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 (42-46) . Reduced class I MHC 
expression could also 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 (47-51) . In some 
experiments, tumor cells which express a class I MHC gene confer 
immunity in naive recipients against the parental tumor (48,49). 
The absolute level of class I MHC expression however, is not the 
only factor which influences the tumorigenicity or immunogenicity 
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 (52) . 
The immune response to tumor cells can be stimulated by 
systemic administration of IL-2 (53) , or IL-2 with LAK cells 
(54,55). Clinical trials using tumor infiltrating lymphocytes 
are also in progress (17) . Recently, several studies have 
examined the tumor suppressive effect of lymphokine production by r 
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 
parental tumor cell line (6) . Expression of IL-4 by plasmacytoma 
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Recombinant DNA Research, Volume 17 
