In order to investigate the nature of the T cell defect associated with the acquired immune deficiency syndrome (AIDS) we studied the ability of peripheral blood mononuclear cells from 8 patients with Kaposi's sarcoma (KS), 2 with opportunistic infection (0I), 23 with AIDS-related symptoms complex (ARC) without KS or 0I (ARC), and 29 heterosexual controls to produce interleukin II (IL-2) on phytohemagglutinin (PHA) stimulation and to respond to exogenously supplied IL-2. Patients with AIDS as well as those with ARC produced adequate levels of IL-2 in response to lectin stimulation when compared to controls (AIDS, 3.07 ± 1.98 units; ARC, 3.03 ± 1.89 units; control, 3.75 ± 1.52 units). However, the ability of these patients' cells to respond in vitro to exogenously supplied IL-2 as measured on short-term PHA-stimulated T cell blasts was found to be severely impaired in patients with AIDS and ARC (AIDS, 22.4 ± 6.0 x 10-3 cpm; ARC, 20.1 ± 4.2 x 10-3 cpm; control, 41.4 ± 4.2 x 10-3 cpm). This impairment was associated with diminished expression of the IL-2 receptor on 7-day-old lectin-stimulated T cells from both patient groups (AIDS, 17.7 ± 5.7; ARC, 36.8 ± 4.4; control, 71.8 ± 1.7). These results should be considered when IL-2 is proposed as potential therapy in the treatment of AIDS. They also suggest that the nature of the AIDS defect is related to impaired hormone receptor expression.
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