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Cross-Reacting Antigens on L5178Y Cells Which Serve as Targets for Cytotoxic T-Lymphocyte Lysis during Establishment of the Tumor Dormant State¹

Department of Pathology and Laboratory Medicine, Hahnemann Medical College, Philadelphia, Pennsylvania 19102

We have attempted to identify the antigen on L5178Y cells that is the target for peritoneal cytotoxic T-lymphocytes (CTL) generated in L5178Y-O (original) immunized and challenged DBA/2 mice during establishment of the L5178Y cell tumor dormant state. These CTL exhibited in vitro lytic activity against methylcholanthrene-induced L5178Y and P815Y cells as well as Gross virus-induced BALB/c cells but not against a variety of other H-2^d-tumor cell lines. The pattern of susceptibility to cell-mediated immune cytolysis was identical to the pattern of AB-dependent complement-mediated cytolysis produced by a rabbit anti-L5178Y antiserum. Quantitative expression of surface H-2^d determinants was not a limiting factor in tumor cell lysis by CTL. The degree of CTL lysis of the susceptible cell lines was directly related to the amount of tumor-associated antigen expressed on the cell surface. The pattern of in vitro susceptibility to CTL lysis correlated well with in vivo transplantation resistance. The L5178Y cell antigen target for both CTL and Ra-anti-L5178Y serum lysis is likely to be either an endogenous AKR ecotropic viral glycoprotein with a molecular weight of 71,000 or one of two cell surface determinants, at M, 85,000 and 135,000. These higher-molecular-weight antigens are neither endogenous AKR ecotropic viral-induced nor murine leukemia virus group-specific precursor structural proteins but may be transformation antigens shared by the susceptible tumor cell lines.

¹ This work was supported by Grants 32575 and 32577 awarded by the National Cancer Institute, Department of Health, Education, and Welfare, and by Biomedical Research Support Grant 1 507 RR-05414.

² Present address: Department of Surgery, Duke University Medical Center, Durham, N.C. 27710.

³ To whom requests for reprints should be sent.

Received 3/17/82. Accepted 6/10/82.