Tumor Cell Evasion Of Killer Cells

Tumor cells may evade killer cell destruction by the production of FasL that induces apoptosis in adversarial TILs, CTLs, and NK cells expressing the Fas marker. Constitutive expression of FasL (CD95L) has been described in NK lymphoma, large granular lymphocytic leukemia, melanoma, hepatocellular he-

Immunotoxicology and Risk Assessment Table 3. Immunodeficiencies with NK Cell Defects

Severe combined immunodeficiency Reticular dysgenesis Common variable immunodeficiency Chediak-Higashi syndrome Leukocyte adhesion deficiency Bloom's syndrome Chronic fatigue syndrome

Reprinted from Pediatric Research, Stiehm, 1993, 33:S2-7, withpermission of Pediatric Research patic carcinoma, and astrocytoma. To prevent autoreactions, the Fas (CD95) molecule is downregulated on tumor cells.

Cytotoxic T cells have different sensitivities to tumor-induced FasL apop-tosis. TILs and cytotoxic CD4 cells are extremely sensitive to FasL-induced apoptosis. In contrast, a lower proportion of CD8 and NK cells can be killed by the Fas death-producing signal.

Tumor cells have developed mechanisms to counter the effects of perforins and granzymes. Many tumors secrete an active form of TGF-fi that inhibits both perforin and the granzyme serine esterase activity. Some tumors also express mutated receptors for perforin that result in binding without the formation of transmembrane pores.

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