The identification of MHC-restricted and tumour-specific cytotoxic T lymphocytes 
(CTLs) provides strong evidence in support of T cell-mediated immune 
surveillance against human tumour cells. These CTLs recognize short peptides 
derived from tumour-associated antigens in conjunction with class I molecules 
expressed on tumour cells. In contrast to these observations there are now 
numerous examples to suggest that a number of tumours escape this CTL-mediated 
control either by down-regulating accessory molecules or by blocking the 
intracellular processing of tumour-specific antigens. Recently a number of 
tumour cell lines have been identified which display a transcriptional 
deficiency of transporters associated with antigen processing (also referred to 
as TAP). The Epstein-Barr virus (EBV)-associated tumour, Burkitt's lymphoma 
(BL), is a classic example in this category. In the present study we have 
restored class I-restricted antigen processing in a BL cell line by transfecting 
a minigene expression vector encoding a CTL epitope derived from EBV linked to 
an endoplasmic reticulum translocation signal sequence. These minigene 
transfected BL cells were not only susceptible to lysis by virus-specific CTL 
but were also capable of efficiently activating an antigen-specific CTL 
response. Interestingly, the immunogenicity of these BL cells was not affected 
by the significantly down-regulated expression of adhesion molecules such as 
LFA1 alpha, LFA1 beta and LFA3. These findings suggest that resistance of tumour 
cells to CTL-mediated immune control can be reversed if the relevant peptide 
epitopes are appropriately presented on the cell surface.