A murine acquired immunodeficiency (
MAIDS) virus transformed B cell line, B6-1710, was shown to express
superantigen activity and stimulate T cell hybridomas to produce
IL-2. However, T cell clones and lines from which B6-1710 reactive hybridomas were established failed to proliferate upon stimulation with B6-1710, while B6-1710 cells were capable of presenting bacterial
superantigen to stimulate both T cell hybridomas and clones. Proliferative response of T cells to
MAIDS virus
superantigen could be detected by the addition of the pharmacological agent
phorbol myristate acetate (PMA). Thus, B6-1710 seems to lack a stimulatory activity necessary for the proliferative response of T cells to the
MAIDS viral
superantigen. In the analysis of the response of naive splenic T cells to the
MAIDS superantigen, T cells recovered from a culture stimulated with B6-1710 cells in the presence of PMA showed no dominant TCR V beta chain usage, while cells recovered from a culture stimulated with B6-1710 alone were dominated by T cells expressing V beta 5, 11, and 12 TCR chains. These results suggest that T cells bearing a majority of TCR V beta chains are capable of responding to B6-1710
superantigen. The avidity of interaction between T cells and viral
superantigen may differ significantly among T cells and those T cells exhibiting weak interaction with
MAIDS virus
superantigen may require additional signals, such as PMA, for an in vitro proliferative response to B6-1710 cells.