Abstract
Cloned CTL have been loaded with the K+ analogue 86Rb+. When mixed with unlabeled target cells, accelerated 86Rb+ release occurs from the CTL. The magnitude of accelerated 86Rb+ release is proportional to the efficacy of the target in standard 51Cr release assays. The signal responsible for accelerated 86Rb+ release has been localized to a postbinding event and has the physiologic requirements of delivery of the lethal hit. Thus, accelerated 86Rb+ release from the CTL represents the first direct observation of a physiologic event within the CTL related to a functional CTL-target interaction.

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