Document 0823
 DOCN  M9460823
 TI    HIV-1 gp120-dependent induction of apoptosis in antigen-specific human T
       cell clones is characterized by 'tissue' transglutaminase expression and
       prevented by cyclosporin A.
 DT    9404
 AU    Amendola A; Lombardi G; Oliverio S; Colizzi V; Piacentini M; Department
       of Biology, University of Rome Tor Vergata, Italy.
 SO    FEBS Lett. 1994 Feb 21;339(3):258-64. Unique Identifier : AIDSLINE
       MED/94156044
 AB    We investigated the effect of cyclosporin (CsA) on HIV-gp120-dependent
       induction of cell death by apoptosis of human T cell clones specific for
       influenza virus haemagglutinin and restricted by HLA-DR1. Preincubation
       of the clones with gp120 induced a large inhibition of their
       proliferation which was paralleled by the induction of apoptosis.
       Exposure to the specific antigen alone was able to trigger apoptosis in
       a significant fraction of cells, this effect was potentiated by
       pretreatment with gp120. Apoptosis was characterized by the typical
       morphological changes and by the expression of 'tissue' Transglutaminase
       (tTG), one of the few characterized effector elements of programmed cell
       death. Interestingly, the tTG protein induction was detectable within
       the first 24 hours following the gp120 treatment and preceded the
       appearance of the typical apoptotic phenotype. Noteworthy, CsA treatment
       prevented the gp120-dependent induction of apoptosis by blocking the
       activation of the Ca(2+)-dependent effector elements such as tTG.
 DE    Apoptosis/*DRUG EFFECTS  Clone Cells  Cyclosporine/*PHARMACOLOGY
       Hemagglutinins, Viral/IMMUNOLOGY  HIV Envelope Protein
       gp120/*PHARMACOLOGY  *HIV-1  HLA-DR1 Antigen/IMMUNOLOGY
       Protein-Glutamine Gamma-Glutamyltransferase/*METABOLISM  Support,
       Non-U.S. Gov't  T-Lymphocytes/IMMUNOLOGY/*PHYSIOLOGY  Viral Envelope
       Proteins/IMMUNOLOGY  JOURNAL ARTICLE

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