Macrophages and resistance to tumours: influence of agents affecting macrophages and delayed-type hypersensitivity on resistance to tumours inducing concomitant immunity.

Abstract

Early, specific concomitant immunity to each of four tumours was inhibited by treatment with silica or carrageenan. Late, non-specific concomitant immunity was, with one exception, not inhibited by these agents. Treatment of non-immune mice with silica at certain critical periods before challenge promoted the growth of four of six syngeneic methylcholanthrene-induced tumours in their feet. Treatment with carrageenan was much less effective. Early and late concomitant immunity were inhibited by one or more agents inhibiting delayed-type hypersensitivity: irradiation, niridazole and reserpine. Irradiation of non-immune mice did not effect the growth of tumours in their feet. Treatment of non-immune mice with niridazole or reserpine actually inhibited the growth of some tumours. It is suggested that (a) mice offer some natural resistance to tumour growth, macrophages perhaps being effectors; (b) some tumour isografts may survive only if an inflammatory reaction occurs; (c) mechanisms akin to those of delayed-type hypersensitivity operate in the expression of concomitant immunity; (d) macrophages are important in early, specific concomitant immunity, but perhaps less so in the late non-specific phase.