Role of "lymphotoxin" in the local anti-tumour action associated with inflammation caused by delayed hypersensitivity responses or intralesional BCG. I. Variations in response of different syngeneic mouse tumours.

The anti-tumour effect induced by a delayed hypersensitivity response (DHSR) unrelated to the tumour or by intra-tumoural inoculation of BCG was studied with 6 syngeneic mouse tumours. The growth of the tumours was followed i.p. or s.c. in suitably sensitized animals either in the presence or absence of the specific antigen required to elicit a DHSR. In a Winn-type assay the growth of tumour cells admixed with sensitized lymphocytes was also determined with and without the eliciting antigens. In addition, the effect of admixing different amounts of BCG with the tumour cells was studied on the growth of the tumours in vivo. The different tumours varied widely in their susceptibility to growth inhibition by a DHSR reaction and by BCG but their order of sensitivity was the same in all of the tests. Analysis of the effector population in the Winn test coupled with the inability to observe an anti-tumour action in mice with defective T-cell function showed that the effector mechanism involved allergized T-cells or more probably products released when these were confronted with the specific antigen. In vitro the relative susceptibility of the different tumour cells to killing by activated macrophages and by NK cells was quite different to that found for in vivo growth inhibition but the in vitro response to lymphotoxin of the different tumours paralleled that produced by inflammation in vivo.