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Pathogenesis and Immunity

Migration ofAntigen-Specific T Cells Away from CXCR4-Binding Human ImmunodeficiencyVirus Type 1gp120

Diana M. Brainard, William G. Tharp, Elva Granado, Nicholas Miller, Alicja K. Trocha, Xiang-Hui Ren, Brian Conrad, Ernest F. Terwilliger, Richard Wyatt, Bruce D. Walker, Mark C. Poznansky
Diana M. Brainard
1Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114
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William G. Tharp
1Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114
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Elva Granado
1Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114
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Nicholas Miller
1Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114
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Alicja K. Trocha
1Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114
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Xiang-Hui Ren
2Division of Experimental Medicine, Beth Israel Deaconess Medical Center, and Harvard Institutes of Medicine
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Brian Conrad
3Department of Mathematics, University of Michigan, Ann Arbor, Michigan 48109
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Ernest F. Terwilliger
2Division of Experimental Medicine, Beth Israel Deaconess Medical Center, and Harvard Institutes of Medicine
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Richard Wyatt
4Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115
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Bruce D. Walker
1Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114
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Mark C. Poznansky
1Partners AIDS Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114
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  • For correspondence: mpoznansky@partners.org
DOI: 10.1128/JVI.78.10.5184-5193.2004
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ABSTRACT

Cell-mediated immunity depends in part on appropriate migration and localization of cytotoxic T lymphocytes (CTL), a process regulated by chemokines and adhesion molecules. Many viruses, including human immunodeficiency virus type 1 (HIV-1), encode chemotactically active proteins, suggesting that dysregulation of immune cell trafficking may be a strategy for immune evasion. HIV-1 gp120, a retroviral envelope protein, has been shown to act as a T-cell chemoattractant via binding to the chemokine receptor and HIV-1 coreceptor CXCR4. We have previously shown that T cells move away from the chemokine stromal cell-derived factor 1 (SDF-1) in a concentration-dependent and CXCR4 receptor-mediated manner. Here, we demonstrate that CXCR4-binding HIV-1 X4 gp120 causes the movement of T cells, including HIV-specific CTL, away from high concentrations of the viral protein. This migratory response is CD4 independent and inhibited by anti-CXCR4 antibodies and pertussis toxin. Additionally, the expression of X4 gp120 by target cells reduces CTL efficacy in an in vitro system designed to account for the effect of cell migration on the ability of CTL to kill their target cells. Recombinant X4 gp120 also significantly reduced antigen-specific T-cell infiltration at a site of antigen challenge in vivo. The repellant activity of HIV-1 gp120 on immune cells in vitro and in vivo was shown to be dependent on the V2 and V3 loops of HIV-1 gp120. These data suggest that the active movement of T cells away from CXCR4-binding HIV-1 gp120, which we previously termed fugetaxis, may provide a novel mechanism by which HIV-1 evades challenge by immune effector cells in vivo.

  • Copyright © 2004 American Society for Microbiology
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Migration ofAntigen-Specific T Cells Away from CXCR4-Binding Human ImmunodeficiencyVirus Type 1gp120
Diana M. Brainard, William G. Tharp, Elva Granado, Nicholas Miller, Alicja K. Trocha, Xiang-Hui Ren, Brian Conrad, Ernest F. Terwilliger, Richard Wyatt, Bruce D. Walker, Mark C. Poznansky
Journal of Virology Apr 2004, 78 (10) 5184-5193; DOI: 10.1128/JVI.78.10.5184-5193.2004

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Migration ofAntigen-Specific T Cells Away from CXCR4-Binding Human ImmunodeficiencyVirus Type 1gp120
Diana M. Brainard, William G. Tharp, Elva Granado, Nicholas Miller, Alicja K. Trocha, Xiang-Hui Ren, Brian Conrad, Ernest F. Terwilliger, Richard Wyatt, Bruce D. Walker, Mark C. Poznansky
Journal of Virology Apr 2004, 78 (10) 5184-5193; DOI: 10.1128/JVI.78.10.5184-5193.2004
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KEYWORDS

HIV Envelope Protein gp120
Receptors, CXCR4
T-Lymphocytes

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