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Inhibition of functional properties of tetanus antigen-specific T-cell
clones by envelope glycoprotein GP120 of human immunodeficiency virus
N Chirmule, VS Kalyanaraman, N Oyaizu, HB Slade and S Pahwa
Department of Pediatrics, North Shore University Hospital, Cornell
University Medical College, Manhasset, NY 11030.
We investigated mechanisms by which the soluble native envelope
glycoprotein gp120 of the human immunodeficiency virus (HIV-1) suppresses
antigen-driven T cell responses. For this study, exogenous interleukin-2
(IL-2)-independent, antigen-specific, CD4 positive, human T-cell clones
were developed by cyclic restimulation with soluble tetanus toxoid antigen.
In the presence of soluble antigen and antigen- presenting cells (APC),
T-cell clones proliferated and secreted IL-2. Purified gp120 suppressed the
proliferative responses of the T-cell clones with concomitant suppression
of IL-2 secretion; proliferative responses of CD8+ T cells preincubated
with gp120 were not inhibited. A short pulse of 20 minutes with gp120 was
sufficient to inhibit the proliferative response of the T-cell clones.
Anti-CD3 monoclonal antibody (MoAb)-driven proliferation of the T-cell
clones was also suppressed by gp120, but responses elicited by mitogens,
phorbol myristate acetate (PMA) plus calcium ionophore, ionomycin, anti-CD2
MoAbs, and a combination of anti-CD3 plus anti-CD28 MoAb driven responses
remained unaffected. Investigation of signal transduction events showed
that antigen-driven early activation signals via translocation of protein
kinase C (PKC), increase in intracellular inositol phosphates, and increase
in intracellular calcium were suppressed in gp120 pretreated, tetanus
toxoid antigen-stimulated T- cell clones. One mechanism of immune
suppression by gp120 may involve interference with the initiation of signal
transduction through the T- cell receptor complex.
Volume 75,
Issue 1,
pp. 152-159,
01/01/1990
Copyright © 1990 by The American Society of Hematology
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