lymphocytes (TIL) selectively lyse cells of the tumor from which 
they were derived (13,14). Macrophages can also kill neoplastic 
cells through antibody-dependent mechanisms (15,16), or by 
activation induced by substances such as BCG (17) . 
Cytokines are important in the anti-tumor response through 
direct action on tumor cells and by activating cellular 
components of the immune system. Tumor necrosis factor-a (TNF-a) 
(18) and lymphotoxin (19) have direct effects on neoplastic cells 
resulting in cell death. Interferon -7 (IFN- 7 ) induces a marked 
increase in surface expression of class I MHC molecules (20,21) 
and synergizes with TNF-a in producing this effect (22) . Colony 
stimulating factors such as G-CSF and GM-CSF activate neutrophils 
and macrophages to lyse tumor cells directly (23) . 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 
(11,24,25). The LAK cells lyse tumor cells without 
pre immunization or MHC restriction (26) . Interleukin-4 (IL-4) 
also generates LAK cells and acts synergistically with IL-2 in 
the generation of tumor specific killer cells (27) . 
Although the immune system can be stimulated to mediate 
tumor cell destruction, the vast majority of malignancies arise 
spontaneously in immunocompetent hosts. This observation 
suggests that tumor cells escape these host defenses by 
mechanisms which are incompletely defined. It has been suggested 
that evolution of tumor cells provides a proliferative advantage 
to successively less immunogenic clones (28) . Deficient 
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