CLONAL DELETION AS DIRECT CONSEQUENCE OF AN INVIVO T-CELL RESPONSE TO BACTERIAL SUPERANTIGEN

To date clonal deletion of peripheral mature T cells is restricted to in vivo model systems characterized by prolonged exposure of mice to antigens and clonal T cell expansion preceding clonal deletion. Here we describe that upon challenge of mice with the superantigen staphylococcal enterotoxin B two immediate events become imposed on ligand-reactive Vbeta8+ T cells in lymph node cells draining the local site of injection. First, and within hours Vbeta selective clonal deletion is initiated via an apoptotic process. Second, the remaining Vbeta8+ T cells first develop a profound state of ligand-specific unresponsiveness and subsequently initiate clonal in vivo growth. It is suggested that the dichotomy of events observed reflects a direct consequence of T cell receptor occupancy in the context of inappropriate signalling.