SIGNAL-TRANSDUCTION DEFECT IN THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME AND AIDS-RELATED COMPLEX

Peripheral blood mononuclear cells from patients with the acquired imm unodeficiency syndrome (AIDS), AIDS-related complex (ARC), and heteros exual controls were stimulated with anti-CD3 monoclonal antibody, phor bol myristate acetate (PMA), or both and H-3 thymidine incorporation a nd IL-2 receptor (IL-2R alpha; CD25;Tac antigen) expression were measu red. In addition, basal plasma membrane potential and plasma membrane potential following anti-CD3 stimulation were compared between the thr ee groups. A significantly reduced DNA synthesis and CD25 expression w as observed in both AIDS and ARC upon stimulation with anti-CD3 or PMA . Although, a significant synergism was observed with anti-CD3 plus PM A stimulation in both AIDS and ARC, and the responses were normalized to the levels of anti-CD3 or PMA response in normal control, the level s were significantly lower than those observed with anti-CD3 plus PMA in controls. Plasma membrane potentials were decreased (membrane depol arized) in both ARC and AIDS (AIDS>ARC), and anti-CD3 had no effect on further depolarization of plasma membrane in AIDS. These data suggest a defect in signal transduction pathway in patients with HIV-1 infect ion.