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MOLECULAR FEATURES OF THE H‐2 CLASS I AND Qa ANTIGENS EXPRESSED ON GROSS VIRUS INDUCED AKR LEUKAEMIAS

It is now well established that T cell receptor structures expressed on effector T lymphocytes recognize ‘non-self’ (processed) peptides present on the surface of antigen presenting cells (APC) (Braciale et al., 1987; Morrack & Kappler, 1986; Townsend et al., 1986). This recognition process is restricted by ‘self’ MHC antigens (Zinkernagel & Doherty, 1974). Specifically, the H-2 Class-1 antigens expressed by neoplastic and virus infected cells are important in antigen recognition by cytotoxic effector T lymphocytes (CTL). Thus, MHC Class-I glycoproteins are peptide-binding molecules essential for ‘non-self’ presentation to CTL (Bjorkman et al., 1987) and therefore may play a central role in immunosurveillance (Festenstein, 1987). An important prediction from the Class-I peptide-binding notion is that APCs must have ‘the appropriate’ Class-I repertoire for effective antigen presentation to the corresponding T cells. The H-2 Class I repertoire is normally dependent on the existence of multiple loci broadly divided in two series : (1) the highly polymorphic H-2D, -K, -L loci and; (2) the less polymorphic Qa/Tla loci, the function of the latter genes being still largely unknown. We have used the AKR Gross virus spontaneous T cell leukemias as a model to investigate the role of the H-2 Class-I D/K/L and Qa/Tla sub-region products in tumour development. Alterations of Class-I antigen profiles which have been observed on neoplastic cells were either: (a) the suppression or loss of specific Class-I antigens and (b) the generation of novel Class-I antigens. While these changes are not observed in all tumour systems, alterations of Class-I antigens in association with the development of tumours may be one of several decisive factors which determine the course of certain malignancies such as leukaemia (Festenstein & Labeta, 1988). Previous findings from our laboratory have shown that certain AKR tumour cell lines not only have an altered balance of syngeneic H-2 Class-I gene products but also unexpectedly express novel Class-I MHC-like epitopes (Festenstein & Schmidt 1981 ; Labeta et al., 1989).