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

Mark C. Hannibal, David M. Markovitz, Gary J. Nabel

Research output: Contribution to journalArticlepeer-review

Abstract

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 κB. 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.

Original languageEnglish (US)
Pages (from-to)1839-1846
Number of pages8
JournalBlood
Volume83
Issue number7
StatePublished - Apr 1 1994
Externally publishedYes

ASJC Scopus subject areas

  • Hematology

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