MECHANISM UNDERLYING SUPERANTIGEN-INDUCED CLONAL DELETION OF MATURE T-LYMPHOCYTES

We observed that peripheral T cells activated in vivo or in vitro by s uperantigens are susceptible to cell death when their antigen receptor is cross-linked with the appropriate anti-alphabeta TCR mAb. TCR liga tion by mAbs specifically drove the T cell clonal deletion in both CD4 + and CD8+ cell subsets. An IL-2/IL-2R interaction seems to be a criti cal step in predisposing superantigen activated cells to death; in fac t, in vivo IL-2R bockade reversed T cell deletion in superantigen plus anti-alphabeta TCR mAb treated mice. TCR ligation by mAbs also produc ed cell death of the relevant targets in in vitro IL-2 activated T cel ls. Surprisingly, no T cell deletion was demonstrable in IL-2 activate d cells following staphylococcal enterotoxin B - TCR interaction, ruli ng out the possibility that superantigen in itself can induce cell dea th. Thus, while superantigen activation opens the cell death program, a subsequent TCR - antigen (self) interaction appears necessary to pro duce clonal deletion in mature T lymphocytes.