, which becomes resistant to streptomycin. This strain could be used in in vivo infections, when CFU quantification was estimated in plates with antibiotic, culminating in greater experimental efficiency and lower contamination. This strain was used in in vivo experiments to evaluate components of the immune system that participates in resistance against lethal dose of bacteria administered intranasally. We showed that Tnf-/-, Ifn-/- or Ccr2-/- mice are more susceptible to infection than wild type mice. However Ccr5-/-, Il17r-/-, Il6-/- or Nod2-/- mice are more resistant to infection than wild type animals. The discovery of these molecules in a lethal infection model in vivo highlights the importance of some components of immunity to resistance during experimental Legionnaires disease and potential therapeutic targets to disease.
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Books on the topic "CCR5"

1

Masters, Jennefer. Myxoma virus induced activation of CC-chemokine receptor 5 (CCR5). Ottawa: National Library of Canada, 2000.

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Pass CCRN! St.Louis, Mo: Mosby, 1996.

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Pass CCRN! 4th ed. St. Louis, Mo: Elsevier, 2013.

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Brorsen, Ann J. Adult CCRN certification review. 2nd ed. Burlington, MA: Jones & Bartlett Learning, 2014.

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R, Rogelet Keri, ed. Pediatric CCRN certification review. Sudbury, MA: Jones & Bartlett Learning, 2012.

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R, Rogelet Keri, ed. Adult CCRN certification review. Sudbury, MA: Jones and Bartlett Publishers, 2009.

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Bhat, B. V. Rajarama. Cocycles of CCR flows. Providence, R.I: American Mathematical Society, 2001.

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Gallagher, A. M. Attitudes to higher education: Report to CCRU and DENI. Belfast: Centre for Research on Higher Education, 1996.

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Horgan, Carmel Mary Teresa. Studies on Mitozolomide (CCRG 81010), a new antineoplastic agent. Birmingham: University of Aston.Department of Pharmacy, 1985.

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Centro Cultural Recoleta (Buenos Aires, Argentina), ed. Testa + Bedel + Benedit: 30 años del CCR. Buenos Aires: Centro Cultural Recoleta, 2010.

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Book chapters on the topic "CCR5"

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Hütter, Gero. "CCR5." In Encyclopedia of Signaling Molecules, 828–32. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101567.

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Hütter, Gero. "CCR5." In Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101567-1.

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Soria, Gali, and Adit Ben-Baruch. "The CCL5/CCR5 Axis in Cancer." In Chemokine Receptors in Cancer, 109–30. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-267-4_7.

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Yasuda, Nobuyoshi. "CCR5 Receptor Antagonist." In The Art of Process Chemistry, 45–75. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527633562.ch2.

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Pryde, David C., and Christopher G. Barber. "CCR5 Antagonists in HIV." In Methods and Principles in Medicinal Chemistry, 207–38. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527631995.ch10.

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Junker, Anna, Artur Kamil Kokornaczyk, Ann Kathrin Strunz, and Bernhard Wünsch. "Selective and Dual Targeting of CCR2 and CCR5 Receptors: A Current Overview." In Topics in Medicinal Chemistry, 187–241. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/7355_2014_40.

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Cornu, Tatjana I., Claudio Mussolino, Kristie Bloom, and Toni Cathomen. "Editing CCR5: A Novel Approach to HIV Gene Therapy." In Advances in Experimental Medicine and Biology, 117–30. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2432-5_6.

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Hütter, Gero. "Transplantation of CCR5-Δ32/Δ32 Stem Cells May Cure HIV Infection." In Stem Cells and Cancer Stem Cells, Volume 13, 35–41. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7233-4_3.

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Webb, Nicholas E., and Benhur Lee. "Quantifying CD4/CCR5 Usage Efficiency of HIV-1 Env Using the Affinofile System." In Methods in Molecular Biology, 3–20. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3046-3_1.

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Price, David. "Maraviroc (Selzentry): The First-in-Class CCR5 Antagonist for the Treatment of HIV." In Modern Drug Synthesis, 17–27. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470768594.ch2.

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Conference papers on the topic "CCR5"

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Hsieh, Chia-Ling, Che-Ming Liu, and Shian-Ying Sung. "Abstract 1559: CCR5-CCRL2 regulates CCL5-induced organ specific metastasis: thein vitroandin vivostudies." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1559.

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Abid, S., E. Marcos, A. Parpaleix, V. Amsellem, M. Breau, A. Houssaini, N. Vienney, et al. "CCR2- and CCR5-Mediated Crosstalk Between Macrophages and Pulmonary-Artery Smooth Muscle Cells Drives Pulmonary Hypertension." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4410.

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Parpaleix, Aurelien, Shariq Abid, Elisabeth Marcos, Valérie Amsellem, Amal Houssaïni, Marielle Breau, Daigo Sawaki, et al. "Targeting CCR2 and CCR5 to inhibit macrophage/pulmonary artery smooth muscle cells cross-talk in pulmonary hypertension." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3066.

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Chang, Hui-Wen, Hui-Ju Li, Chia-Ling Hsieh, and Shian-Ying Sung. "Abstract 302: CCR5 and CCRL2 accommodating responses to CCL5 induces directional cancer cells migration and organ specific metastasis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-302.

