Publications & Reports

Infection and apoptotic cell death of CD4+ T cells during an immune response to HIV-1-pulsed dendritic cells.

Cameron PU, Pope M, Gezelter S, Steinman RM
Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

Abstract

Interacting dendritic cells and helper CD4+ lymphocytes form a microenvironment that is permissive for HIV-1 replication. The virus need only be pulsed initially onto the dendritic cells, which then transfer HIV-1 to the lymphocytes that are responding to presented antigens or superantigens. We have pursued underlying mechanisms in this system, because it provides a model for the infection of antigen-reactive, primary T cells. Pulsing the T cells with HIV-1 results in much less of a subsequent infection than does pulsing the dendritic cells. The latter pulse occurs effectively in the presence of AZT. Direct examination of the interacting dendritic cells and T cells reveals extensive production of p24 by many of the lymphocytes, including syncytia. The majority of the responding T cells die during the coculture. Apoptosis accounts for much of this death as revealed by in situ nick translation assays for DNA endonucleolysis, and hypodiploid profiles on staining with DNA-binding dyes. Therefore the microenvironment that is generated between antigen-presenting dendritic cells and T cells reveals the cytopathic potential of HIV-1, because there is such extensive and rapid death by apoptosis of antigen-reactive T cells.

Publication

  • Journal: AIDS Research and Human Retroviruses
  • Published: 01/01/1994
  • Volume: 10
  • Issue: 1
  • Pagination: 61-71