Soluble suppressor factors from PBMC of AIDS patients inhibit T-cell-dependent immune responses, suggesting a mechanism for immune suppression in AIDS.
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Should not yet change AIDS management; leaves open whether reducing agents could restore immune function in patients.
Supernatants from PBMC obtained from certain patients with AIDS or its prodrome were capable of depressing pokeweed mitogen-driven immunoglobulin production and the proliferative response of T cells to specific antigen. These soluble suppressor factors (SSF) were present in uniquely high concentrations, and were the product of an interaction of T lymphocytes with adherent cells. T-cell independent functions were not modified by soluble suppressor factors. Restoration of immunoglobulin synthesis in SSF-treated cultures was realized by addition of reducing agents such as 2-mercaptoethanol, suggesting inhibitory mechanisms possibly related to that of Con A-induced soluble immune response suppression, and perhaps offering clues to clinically applicable substances capable of modifying such responses. A relationship between SSF-AIDS and a human retrovirus LAV/HTLV III, linked etiologically to AIDS and its prodromes, is suggested by studies of SSF-like substances released by human T-T cell hybridomas derived from LAV+ patients.
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Laurence et al. (1984) studied this question.
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