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Multiple cis-acting elements in the human immunodeficiency virus type 2
enhancer mediate the response to T-cell receptor stimulation by antigen in
a T-cell hybridoma line
MC Hannibal, DM Markovitz and GJ Nabel
Howard Hughes Medical Institute, Department of Internal Medicine,
University of Michigan Medical Center, Ann Arbor 48109-0650.
Transcription directed by the human immunodeficiency virus type 2 long
terminal repeat (HIV-2 LTR) responds to T-cell antigen receptor signaling.
Agents that stimulate T-cell signaling pathways activated by the antigen
receptor, such as phorbol ester, plant lectin, or anti-CD3 antibody
treatment, have been shown to increase transcription directed by the HIV-2
LTR. In this study, we examine the activation of the HIV-2 LTR in T cells
stimulated with the physiologic ligand of the T-cell receptor, antigenic
peptide presented by a major histocompatibility molecule. HIV-2 reporter
plasmids were transfected into the antigen- specific T-cell hybridoma,
2B4.11, where they responded to antigen- dependent activation. This
antigen-mediated transcriptional activation of the HIV-2 enhancer required
the presence of at least four regulatory elements in the HIV-2 enhancer,
including two purine boxes, PuB1 and PuB2, an AP-1/CREB-like element
(pets), and kappa B. This finding suggests that signals emanating from the
antigen receptor act coordinately on a set of transcription factors that
bind to conserved HIV-2 regulatory elements. Despite differences in the
organization of potentially related enhancer elements in HIV-2 and IL-2,
these enhancers exploit a similar signal transduction pathway to induce
gene expression in antigen-activated T cells.
Volume 83,
Issue 7,
pp. 1839-1846,
04/01/1994
Copyright © 1994 by The American Society of Hematology
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