Abstract:
AIDS is characterized by a progressive decline in the number of CD4+ T cells. This is preceded by an early selective defect in the proliferation of these cells to recall antigens [1-3], pokeweed mitogen (PWM) [4-6] and to superantigens (SAg) [4,7]. In contrast, the proliferative response to phytohaemagglutinin (PHA) remains intact [1,2,5]. We and others have shown that the proliferative defect in response to some stimuli was in fact due to the induction of cell death [4,7]. The activation-induced cell death mechanism that explains the proliferative defects observed in vitro might also account for the progressive in vivo deletion of CD4+ T cells. Indeed, studies performed on different models of primates have shown that induction of cell death in CD4+ T cells was detected only when T cells were isolated from animals infected with a type of retrovirus that induces an AIDS-like disease [8]. This correlation prompted us to analyse further the mechanism of HIV-induced activation cell death to determine the specificity and rate of induction of cell death. T cells from HIV-infected individuals were activated with superantigens and the V beta T cell receptor (TCR) expression analysed. Data presented here show that cell death is restricted to activated CD4+ T cells, and does not affect bystander cells. More importantly, addition of anti-CD28 MoAb specifically inhibited the induction of apoptosis, raising possibilities for therapy.
Keywords: Antibodies, Monoclonal/PHARMACOLOGY/*THERAPEUTIC USE Antigens, CD28/*IMMUNOLOGY Apoptosis/IMMUNOLOGY Base Sequence Cell Division/IMMUNOLOGY Child *Clonal Deletion CD4-Positive T-Lymphocytes/*IMMUNOLOGY Enterotoxins/PHARMACOLOGY Flow Cytometry Human HIV Infections/*IMMUNOLOGY/*THERAPY Immunosuppressive Agents/PHARMACOLOGY Lymphocyte Transformation/*IMMUNOLOGY Molecular Sequence Data Polymerase Chain Reaction Staphylococcus aureus/IMMUNOLOGY Superantigens/IMMUNOLOGY Support, Non-U.S. Gov't Twins, Monozygotic JOURNAL ARTICLE 961130
M96B1844
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