The Experts below are selected from a list of 5319 Experts worldwide ranked by ideXlab platform

Philip M Murphy - One of the best experts on this subject based on the ideXlab platform.

  • molecular cloning of leukotactin 1 a novel human Beta chemokine a chemoattractant for neutrophils monocytes and lymphocytes and a potent agonist at cc chemokine receptors 1 and 3
    Journal of Immunology, 1997
    Co-Authors: Byung S Youn, Massimo Locati, Shang M Zhang, Doo H Park, James E Pease, Kathleen Antol, Hal E. Broxmeyer, Philip M Murphy, Byoung S Kwon
    Abstract:

    A new member of human Beta-chemokine cDNA was isolated and named leukotactin-1 (Lkn-1). Lkn-1, along with murine macrophage inflammatory protein-related protein-1 and -2, defines a subgroup of Beta-Chemokines based on two conserved cysteines in addition to the four others conserved in all Beta-Chemokines. The putative mature Lkn-1 is composed of 92 amino acids with a calculated m.w. of 10,162. The Lkn-1 gene was mapped to human chromosome 17, region q12. Recombinant Lkn-1 was a potent chemoattractant for neutrophils, monocytes, and lymphocytes and induced calcium flux in these cells. Lkn-1 specifically induced calcium flux in CCR1- and CCR3-expressing HOS cell lines. Lkn-1 suppressed colony formation by human granulocyte-macrophage, erythroid, and multipotential progenitor cells stimulated by combinations of growth factors. Hence, we have isolated and characterized a human C6 Beta-chemokine that is a potent agonist at CCR1 and CCR3 and shows broad biologic activities, including leukocyte chemoattraction.

  • cloning chromosomal localization and rna expression of a human β chemokine receptor like gene
    DNA and Cell Biology, 1995
    Co-Authors: Christophe Combadiere, Sunil K. Ahuja, Philip M Murphy
    Abstract:

    A human cDNA encoding a putative G protein-coupled receptor designated chemokine Beta receptor-like 1 (CMKBRL1) was isolated from an eosinophilic leukemia library. Its deduced sequence is approximately 40% identical to previously cloned receptors for the Beta Chemokines macrophage inflammatory protein-1 alpha (MIP-1 alpha), RANTES, and monocyte chemoattractant protein-1 (MCP-1), which are chemoattractants for blood leukocytes, and is 83% identical to the product of the orphan rat cDNA RBS 11. Like the MIP-1 alpha/RANTES receptor, CMK-BRL1 is encoded by a small, single-copy gene that maps to chromosome 3p21 and is expressed in leukocytes. However, two screening assays with a broad panel of Chemokines failed to identify its ligand. CMKBRL1 mRNA was detectable by Northern blot hybridization in neutrophils and monocytes, but not eosinophils, and was also found in eight solid organs that were tested with particularly high expression in brain. The RNA distribution of the known Beta chemokine receptors was overlapping but distinct from that of CMKBRL1. MIP-1 alpha/RANTES receptor mRNA was detectable in neutrophils, monocytes, eosinophils, and in all eight solid organs tested, with particularly high expression in placenta, lung, and liver. MCP-1 receptor mRNA was found in monocytes, lung, liver, and pancreas. These results suggest that the ligand for the putative CMKBRL1 receptor is a Beta chemokine that targets both neutrophils and monocytes. Moreover, the RNA distributions suggest that CMKBRL1, the MIP-1 alpha/RANTES receptor, and the MCP-1 receptor may have both overlapping and distinct biological roles.

  • Molecular piracy of mammalian interleukin-8 receptor type B by herpesvirus saimiri.
    Journal of Biological Chemistry, 1993
    Co-Authors: Sunil K. Ahuja, Philip M Murphy
    Abstract:

