Abstract
Experiments were carried out relevant to the mechanisms involved in tumor ‘concomitant immunity’. Mice bearing 3LL, B16, EL4 or the methylcholanthrene‐induced T‐10 tumors were capable of completely suppressing the growth of a subsequent intra footpad graft of tumor cells. The observed inhibitory activity exerted by the primary tumor increased with the increase in size of the tumor and reached its maximum at the latest period of tumor growth when the immune response of the tumor‐bearing host was largely suppressed. In T‐cell‐depleted animals (B mice or nude mice), the inhibitory effect exerted by the first tumor on the subsequently implanted tumor graft was as effective as in normal mice. Hence it appears that concomitant immunity is not mediated via a T‐cell‐dependent immune reaction. The observed inhibitory effect was tumor‐nonspecific. Mice bearing a 3LL tumor manifested resistance to the reinoculation of 3LL, B16 or EL4 tumor cells. Similarly, mice bearing B16, EL4 or T‐10 tumors arrested the growth of reinoculated 3LL tumor cells. Hence, concomitant immunity is not a result of specific immune response. Metastases can be considered as ‘naturally’ occurring secondary grafts. Indeed, we found that the local tumors exert a strong inhibitory effect on their lung metastases. Thus, the surgical removal of the local 3LL tumor led to an acceleration of metastatic growth in the lungs. Such acceleration took place even when the local tumor grew in immune‐suppressed mice. It appears, therefore, that ‘concomitant immunity’ and the suppression of metastatic growth exerted by the local tumor, are based on similar mechanisms.