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*
Laboratoire d’Immunologie, Institut de Recherches Cliniques de Montréal, Montréal, Québec, Canada;
Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, Québec, Canada;
Department of Immunology, University of Toronto and the Wellesley Hospital Research Institute, Toronto, Ontario, Canada; and
§
Département de Microbiologie et Immunologie, Faculté de Médecine, Université de Montréal, Montréal, Québec, Canada
Binding of the HIV envelope glycoprotein gp120 to CD4 inhibits T
cell activation. We have used a murine T cell clone transfected with
either wild-type human CD4 or mutated forms of CD4 to characterize the
pathways involved in this inhibitory effect of gp120. Ag-induced
proliferation of T cell clones transfected with human CD4 was
completely inhibited in the presence of gp120, even though stimulation
of this clone is independent of a CD4/MHC class II interaction. In
addition, our results demonstrate that the inhibition by gp120 is not
due to the sequestration of lck from TCR and does not require
activation of lck by gp120. This suggests that CD4 can regulate the
initiation of T cell activation independently of its interaction with
lck. Moreover, we demonstrate that the nonresponsiveness induced by
gp120 can be reversed by soluble CD4 when added early after onset of
stimulation and that gp120 exerts its inhibitory effect when cells are
in the G0 
1 phase of the cell
cycle.
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