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

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