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M9550247.TXT
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1995-03-04
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Document 0247
DOCN M9550247
TI Tat-expressing Jurkat cells show an increased resistance to different
apoptotic stimuli, including acute human immunodeficiency virus-type 1
(HIV-1) infection.
DT 9505
AU Gibellini D; Caputo A; Celeghini C; Bassini A; La Placa M; Capitani S;
Zauli G; Institute of Microbiology, University of Ferrara, Italy.
SO Br J Haematol. 1995 Jan;89(1):24-33. Unique Identifier : AIDSLINE
MED/95134677
AB Human CD4+ T lymphoblastoid Jurkat cells were stably transfected with
two different plasmid vectors containing the cDNA of human
immunodeficiency virus-type 1 (HIV-1) tat gene under the control of
either the promoter of simian virus 40 (pRPneo/tat) or the long terminal
repeat region of SL3 murine leukaemia virus (pRPneo/SL3/tat). Both
pRPneo/tat and pRPneo/SL3/tat Jurkat cell lines showed a constant and
high production of bioactive Tat in transient co-transfection assays
with an HIV-1 long terminal repeat (LTR)-chloramphenicol
acetyltransferase (CAT) reporter plasmid. Tat-positive and
mock-transfected Jurkat cells were cultured with various cytotoxic
agents, which have been associated to the progressive loss of CD4
T-lymphocytes characteristic of HIV-1 disease. In the presence of
recombinant tumour necrosis factor-alpha (TNF-alpha), anti-fas antibody,
Leu3a anti-CD4 antibody, the percentage of apoptosis, evaluated in a
24-72 h short-term assay, was lower (P < 0.05) in tat-positive Jurkat
cells than in mock-transfected controls. The low susceptibility to the
cytotoxic activity of TNF-alpha and anti-fas antibody of tat-transfected
cells was confirmed by counting viable cells up to 15 d of culture.
Also, recombinant Tat protein was able to prevent the increase of
apoptosis induced in mock-transfected Jurkat by TNF-alpha. Of note,
tat-expressing cells showed a better survival with respect to
mock-transfected control cells even when acutely infected with high
doses (500,000 cpm of reverse transcriptase) of HIV-1 (strain IIIB) or
treated with heat-inactivated HIV-1. These data demonstrate that the
expression of the regulatory HIV-1 Tat protein is able to rescue Jurkat
lymphoblastoid cells from apoptosis induced by a variety of cytotoxic
agents. Since Tat protein expression is restricted to the initial phases
of an active HIV-1 replication, the anti-apoptotic effect of Tat could
have the physiological significance of selectively protecting HIV-1
producing cells from death, at least for the time necessary to allow
virus production and spreading.
DE Antibodies, Monoclonal/PHARMACOLOGY Antigens, CD4/ANALYSIS/IMMUNOLOGY
Antigens, Surface/ANALYSIS/IMMUNOLOGY Apoptosis/*GENETICS CD4-Positive
T-Lymphocytes/*PATHOLOGY/ULTRASTRUCTURE *Genes, tat Human HIV
Infections/*GENETICS HIV-1/*GENETICS Plasmids/GENETICS Support,
Non-U.S. Gov't Transfection Tumor Cells, Cultured Tumor Necrosis
Factor/PHARMACOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).