A novel strategy of c-myc oncogene in NK activity regulation not related to the W6/32 MHC class-I epitope.

The c-myc gene encodes a nuclear protein whose precise function is still not fully understood. Introduction of a c-myc gene into a number of cell lines leads to an increase in their susceptibility to NK-cell lysis. It was reported earlier that c-myc can induce a decrease in the membrane expression of the MHC class-I molecules and this may be one of the factors that render target cells relatively more susceptible to NK lysis. In this contribution, we show, in a human LCL line transfected with a constitutively active c-myc gene, an increased sensitivity to NK lysis, which correlates with an augmented effector-target binding ability of c-myc-transfected LCLs and with a high ICAM-I expression rather than with down-regulation of MHC class-I W6/32 epitope expression.