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M9490427.TXT
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1994-09-19
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Document 0427
DOCN M9490427
TI Understanding the CD4 molecule: surface expression and function.
DT 9411
AU Morrison WJ; Offner H; Vandenbark AA; Neuroimmunology Research
Laboratory, Veterans Administration; Medical Center, Portland, OR 97207.
SO J Neurosci Res. 1994 May 1;38(1):1-5. Unique Identifier : AIDSLINE
MED/94335009
AB Surface expression of the CD4 glycoprotein molecule is postulated to
facilitate antigen recognition through the T cell receptor (TCR) and is
itself a receptor for human immunodeficiency virus (HIV)-gp120
glycoprotein. Both antigen-stimulated TCR activation and HIV infectivity
can be blocked by whole anti-CD4 antibodies. Although selective
modulation of CD4 from the surface by gangliosides (GM1) blocks HIV
infectivity, it enhances associated TCR function. Enhanced TCR function
has also been observed after intracellular delivery of synthetic CD4
mRNA-antisense oligodeoxynucleotides (ODN) that block de novo synthesis
of CD4. These specific CD4 modulations were mechanistically different
from one another yet they both selectively removed the CD4 molecule from
the T cell surface and enhanced antigen-stimulated function through the
TCR. The proposed role of CD4 during TCR function and HIV infectivity
was developed, in part, according to decreases following CD4 antagonism
by whole antibody or down-modulation of CD4 by phorbol-stimulated
protein kinase C activity. Selective CD4 modulations have independently
redefined the specific contributions of CD4 surface expression during T
cell activation and may establish a role for CD4 receptor subtypes
during HIV-1 infection of CD4+ cells.
DE Animal Antigens, CD4/BIOSYNTHESIS/GENETICS/*IMMUNOLOGY Human HIV
Infections/IMMUNOLOGY Support, Non-U.S. Gov't Support, U.S. Gov't,
Non-P.H.S. T-Lymphocytes/ENZYMOLOGY/IMMUNOLOGY JOURNAL ARTICLE REVIEW
REVIEW, TUTORIAL
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).