    Abstract Viruses are known to acquire and modify the genes of their hosts to attain a survival advantage in the host environment. Herpesvirus saimiri (HVS) is a T-lymphotropic virus that causes fatal lymphoproliferative diseases in several non-human primates. The gene ECRF3 of HVS was most likely acquired from a primate host. ECRF3 encodes a putative seven-transmembrane-domain receptor that is remotely related (approximately 30% amino acid identity) to the known mammalian alpha and Beta chemokine receptors, namely interleukin-8 receptor (IL8R) types A and B and the MIP-1 alpha/RANTES receptor, respectively. Chemokines regulate the trafficking, activation, and, in some cases, proliferation of myeloid and lymphoid cell types. We now show that ECRF3 encodes a functional receptor for the alpha Chemokines IL-8, GRO/melanoma growth stimulatory activity (MGSA), and NAP-2 but not for Beta Chemokines, a specificity identical to that of IL8RB. Paradoxically, IL8RA shares 77% amino acid identity with IL8RB but is not a receptor for GRO/MGSA or NAP-2. This is the first functional characterization of a viral seven-transmembrane-domain receptor. It suggests a novel role for alpha Chemokines in the pathogenesis of HVS infection by transmembrane signaling via the product of ECRF3.

Anjali Singh - One of the best experts on this subject based on the ideXlab platform.

  • potential role for cd63 in ccr5 mediated human immunodeficiency virus type 1 infection of macrophages
    Journal of Virology, 2003
    Co-Authors: Jana J Von Lindern, Daniel R Rojo, Kathie Grovitferbas, Christine Yeramian, Cheng Deng, Georges Herbein, Monique R Ferguson, Todd C Pappas, Julie M Decker, Anjali Singh
    Abstract:

    Macrophages and CD4(+) lymphocytes are the principal target cells for human immunodeficiency virus type 1 (HIV-1) infection, but the molecular details of infection may differ between these cell types. During studies to identify cellular molecules that could be involved in macrophage infection, we observed inhibition of HIV-1 infection of macrophages by monoclonal antibody (MAb) to the tetraspan transmembrane glycoprotein CD63. Pretreatment of primary macrophages with anti-CD63 MAb, but not MAbs to other macrophage cell surface tetraspanins (CD9, CD81, and CD82), was shown to inhibit infection by several R5 and dualtropic strains, but not by X4 isolates. The block to productive infection was postfusion, as assessed by macrophage cell-cell fusion assays, but was prior to reverse transcription, as determined by quantitative PCR assay for new viral DNA formation. The inhibitory effects of anti-CD63 in primary macrophages could not be explained by changes in the levels of CD4, CCR5, or Beta-Chemokines. Infections of peripheral blood lymphocytes and certain cell lines were unaffected by treatment with anti-CD63, suggesting that the role of CD63 in HIV-1 infection may be specific for macrophages.

Louis Flancbaum - One of the best experts on this subject based on the ideXlab platform.

  • cellular immunotherapy of advanced human immunodeficiency virus type 1 infection using autologous lymph node lymphocytes effects on chemokine production
    The Journal of Infectious Diseases, 1999
    Co-Authors: Pierre L Triozzi, Wayne Aldrich, Herbert S Bresler, Michael F Para, Louis Flancbaum
    Abstract:

    A pilot study was undertaken in patients with human immunodeficiency virus type 1 (HIV-1) infection to examine the effects of infusing autologous lymph node lymphocytes that had been cultured ex vivo in conditions designed to maximize the specific secretion of HIV-1-suppressive factors, including Beta Chemokines. Ten patients with CD4 cell counts between 119 and 436/microliter on antiretroviral drugs received a single infusion of CD4 and CD8 lymph node lymphocytes. There were no serious acute or chronic adverse clinical effects. Increases in serum levels of macrophage inflammatory protein 1Beta (MIP-1Beta) and increases in the production of MIP-1Beta by peripheral blood lymphocytes in response to HIV-1 env were observed. Increases in CD4 and CD8 cell counts and skin test reactivity to recall antigens and decreases in HIV-1 virus load were also observed. This cellular immunotherapy can modulate Beta chemokine production in patients with advanced HIV-1 infection and may contribute immunorestorative and antiviral activities.

P E Jolly - One of the best experts on this subject based on the ideXlab platform.

