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).