A T Cell Clone Which Reflects the Functional Defects Observed in the T Cells of AIDS Patients
Infection of T cells by the Human Immunodeficiency Virus (HIV) renders the body susceptible to attack by opportunistic infections as these cells of the immune system are not only killed by the virus, but are also rendered defective in their function (1,2,3,4). It is well documented that T cell defects associated with HIV infection in AIDS patients include reduced production of the lymphokine, IL-2, and an inability to mobilize Ca++ following mitogenic or antigenic stimulation. T cell dysfunction has also been attributed to downmodulation of CD3 and CD4, possibly as a result in their uncoupling (5,6,7). Since many of these events that lead to T cell activation are under some of the same controls as events involved in the activation of HIV (8–9), a T cell model system to study physiologic influences on HIV expression and the effects of the virus on the cell’s activation signals would be of great value.
KeywordsHuman Immunodeficiency Virus Jurkat Cell Acquire Immunodeficiency Syndrome Inositol Triphosphate Cell Model System
Unable to display preview. Download preview PDF.
- 12.Tong-Starksen, S., P.A. Luciew, and B.M. Peterlin. 1989. Signaling through T Lymphocyte proteins, TCR/CD3 and CD28, activates the HIV-1 long terminal repeat. J. Immunol. 142: 702–707.Google Scholar
- 14.Mauger, B., A. Weiss, J. Imboden, T. Laing, and J.D. Stobo. 1987. The role of protein kinase C in transmembrane signaling by the T-cell antigen receptor complex: effects of stimulation with soluble or immobilized CD3 antibodies. J. Immunol. 139: 2755.Google Scholar