expression of class I MHC molecules limits the ability of tumor 
cells to present antigens to cytotoxic T cells. Freshly isolated 
cells from naturally occurring tumors frequently lack class I MHC 
antigen completely or show decreased expression (29-33) . Reduced 
class I MHC expression is thought to facilitate growth of these 
tumors when transplanted into syngeneic recipients. Several 
tumor cell lines which exhibit low levels of class I MHC proteins 
become less oncogenic when expression vectors encoding the 
relevant class I MHC antigen are introduced into them (34-38) . 
In some experiments, tumor cells which express a class I MHC gene 
confer immunity in naive recipients against the parental tumor 
(35,36). The absolute level of class I MHC expression however, 
is not the only factor which influences the tumorigenicity or 
immunogen icity of tumor cells. In one study, mouse mammary 
adenocarcinoma cells, treated with 5-azacytidine and selected for 
elevated levels of class I MHC expression did not display altered 
tumorigenicity compared to the parent line (39) . 
A variety of methods can be used to augment the immune 
response against tumor cells. These include systemic 
administration of IL-2 (40), or IL-2 with LAK cells (41,42). 
Clinical trials using tumor infiltrating lymphocytes are 
currently in progress (43) . Recently, several studies have 
examined the tumor suppressive effect of lymphokine production by 
genetically altered tumor cells. The introduction of tumor cells 
transfected with an IL-2 expression vector into syngeneic mice 
stimulated an MHC class I restricted cytolytic T lymphocyte 
response which protected against subsequent rechallenge with the 
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