Subtherapeutic numbers of tumour-sensitized, L3T4+, Ly 1+2- T cells are needed for endotoxin to cause regression of an established immunogenic tumour.

The immunological requirements for endotoxin-induced regression of an established subcutaneous tumour (SA 1 sarcoma) were investigated by employing tumour-bearing T-cell deficient mice as test recipients, and mice generating concomitant immunity, or Corynebacterium parvum-augmented concomitant immunity, as donors of sensitized T cells. It was found that endotoxin failed to cause regression of an established tumour in T-cell deficient recipients unless they were infused 2 days earlier with a subtherapeutic number of T cells from donors generating concomitant immunity. The donor T cells that primed the recipient tumour for endotoxin-induced regression displayed the L3T4+, Ly 1+2- membrane phenotype. T-cell priming for endotoxin-induced regression was specific and localized, as evidenced by the results of experiments that employed recipients simultaneously bearing two different syngeneic tumours. Infusing these recipients with T cells sensitized to one tumour primed that tumour, but not the other, for endotoxin-induced regression. The ultimate effector mechanism of regression also appeared to be specific, in that a mixed tumour made up of YAC1 lymphoma cells plus SA1 sarcoma cells underwent complete regression only in recipients infused with both YAC1-sensitized and SA1-sensitized T cells. These results indicate that, whereas endotoxin-induced tumour necrosis may not depend on an anti-tumour immune response, regression of the ring of living tumour tissue that surrounds the area of necrosis is specifically accomplished by an acquired population of tumour-sensitized L3T4+ T cells.