       Document 3235
 DOCN  M94A3235
 TI    Monomeric HIV-gp120 induces both inhibition of cell proliferation and
       apoptosis.
 DT    9412
 AU    Tuosto L; Lorenzetti S; Cundari E; Moretti S; Lombardi G; Piccolella E;
       Dept. Cell. and Develop. Biology, Univ. of Rome, Italy.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):122 (abstract no. PA0106). Unique
       Identifier : AIDSLINE ICA10/94369340
 AB    Infection with human immunodeficiency virus (HIV) results in a
       progressive impairment of immune responses, partly due to the defect
       induced in T cells following the interaction of the HIV-envelope
       glycoprotein (gp120) and/or anti-CD4 antibodies with CD4 molecules.
       These effects have been reported as inhibition of mitogen- and
       antigen-induced T cell proliferation, and induction of apoptosis.
       However, it is not clear if cross-linking of CD4 molecules by HIV gp120
       or anti-CD4 antibodies is required to induce either the impairment of
       cell proliferation or the induction of apoptosis in antigen-primed
       lymphocytes. To this aim we have analyzed the effect of monomeric gp120
       and anti-CD4 antibodies on proliferative response and
       apoptosis-induction on a panel of antigen-specific T cell clones and
       freshly isolated CD4+ T lymphocytes. We found new experimental
       conditions able to induce apoptosis by involvement of CD4 molecules
       without cross-linking of HIV gp120 and CD4 antibodies. Our results
       clearly demonstrate that: a) the need for CD4 cross-linking is
       restricted only to fresh purified CD4+ lymphocytes stimulated by
       anti-CD3 antibody, while antigen-specific T cell clones are sensible to
       programmed cell death mediated by monomeric gp120; b) soluble anti-CD4
       antibodies are able to induce apoptosis in both fresh T lymphocytes and
       antigen-specific T cell clones. Our results suggest that during HIV
       infection anti-CD4 antibodies and gp120 could contribute to the
       unresponsiveness state and programmed cell death of CD4+ uninfected T
       lymphocytes during an antigen-stimulation.
 DE    Antibodies/PHARMACOLOGY  Antigens, CD/IMMUNOLOGY/PHYSIOLOGY  Antigens,
       CD4/IMMUNOLOGY/PHYSIOLOGY  *Apoptosis  Cell Division  Clone Cells
       Comparative Study  Human  HIV/*PHYSIOLOGY  HIV Envelope Protein
       gp120/IMMUNOLOGY/*METABOLISM  In Vitro  *Lymphocyte Transformation
       T-Lymphocytes/CYTOLOGY/IMMUNOLOGY/*MICROBIOLOGY  T4
       Lymphocytes/CYTOLOGY/IMMUNOLOGY/*MICROBIOLOGY  MEETING ABSTRACT

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

