Cross-linking of Fcγ receptors activates HIV-1 long terminal repeat-driven transcription in human monocytes

Erdyni N. Tsitsikov*, Ramsay Fuleihan, Ken Mclntosh, Paul R. Scholl, Raif S. Geha

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Elevation of the levels of circulating immune complexes frequently accompanies HIV-1 infection and is a prognostic indicator of clinical progression from asymptomatic infection to AIDS. Here we report that cross-linking of FcγRI or FcγRII by adherent human IgG or by specific anti-FcγR mAb activates HIV-1 gene expression in the human monocytic cell line BF24 and increased HIV RNA expression in monocytes from HIV infected patients as assayed by reverse transcription-PCR. In THP-1 cells, FcγR cross-linking induced NF-κB, which is known to bind to the regulatory region of the long terminal repeat (LTR) of HIV-1 and to activate HIV-1 transcription. Anti-TNF-α antibody but not anti-IL-1β antibody strongly inhibited both the induction of HIV-1-LTR-driven transcription and the induction of NF-κB by FcγR cross-linking. These results indicate that FcγR can mediate a TNF-α-dependent induction of HIV-1 gene transcription and suggest that immune complexes may contribute to the pathophysiology of HIV-1 infection by augmenting viral replication in monocytes.

Original languageEnglish (US)
Pages (from-to)1665-1670
Number of pages6
JournalInternational Immunology
Issue number10
StatePublished - Oct 1995


  • HIV-1-LTR
  • Immune complexes
  • NF-κB
  • TNF

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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