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Agarwal, Alpna, Eron Oronsaye, Arthur Nadas, Susan Zolla-Pazner, and Timothy Cardozo. "CCR5/CXCR4 discriminating sites in the HIV-1 gp120 core." In the 2nd ACM Conference. New York, New York, USA: ACM Press, 2011. http://dx.doi.org/10.1145/2147805.2147888.

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Zhao, W., RL Toonkel, M. Sole, AC Borczuk, and CA Powell. "Lung Adenocarcinoma Invasion by TGFBRII Deficient Cells Requires RANTES/CCR5." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5133.

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Halama, Niels, Inka Zoernig, Anna Berthel, Christoph Kahlert, Fee Klupp, Meggy Suarez-Carmona, Karsten Brand, et al. "Abstract 3021: CCR5 inhibition: macrophage repolarization therapy for colorectal cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3021.

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Silva, Thauane, Gabrielle Vale, André Ferreira, Dumith Bou-Habib, Marilda Siqueira, Thiago Lopes, and Milene Miranda. "Modulation of host antiviral restriction factors by ccr5 and cxcr4 ligands." In IV International Symposium on Immunobiologicals & VII Seminário Anual Científico e Tecnológico. Instituto de Tecnologia em Imunobiológicos, 2019. http://dx.doi.org/10.35259/isi.sact.2019_32700.

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Halama, Niels, Inka Zoernig, Anna Berthel, Christoph Kahlert, Fee Klupp, Meggy Suarez-Carmona, Juergen Krauss, et al. "Abstract B037: Macrophage repolarization therapy in metastatic colorectal cancer: CCR5 inhibition." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b037.

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Barroso, Edmilson Pereira, Jorgimar Peres Ferreira, Fabiana Souza da Silva, Abigail Gonçalves da Silva, Maria Rafaela da Costa Martins, and Eder Ferreira de Arruda. "HIV: O USO TERAPÊUTICO DE CÉLULAS-TRONCO HEMATOPOIÉTICAS SEM CCR5 FUNCIONAL." In I CONGRESSO NORTE NORDESTE DE ANÁLISES CLÍNICAS E TOXINOLOGIA (ONLINE). EDITORA OMNIS SCIENTIA, 2021. http://dx.doi.org/10.47094/iconnact.2020/60-63.

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Reports on the topic "CCR5"

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Chen, Liangyu, Shi Yin, Yunqing Hou, Ying Liu, Shulei Li, Hui Xue, and Jiamei Liu. The therapeutic effect of inhibition of CCR5 on animal models of stroke or traumatic brain injury: A Systematic review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0026.

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Adair, M. The CCRS Quicklook Swath Browser. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2000. http://dx.doi.org/10.4095/219632.

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Adair, M. The CCRS Quicklook Swath Browser. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2000. http://dx.doi.org/10.4095/219646.

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Cyr, I., and Th Toutin. RADARSAT-1 Stereo Advisor on CCRS Web. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2001. http://dx.doi.org/10.4095/219705.

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Graham, D. F., A. N. Rencz, and V. H. Singhroy. GSC - CCRS Storefront Project, conclusions from selected projects. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1994. http://dx.doi.org/10.4095/193706.

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Vachon, P. W., A. L. Gray, and K. E. Mattar. RADARSAT and ERS Repeat-Pass SAR Interferometry at CCRS. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1998. http://dx.doi.org/10.4095/219176.

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7

Zou, Chenghui, Weng Zhang, Mao Li, Dan He, Yujie Han, and Mao Lu. A meta-analysis of association between CCL5、CCL11、CCL17 polymorphisms and AD. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0148.

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Abstract:
Review question / Objective: At present, many studies on the association between CCL5、CCL11、CCL17 polymorphisms and atopic dermatitis（AD）are inconsistent. We conducted this meta-analysis of Case control trial to evaluate the association between CCL5、CCL11、CCL17 polymorphisms and atopic dermatitis（AD). Condition being studied: Since the discovery of cytokines, and in particular the role of chemokines in the progression of AD, many clinical studies have been carried out around the world to explore the association of AD with chemokine polymorphism. However, the quality, type and conclusions of studies on the correlation between chemokine polymorphism and AD are inconsistent. Foreign studies have shown that chemokine polymorphism is statistically significant in relation to AD. Studies by Menzies-Gow A et al have shown that a new therapeutic strategy targeting to block CCL11 signal has been proven to significantly improve patients with moderate to severe AD. However, some foreign studies have also reported that chemokine polymorphism is unrelated to AD.
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Bentz, Dale P., Xiuping Feng, Claus-Jochen Haecker, and Paul E. Stutzman. Analysis of CCRL proficiency cements 135 and 136 using CEMHYD3D. Gaithersburg, MD: National Institute of Standards and Technology, 2000. http://dx.doi.org/10.6028/nist.ir.6545.

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9

Wolfe, S. A. Permafrost science at ESS: a workshop on GSC/CCRS scientific opportunities. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2010. http://dx.doi.org/10.4095/263373.

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10

McGurrin, B. Remote Sensing Information: How and Why CCRS Developed an Online Database. Natural Resources Canada/CMSS/Information Management, 1990. http://dx.doi.org/10.4095/217657.

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