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 language | English (US) |
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Pages (from-to) | 1665-1670 |
Number of pages | 6 |
Journal | International Immunology |
Volume | 7 |
Issue number | 10 |
DOIs | |
State | Published - Oct 1995 |
Funding
This work was supported by USPHS grants nos AI-29906-04 (HIV-RSG) and AI-01091-02 (KO8-R.F). E. N. T. was supported by F Hoffman La-Roche, Basel, Switzerland.
Keywords
- HIV-1-LTR
- Immune complexes
- NF-κB
- TNF
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology