Clonal deletion as direct consequence of an in vivo T cell response to bacterial superantigen

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Abstract
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 Vβ8+ T cells in lymph node cells draining the local site of injection. First, and within hours Vβ selective clonal deletion is initiated via an apoptotic process. Second, the remaining Vβ8+ 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.