Immunotherapy involving CTL is an attractive alternative for treatment
of various malignancies. One of the approaches currently being explor
ed for immune targeting of human cancers involves potentiation of immu
nogenicity of malignant cells by gene transduction. This strategy is u
ndoubtedly influenced by the ability of the malignant cells to endogen
ously process and present target epitopes on their cell surface for im
mune recognition by CTL. However, there is increasing evidence to sugg
est that a large proportion of human cancers escape CTL-mediated immun
e surveillance by selectively down-regulating the expression of MHC cl
ass I molecules and peptide transporter genes. Understanding and molec
ular analysis of these immunologically relevant genetic defects in tum
ours is very important before translating preclinical studies of immun
otherapy to rational clinical trials. Careful consideration of these p
otential limitations may lead to the development of novel immunotherap
eutic strategies and, potentially, prevention of tumour progression or
development.