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 journalArticle

14 Citations (Scopus)

Abstract

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
Volume7
Issue number10
DOIs
StatePublished - Oct 1 1995

Fingerprint

HIV Long Terminal Repeat
Monocytes
Fc Receptors
Transcription
Receptor
Linking
HIV-1
Infection
Tumor Necrosis Factor
Proof by induction
Antibody
Antibodies
Pathophysiology
Antigen-Antibody Complex
Cell
HIV Infections
RNA
Progression
Gene expression
Replication

Keywords

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

ASJC Scopus subject areas

  • Statistics, Probability and Uncertainty
  • Applied Mathematics
  • Public Health, Environmental and Occupational Health
  • Neuropsychology and Physiological Psychology
  • Transplantation
  • Immunology

Cite this

Tsitsikov, Erdyni N. ; Fuleihan, Ramsay ; Mclntosh, Ken ; Scholl, Paul R. ; Geha, Raif S. / Cross-linking of Fcγ receptors activates HIV-1 long terminal repeat-driven transcription in human monocytes. In: International Immunology. 1995 ; Vol. 7, No. 10. pp. 1665-1670.
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Cross-linking of Fcγ receptors activates HIV-1 long terminal repeat-driven transcription in human monocytes. / Tsitsikov, Erdyni N.; Fuleihan, Ramsay; Mclntosh, Ken; Scholl, Paul R.; Geha, Raif S.

In: International Immunology, Vol. 7, No. 10, 01.10.1995, p. 1665-1670.

Research output: Contribution to journalArticle

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T1 - Cross-linking of Fcγ receptors activates HIV-1 long terminal repeat-driven transcription in human monocytes

AU - Tsitsikov, Erdyni N.

AU - Fuleihan, Ramsay

AU - Mclntosh, Ken

AU - Scholl, Paul R.

AU - Geha, Raif S.

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N2 - 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.

AB - 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.

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