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M9650292.TXT
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1996-03-09
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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).