Identification of signalling molecules and surface structures determining the interaction between natural killer (NK) effector cells and tumor targets.

Project Details


In the CIMM lab a mouse T lymphona model (BW) was developed to study immune escape mechanisms. As such a correlation was established between expression of H-2D major histocompatibility complex (MHC) class 1 and resistance to NK cells, which is accompanied by an enhanced metastatic capability of the BW cells. The present study will on the one hand delineate the importance of tumor-derived peptidesequences in teh H-2D-mediated inactivation of NK cells and on the other hand optimal LAK populations for adoptive transfer will be generated. Indeed, in certain BW variants, deficiencies at the level of the proteasome will be accompanied by an enhanced susceptibility to NK cells, which can point to a peptide specificity of NK inhibition in the mouse system. The identification and subsequent inactivation of these inhibitory tumor-derived antigens can lead to efficient anticancer vaccination strategies. Interestingly, in contrast to current views, we were able to demonstrate that MHC class 1-mediated inactivation of NK cells is not insuperable. Indeed, activity could be enforced by treating NK cells with IL-12. Profound analysis of the phenomeneon of costimulation of NK and the receptors involved, could have important implications for the use of selective NK/LAK populations in adoptive transfer experiments.
Effective start/end date1/01/9931/12/99


  • natural killer cells
  • tumorvaccination
  • peptides
  • PCR

Flemish discipline codes

  • Basic sciences
  • Materials engineering