Mechanism underlying superantigen-induced clonal deletion of mature T lymphocytes

Abstract

We observed that peripheral T cells activated in vivo or in vitro by superantigens are susceptible to cell death when their antigen receptor is cross-linked with the appropriate anti-αβ TCR mAb. TCR ligation by mAbs specifically drove the T cell clonal deletion in both CD4⁺ and CD8⁺ cell subsets. An IL-2/1L-2R interaction seems to be a critical step In predisposing superantigen activated cells to death; In fact, in vivo IL-2R bockade reversed T cell deletion In superantlgen plus anti-αβ TCR mAb treated mice. TCR ligatlon by mAbs also produced cell death of the relevant targets in in vitro IL-2 activated T cells. Surprisingly, no T cell deletion was demonstrable in IL-2 activated cells following staphylococcal enterotoxin B - TCR Interaction, ruling out the possibility that superantigen in Itself can induce cell death. Thus, while superantigen activation opens the cell death program, a subsequent TCR-antigen (self) Interaction appears necessary to produce clonal deletion in mature T lymphocytes.