lymphokine-activated killer (LAK) cells (25) . Cytolytic T cells 
which infiltrate tumors have been isolated and characterized 
(26) . These tumor infiltrating lymphocytes (TIL) selectively 
lyse cells of the tumor from which they were derived (10,27). 
Macrophages can also kill neoplastic cells through antibody- 
dependent mechanisms (28,29), or by activation induced by 
substances such as BCG (30) . 
Cytokines can also participate in the anti-tumor response, 
either by a direct action on cell growth or by activating 
cellular immunity. The cytostatic effects of tumor necrosis 
factor-a (TNF-a) (31) and lymphotoxin (32) can result in 
neoplastic cell death. Interferon -7 (IFN- 7 ) markedly increases 
class I MHC cell surface expression (33,34) and synergizes with 
TNF-a in producing this effect (35) . Colony stimulating factors 
such as G-CSF and GM-CSF activate neutrophils and macrophages to 
lyse tumor cells directly (36) , and interleukin-2 (IL-2) 
activates Leu-19+ NK cells to generate lymphokine activated 
killer cells (LAK) capable of lysing autologous, syngeneic or 
allogeneic tumor cells but not normal cells (25,37,38). The LAK 
cells lyse tumor cells without preimmunization or MHC restriction 
(39) . Interleukin-4 (IL-4) also generates LAK cells and acts 
synergistically with IL-2 in the generation of tumor specific 
killer cells (40) . 
Since most malignancies arise in immunocompetent hosts, it 
is likely that tumor cells have evolved mechanism to escape host 
defenses, perhaps through evolution of successively less 
immunogenic clones (41) . Deficient expression of class I MHC 
Recombinant DNA Research, Volume 17 
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