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(Received for publication, June 13, 1996, and in revised form, September 10, 1996)
From the Hans-Spemann-Laboratorium, Max-Planck-Institut für
Immunbiologie, Stübeweg 51, D-79108 Freiburg, Germany
The early transcription unit 3 (E3) of human
adenoviruses encodes proteins which appear to subvert host defense
mechanisms. For example, the E3/19K protein inhibits the transport of
major histocompatibility complex (MHC) class I molecules to the cell surface and thereby prevents cell lysis by cytotoxic T cells. Tumor
necrosis factor
Volume 271, Number 47,
Issue of November 22, 1996
pp. 30249-30255
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
Induces the Adenovirus Early 3 Promoter
by Activation of NF-
B
(TNF) stimulates expression of MHC molecules on the
cell surface of normal cells but not of E3+ cells, rather,
a further reduction of MHC expression is evident. This was attributed
to the increased expression of E3/19K upon TNF treatment, an effect
also observed for other E3 proteins. We investigated the mechanism of
the TNF-mediated up-regulation of E3 products. We show that TNF
stimulates expression of a luciferase reporter gene driven by the E3
promoter. Mutation of individual transcription factor binding sites
within the E3 promoter reveals the importance of the NF-
B binding
site 2 for TNF inducibility. Electrophoretic mobility shift assays
using antibodies directed against various members of the NF-B family
demonstrate that stimulation by TNF is mediated by the p50-p65 NF-B
complex. TNF inducibility does not depend on coexpression of E1A and
can be observed during infection. Interestingly, the E3 promoter seems
to be the only early promoter responsive to TNF and the only adenovirus
promoter containing an NF-B site. The implications of this
regulatory mechanism for the adenovirus life cycle and its pathogenesis
are discussed.
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