Abstract
We investigated the role of ICAM-3 in DC-SIGN-mediated human immunodeficiency virus (HIV) infection of CD4(+) T cells. Our results demonstrate that ICAM-3 does not appear to play a role in DC-SIGN-mediated infection of CD4(+) T cells as virus is transmitted equally to ICAM-3(+) or ICAM-3(-) Jurkat T cells. However, HIV-1 replication is enhanced in ICAM-3(-) cells, suggesting that ICAM-3 may limit HIV-1 replication. Similar results were obtained when SIV replication was examined in ICAM-3(+) and ICAM-3(-) CEMx174 cells. Furthermore, while ICAM-3 has been proposed to play a co-stimulatory role in T cell activation, DC-SIGN expression on antigen presenting cells did not enhance antigen-dependent activation of T cells. Together, these data indicate that while ICAM-3 may influence HIV-1 replication, it does so independent of DC-SIGN-mediated virus transmission or activation of CD4(+) T cells.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, CD / genetics
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Antigens, CD / physiology*
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CD4-Positive T-Lymphocytes / immunology
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CD4-Positive T-Lymphocytes / virology
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Cell Adhesion Molecules / deficiency
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Cell Adhesion Molecules / genetics
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Cell Adhesion Molecules / physiology*
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Cell Line
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HIV-1 / immunology
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HIV-1 / pathogenicity
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HIV-1 / physiology*
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Humans
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Jurkat Cells
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Lectins, C-Type / genetics
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Lectins, C-Type / physiology*
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Lymphocyte Activation
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / physiology*
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Recombinant Proteins / genetics
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Recombinant Proteins / metabolism
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Simian Immunodeficiency Virus / pathogenicity
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Simian Immunodeficiency Virus / physiology
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Solubility
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Virus Replication / physiology
Substances
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Antigens, CD
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Cell Adhesion Molecules
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DC-specific ICAM-3 grabbing nonintegrin
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ICAM3 protein, human
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Lectins, C-Type
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Receptors, Cell Surface
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Recombinant Proteins