Article révisé par les pairs
Résumé : The precise mechanism of action of BCG in bladder cancer treatment is still poorly understood. The question remains whether bladder tumour cells are destroyed in an aspecific manner by polyclonally activated killer cells or targetted by specifically activated T-cells recognizing cognate cpitopes. We tested therefore the lymphoproliferation of peripheral blood lymphocytes against the secreted fibroncctin-binding antigen 85 complex from BCG (AG 85) in patients with superficial bladder tumours (TCC) prior to any BCG treatment. Using a whole blood assay, T-cell response against BCG and AG 85 was investigated in 80 patients with superficial bladder tumours prior to BCG treatment and in 34 control subjects without malignancy matched for age and sex. both groups without past history of tuberculosis. Lymphoproliferation was measured by means of a tritiated thymidine uptake assay on day 7 of culture. In patients with superficial TCC, a significant lymphoproliferative response before any BCG treatment against whole BCG antigen and AG 85 was observed in 32/80 (40.0%) and 51/80 (63.7%) patients respectively. In the control group 3 patients (8.8%) had a significant lymphoproliferation (but significantly lower than bladder cancer patients) against BCG and against AG 85 (p<0.001 and p<0.00001 respectively). Patients with superficial TCC demonstrate a clear increased lymphoproliferation against mycobacterial antigens prior to any BCG treatment. Our data suggest the possible existence of bladder cancer antigens cross-reactive with mycobacterial antigens and especially the major secreted fibronectin-binding antigen from BCG culture filtrate, AG 85. This could imply that BCG possibly acts through botli a nonspecific and a specific targetting of activated T-cells.