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Preparation and Use of HIV-1 Infected Primary CD4+ T-Cells as Target Cells in Natural Killer Cell Cytotoxic Assays
Published on: March 14, 2011
Crosslinking CD4 by human immunodeficiency virus gp120 primes T cells for activation-induced apoptosis
N K Banda1, J Bernier, D K Kurahara
1Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
Insights
Human immunodeficiency virus (HIV) infection depletes CD4+ T cells. HIV's gp120 protein triggers activation-induced cell death in CD4+ T cells, explaining immune deficiency in acquired immune deficiency syndrome (AIDS).
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human immunodeficiency virus (HIV) infection causes a significant reduction in CD4+ T lymphocytes.
- The precise mechanism behind this CD4+ T cell depletion remains unclear, as few cells are productively infected.
Purpose of the Study:
- To investigate the mechanism of CD4+ T cell depletion during HIV infection.
- To determine if HIV envelope protein gp120 contributes to T cell death.
Main Methods:
- Crosslinking of gp120 bound to human CD4+ T cells.
- Stimulation of T cell receptor signaling.
Main Results:
- Crosslinking gp120 and activating T cell receptor signaling induced activation-dependent cell death (apoptosis) in CD4+ T cells.
- Picomolar concentrations of gp120 were sufficient to prime T cells for this death pathway.
- This mechanism may explain CD4+ T cell depletion in acquired immune deficiency syndrome (AIDS), especially during co-infections.
Conclusions:
- HIV gp120 can induce apoptosis in CD4+ T cells through activation-dependent pathways.
- This finding provides a potential mechanism for CD4+ T cell loss in AIDS.
- The results also offer insights into enhanced HIV infection by certain antibodies and the progression to AIDS despite antiviral immunity.
Abstract:
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 activation-induced 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.
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