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M9460667.TXT
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1994-06-25
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Document 0667
DOCN M9460667
TI HIV-1 Nef activity in murine T cells. CD4 modulation and positive
enhancement.
DT 9408
AU Rhee SS; Marsh JW; Laboratory of Molecular Biology, National Institute
of Mental; Health, Bethesda, MD 20892.
SO J Immunol. 1994 May 15;152(10):5128-34. Unique Identifier : AIDSLINE
MED/94230994
AB Immediately after infection of the targeted cell by HIV-1, proviral gene
expression is limited to the three regulatory proteins, Tat, Rev, and
Nef, with the nef transcript representing nearly 80% of total
expression. Additionally, simian immunodeficiency virus Nef has been
shown to be essential for high in vivo titer and the development of
immunodeficiency. Recent findings demonstrate that the negative effects
of Nef expression, as first defined in transformed T cell lines, are not
present when Nef is expressed in primary human T cells or in T cells
from transgenic mice, in which one sees moderate positive enhancements
of HIV replication and the T cell activation process, respectively. We
find that Nef expression in an Ag-specific murine T cell hybridoma
results in both the down-modulation of CD4, as seen in primary cells and
human T cell lines, and a positive enhancement of the TCR response to
stimuli. Examination of a CD4- cell demonstrated that the positive
enhancement is independent of CD4 expression or modulation. CD4
down-modulation is shown to be caused by a post-Golgi, acid-dependent
process, which dramatically decreases the lifespan of the CD4 molecule.
The TCR, Thy Ag, and CD45 remained unchanged in their surface
expression. These findings suggest that Nef alters the normal routing
and residencies of the CD4 molecule and that the positive effect of Nef
on T cell activation is independent of this modulation.
DE Animal Antigens, CD4/*ANALYSIS Cell Line Down-Regulation (Physiology)
Gene Products, nef/*PHYSIOLOGY HIV-1/*PATHOGENICITY
Interleukin-2/BIOSYNTHESIS Lymphocyte Transformation Mice Receptors,
Antigen, T-Cell/PHYSIOLOGY Support, U.S. Gov't, P.H.S.
T-Lymphocytes/*IMMUNOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).