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Science 29 July 1988:
Vol. 241. no. 4865, pp. 573 - 576
DOI: 10.1126/science.2899908
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Articles

Science, Vol 241, Issue 4865, 573-576
Copyright © 1988 by American Association for the Advancement of Science

articles

HIV-1-infected T cells show a selective signaling defect after perturbation of CD3/antigen receptor

GP Linette, RJ Hartzman, JA Ledbetter, and CH June

Department of Microbiology, Georgetown University School of Medicine, Washington, DC 20007.

The binding of antigen or monoclonal antibody to the T cell receptor for antigen or the closely associated CD3 complex causes increases in the concentration of intracellular ionized calcium and subsequent cell proliferation. By measuring second messenger production in primary cultures of human immunodeficiency virus (HIV-1)--infected T cells stimulated with monoclonal antibodies specific for either CD3 or CD2, a specific impairment of membrane signaling was revealed. The HIV-1--infected T cells were unable to mobilize Ca2+ after stimulation with anti-CD3, whereas CD2-induced calcium mobilization remained intact. Furthermore, the HIV-1--infected cells proliferated poorly after CD3 stimulation, although the cells retained normal DNA synthesis in response to interleukin-2 stimulation. These results show that the signals initiated by CD2 and CD3 can be regulated independently within the same T cell; uncoupling of signal transduction after antigen-specific stimulation provides a biochemical mechanism to explain, in part, the profound immunodeficiency of patients with HIV-1 infection.


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CELL-RECEPTOR FUNCTION IN HIV INFECTION.
(1988)
Journal Watch (General) 1988, 8
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Science. ISSN 0036-8075 (print), 1095-9203 (online)