Introduction

MHC antigens and the immune system

Since the report by Mitchison in the early 1950s demonstrating that cellmediated, rather than humoral, immunity played a greater role in tumour rejection (Mitchison, 1953), its primacy in tumour rejection has become an increasingly accepted mechanism by most immunologists. This has mainly been attributed to specific immunity involving MHC antigens as restriction element and to a lesser extent the non-specific immunity involving LAK/NK activity (Jabrane-Ferrat et al., 1990; Mule et al., 1984).

It has long been established that the MHC antigens are an individual's fingerprint and they exist in two forms, the class I and class II antigens. Zinkernagel & Doherty (1979) showed that they act as associative molecules for presentation of non-self antigens to CTLs and TH cells, respectively. The critical role of CTLs for regulating resistance to viral infection (McMichael et al., 1977) as well as in graft and tumour rejection in experimental models (Hui, Grosveld & Festenstein, 1984; Wallich et al., 1985) has previously been reported. TH cells have been shown to act mainly as an immune amplifier, since their stimulation results in the production of a series of immunoreactive cytokines, such as IL-2, which in turn are critical for initiating immune responses, including activation of CTLs (Greenberg et al., 1988).