  • effect of Beta Chemokines on human immunodeficiency virus type 1 replication binding uncoating and ccr5 receptor expression in human monocyte derived macrophages
    Journal of Human Virology, 1999
    Co-Authors: Y Jiang, P E Jolly
    Abstract:

    OBJECTIVES We examined the effect and time of addition of Beta-Chemokines on human immunodeficiency virus type 1 (HIV-1) replication, binding, and uncoating in human macrophages and measured CCR5 receptor expression during virus binding and uncoating. METHODS Macrophages were treated with Beta-Chemokines before infection, at infection, or postinfection, and virus replication was determined by p24 antigen level. Binding and uncoating of 35[S]-methionine-labeled HIV-1 was measured. CCR5 expression was determined by flow cytometry. RESULTS The Beta-Chemokines potently inhibited virus replication. The strongest inhibition occurred when cultures were pretreated and maintained with Beta-Chemokines. Beta-Chemokines also caused strong inhibition of viral uncoating and a considerable decrease in CCR5 expression during uncoating. CONCLUSIONS CCR5 receptors appear to be internalized and recycled to the cell surfaces during HIV entry. The down-regulation of CCR5 expression by Beta-Chemokines during virus uncoating probably accounts for the reduction in virus uncoating (entry) and hence in virus replication.

Adolfo Toledano Gasca - One of the best experts on this subject based on the ideXlab platform.

  • hippocampal ccr5 rantes elevations in a rodent model of post traumatic stress disorder maraviroc a ccr5 antagonist increases corticosterone levels and enhances fear memory consolidation
    Biomolecules, 2020
    Co-Authors: Jose Joaquin Merino, Vilma Munetongomez, Cesar Munetongomez, Maria Angeles Perezizquierdo, Maria Loscertales, Adolfo Toledano Gasca
    Abstract:

    Background: Contextual fear conditioning (CFC) is a rodent model that induces a high and long-lasting level of conditioning associated with traumatic memory formation; this behavioral paradigm resembles many characteristics of posttraumatic stress disorder (PSTD). Chemokines (chemotactic cytokines) play a known role in neuronal migration and neurodegeneration but their role in cognition is not totally elucidated. Aim: We ascertain whether CCR5/RANTES Beta Chemokines (hippocampus/prefrontal cortex) could play a role in fear memory consolidation (CFC paradigm). We also evaluated whether chronic stress restraint (21 days of restraint, 6-h/day) could regulate levels of these Beta Chemokines in CFC-trained rats; fear memory retention was determined taking the level of freezing (context and tone) by the animals as an index of fear memory consolidation 24 h after CFC training session; these Chemokines (CCR5/RANTES) and IL-6 levels were measured in the hippocampus and prefrontal cortex of chronically stressed rats, 24 h after CFC post-training, and compared with undisturbed CFC-trained rats (Experiment 1). In Experiment 2, rats received 1 mA of footshock during the CFC training session and fear memory consolidation was evaluated at 12 and 24 h after CFC training sessions. We evaluated whether RANTES levels could be differentially regulated at 12 and 24 h after CFC training; in Experiment 3, maraviroc was administered to rats (i.m: 100 mg/Kg, a CCR5 antagonist) before CFC training. These rats were not subjected to chronic stress restraint. We evaluated whether CCR5 blockade before CFC training could increase corticosterone, RANTES, or IL-6 levels and affects fear memory consolidation in the rats 24-h post-testing compared with vehicle CFC-trained rats. Results: Elevations of CCR5/RANTES chemokine levels in the hippocampus could have contributed to fear memory consolidation (24 h post-training) and chronic stress restraint did not affect these Chemokines in the hippocampus; there were no significant differences in CCR5/RANTES levels between stressed and control rats in the prefrontal cortex (Experiment 1). In Experiment 2, hippocampal CCR5/RANTES levels increased and enhanced fear memory consolidation was observed 12 and 24 h after CFC training sessions with 1 mA of footshock. Increased corticosterone and CCR5/RANTES levels, as well as a higher freezing percentage to the context, were found at 24 h CFC post-testing in maraviroc-treated rats as compared to vehicle-treated animals (experiment-3). Conversely, IL-6 is not affected by maraviroc treatment in CFC training. Conclusion. Our findings suggest a role for a hippocampal CCR5/RANTES axis in contextual fear memory consolidation; in fact, RANTES levels increased at 12 and 24 h after CFC training. When CCR5 was blocked by maraviroc before CFC training, RANTES (hippocampus), corticosterone levels, and fear memory consolidation were greater than in vehicle CFC-trained rats 24 h after the CFC session.