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*
The Wallenberg Laboratory, Section for Tumour Immunology, Department of Cell and Molecular Biology, University of Lund, and
Pharmacia & Upjohn, Lund, Sweden; and
Department of Biology and Molecular Biology Institute, San Diego State University, San Diego, CA 92182
The role of Rel and activation protein-1 (AP-1) in IL-2 promoter
activity in B7-1- and leukocyte function-associated Ag-3
(LFA-3)-costimulated T cells has been evaluated. We demonstrate that
overexpression of c-Jun but not c-Fos increases IL-2 promoter activity
in both B7-1- and LFA-3-costimulated Jurkat T cells. Cotransfection of
both c-Jun and c-Fos substitutes for B7-1 costimulation in driving an
activation protein-1 response element but not for the IL-2 promoter.
Overexpression of Rel proteins demonstrated that p65-expressing Jurkat
cells transcribed equally well a nuclear factor 
ß reporter
construct when costimulated with B7-1 or LFA-3, but transcription of
IL-2 promoter or CD28 response element (CD28RE)-driven reporters was
superior in B7-1-costimulated cells. Combined expression of c-Jun and
p65 induced vigorous transcription of IL-2 promoter- and CD28RE-driven
reporter constructs in both LFA-3- and B7-1-costimulated Jurkat cells.
Mutating the CD28RE but not the upstream nuclear factor ß-binding
site in the IL-2 promoter reduced B7-1-driven transcription >90%. The
results implicates a major role of the CD28RE in the integration of
p65/c-Jun-mediated transcription within the IL-2 promoter. We suggest
that the transition from an autocrine LFA-3-driven immune response to a
B7--induced paracrine immune response involves the activation of c-Jun
and p65, which target the CD28RE region of the IL-2 promoter.
This article has been cited by other articles:
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