A xenogeneic serum directed at alloimmune CTL is shown to block H-2-restricted anti-viral CTL activity. Extensive absorption studies with targets and effector cells indicate that the blocking is at the level of the CTL and not the target cells. Inhibition is demonstrated for influenza-specific cytotoxicity operating in the context of 3 distinct H-2 haplotypes, suggesting that the serum is not directed at antigen-recognition structures. Kinetic studies on the addition of RAT to an ongoing 51Cr release assay further support the hypothesis that inhibition is not operating via the idiotypic region of the antigen receptor. We suggest that RAT is specific for CTL surface structures involved in nonrecognition events--possibly the lytic sites or a conserved region (idiotype-negative) of th antigen-binding receptor.
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