Staphylococcal enterotoxin B (SEB) is a potent polyclonal activator of both human and murine T cells. We previously reported data which show that SEB-induced T cells suppress antibody secretion by various mouse plasmacytoma cell lines. This suppression of antibody secretion was found to be both idiotype and isotype nonspecific, and the suppressor cell bears the CD5-positive CD8-negative cell surface phenotype. The present studies demonstrate that accessory cells are required in the SEB-primed spleen cell (SEB-PSC) population in order for this population to mediate suppression. The suppressive activity of SEB-PSC is abrogated following accessory cell depletion by passage over Sephadex G-10 columns. B cell depletion using nylon-wool also abrogates suppression mediated by SEB-PSC. The addition of nonelicited adherent peritoneal exudate cells (PECs) restores suppressive activity to accessory cell-depleted SEB-PSC. The restoration of suppression by the PECs is not major histocompatibility complex restricted, since both syngeneic and allogeneic PECs can carry out this activity. In addition, it is not necessary for the accessory cells to be metabolically active in order to participate in the suppressive activity. This is based on results demonstrating that gluteraldehyde fixation, at levels reported to eliminate metabolic activity, does not affect the ability of PECs to restore suppression to Sephadex G-10-depleted SEB-PSC. The results are consistent with the well established requirement for accessory cells in the function of antigen-induced suppressor T cells.
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