Document 0292 DOCN M9650292 TI Cross-linking of Fc gamma receptors activates HIV-1 long terminal repeat-driven transcription in human monocytes. DT 9605 AU Tsitsikov EN; Fuleihan R; McIntosh K; Scholl PR; Geha RS; Division of Immunology, Children's Hospital, Boston, MA 02115,; USA. SO Int Immunol. 1995 Oct;7(10):1665-70. Unique Identifier : AIDSLINE MED/96128660 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 Fc gamma RI or Fc gamma RII by adherent human IgG or by specific anti-Fc gamma R 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, Fc gamma R cross-linking induced NF-kappa B, 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-alpha antibody but not anti-IL-1 beta antibody strongly inhibited both the induction of HIV-1-LTR-driven transcription and the induction of NF-kappa B by Fc gamma R cross-linking. These results indicate that Fc gamma R can mediate a TNF-alpha-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. DE Acquired Immunodeficiency Syndrome/*BLOOD/IMMUNOLOGY/VIROLOGY Antibodies, Monoclonal/IMMUNOLOGY Antigen-Antibody Complex/*IMMUNOLOGY Base Sequence Chloramphenicol Acetyltransferase/BIOSYNTHESIS/GENETICS *Gene Expression Regulation, Viral Genes, Reporter Human *HIV Long Terminal Repeat HIV-1/GENETICS/PHYSIOLOGY IgG/*IMMUNOLOGY Immunoglobulins, Fab/IMMUNOLOGY *Immunologic Capping Leukemia, Monocytic, Acute/PATHOLOGY Molecular Sequence Data Monocytes/*IMMUNOLOGY/VIROLOGY NF-kappa B/METABOLISM Receptors, IgG/*IMMUNOLOGY Recombinant Fusion Proteins/BIOSYNTHESIS RNA, Viral/BIOSYNTHESIS/GENETICS Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. *Transcription, Genetic Tumor Cells, Cultured Tumor Necrosis Factor/PHYSIOLOGY JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).