Abstract
The alpha4beta7 integrin has been shown to serve as a coreceptor for HIV. One anti-alpha4 integrin agent (natalizumab) has been approved for the treatment of multiple sclerosis and Crohn's disease. We found that activation of CD4+ T cells with retinoic acid induced the upregulation of alpha4 and beta7 integrins. However, natalizumab failed to block the replication of HIV-1 strains in lymphoid MT-4 cells or CD4+ T cells at concentrations up to 125microg/ml. Our results suggest that alpha4 integrins are not essential cofactors for HIV replication.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Anti-HIV Agents / pharmacology*
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Antibodies, Monoclonal / pharmacology*
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Antibodies, Monoclonal, Humanized
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CD4-Positive T-Lymphocytes / virology
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Dose-Response Relationship, Drug
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Drug Evaluation, Preclinical / methods
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HIV-1 / drug effects*
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HIV-1 / physiology
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Humans
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Integrin alpha4 / immunology*
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Lymphocyte Activation / drug effects
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Natalizumab
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U937 Cells
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Virus Replication / drug effects
Substances
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Anti-HIV Agents
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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Natalizumab
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Integrin alpha4