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B and AP-1 Transcription Factors1
*
Centre de Recherches de Biochimie Macromoléculaire, Laboratoire d’Immunologie des Infections Rétrovirales, Institut de Biologie, Montpellier, France; and
Centre de Biochimie, Nice, France
Although the molecular mechanisms by which the HIV-1 triggers
either T cell activation, anergy, or apoptosis remain poorly
understood, it is well established that the interaction of HIV-1
envelope glycoproteins with cell surface CD4 delivers signals to the
target cell, resulting in activation of transcription factors such as
NF-
B and AP-1. In this study, we report the first evidence
indicating that kinases MEK-1 (MAP kinase/Erk kinase) and ERK-1
(extracellular signal-regulated kinase) act as intermediates in the
cascade of events that regulate NF-B and AP-1 activation upon HIV-1
binding to cell surface CD4. We found that CEM cells transfected with
dominant negative forms of MEK-1 or ERK-1 do not display NF-B
activation after HIV-1 binding to CD4. In contrast, NF-B activation
was observed in these cells after PMA stimulation. Although the
different cell lines studied expressed similar amounts of CD4 and
p56lck, HIV-1 replication and HIV-1-induced
apoptosis were slightly delayed in cells expressing dominant negative
forms of MEK-1 or ERK-1 compared with parental CEM cells and cells
expressing a constitutively active mutant form of MEK-1 or wild-type
ERK-1. In light of recently published data, we propose that a positive
signal initiated following oligomerization of CD4 by the virus is
likely to involve a recruitment of active forms of
p56lck, Raf-1, MEK-1, and ERK-1, before AP-1
and NF-B activation.
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