The specificity of H-2-restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus-induced tumors I. Isolation of a selectively resistant variant tumor subclone

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Abstract
The AKR.H‐2bSL1 tumor cell line is susceptible to H‐2Kb‐restricted cytotoxic T lymphocytes (CTL) directed against the subclass of AKR endogenous leukemia virus‐induced tumors that express the Gross cell surface antigen (anti‐AKR/Gross virus CTL). A variant subclone (cl.18‐5) of AKR.H‐2bSL1 was isolated, whose susceptibility to lysis by conventional or cloned lines of anti‐AKR/Gross virus CTL was approximately 5% or less than that of the parental tumor. The cl.18‐5 variant was also ineffective when used as an in vivo priming cell or an in vitro stimulator cell in the generation of anti‐AKR/Gross virus CTL or as an unlabeled target cell in competitive inhibition assays. These results implied that the failure of cl.18‐5 to be lysed was due to a lack of recognition by the CTL. In contrast, cl.18‐5 was able to be lysed by and stimulate the generation of predominantly H‐2Db‐restricted CTL with apparent specificity for AKR minor histocompatibility antigens. The variant line was also about as susceptible as the parental AKR.H‐2bSL1 line to both allogeneic CTL and to H‐2Kb‐restricted, TNP‐specific CTL. Thus, the lack of recognition of cl.18‐5 by anti‐AKR/Gross virus CTL did not appear to be due to a failure to express functional H‐2 products or to a generalized insusceptibility to H‐2‐restricted CTL. Rather, cl.18‐5 appeared to be a selective variant and a useful probe for studying the specificity of anti‐AKR/Gross virus CTL.

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