Crossllnklng CD4 by human immunodeficiency virus gp120 primes T cells for activation-induced apoptosis

Nirmal K. Banda, Jacques Bernier, David K. Kurahara, Roland Kurrle, Nancy Haigwood, Rafik P. Sekaly, Terri Helman Finkel

    Research output: Contribution to journalArticlepeer-review

    612 Scopus citations


    During human immunodeficiency virus (HIV) infection there is a profound and selective decrease in the CD4+ population of T lymphocytes. The mechanism of this depletion is not understood, as only a small fraction of all CD4+ cells appear to be productively infected with HIV-1 in seropositive individuals. In the present study, crosslinking of bound gp120 on human CD4+ T cells followed by signaling through the T cell receptor for antigen was found to result in activation-dependent cell death by a form of cell suicide termed apoptosis, or programmed cell death. The data indicate that even picomolar concentrations of gp120 prime T cells for activationinduced cell death, suggesting a mechanism for CD4+ T cell depletion in acquired immune deficiency syndrome (AIDS), particularly in the face of concurrent infection and antigenic challenge with other organisms. These results also provide an explanation for the enhancement of infection by certain antibodies against HIV, and for the paradox that HIV appears to cause AIDS after the onset of antiviral immunity.

    Original languageEnglish (US)
    Pages (from-to)1099-1106
    Number of pages8
    JournalJournal of Experimental Medicine
    Issue number4
    StatePublished - Oct 1 1992

    ASJC Scopus subject areas

    • Immunology and Allergy
    • Immunology

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