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

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Abstract
The C‐myc gene encodes a nuclear protein whose precise function is still not folly 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‐1 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 1CAM‐1 expression rather than with down‐regulation of MHC class‐l W6/32 epitope expression.

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