Document 0162
 DOCN  M95A0162
 TI    Cross-linking of CD30 induces HIV expression in chronically infected T
       cells.
 DT    9510
 AU    Biswas P; Smith CA; Goletti D; Hardy EC; Jackson RW; Fauci AS;
       Laboratory of Immunoregulation, National Institute of Allergy and;
       Infectious Diseases, National Institutes of Health, Bethesda,; Maryland
       20892-2520, USA.
 SO    Immunity. 1995 Jun;2(6):587-96. Unique Identifier : AIDSLINE
       MED/95316714
 AB    CD30, a member of the tumor necrosis factor (TNF) receptor family, is
       expressed constitutively on the surface of the human T cell line ACH-2,
       which is chronically infected with human immunodeficiency virus type-1
       (HIV)-1. We demonstrate that cross-linking CD30 with an
       anti-CD30-specific monoclonal antibody, which mimics the described
       biological activities of the CD30 ligand (CD30L), results in HIV
       expression. CD30 cross-linking does not alter proliferation of ACH-2
       cells and the induction of HIV expression is not mediated by endogenous
       TNF alpha/beta. Furthermore, cross-linking of CD30 leads to NF-kappa B
       activation and enhanced HIV transcription. Thus, CD30-CD30L interactions
       mediate the induction of HIV expression by a kappa B-dependent pathway
       that is independent of TNF. This mechanism may be important in the
       activation of HIV expression from latently infected CD4+ T cells,
       especially in lymphoid organs where cell to cell contact is conducive to
       receptor-ligand interactions.
 DE    Antibodies, Monoclonal/IMMUNOLOGY  Antigens, CD30/*IMMUNOLOGY  Blotting,
       Northern  Cell Line  Chloramphenicol Acetyltransferase/ANALYSIS  Cross
       Reactions/IMMUNOLOGY  Human  HIV/*GROWTH & DEVELOPMENT
       Immunophenotyping  Lymphocyte Transformation  NF-kappa B/BIOSYNTHESIS
       Reverse Transcriptase/ANALYSIS  Support, Non-U.S. Gov't
       T-Lymphocytes/*IMMUNOLOGY/VIROLOGY  Tumor Necrosis Factor/BIOSYNTHESIS
       Virus Activation/*IMMUNOLOGY  JOURNAL ARTICLE

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