Abstract
Carrageenan (Cg) was tested for its effects on the growth of, and immunity to, 2 methylcholanthrene-induced syngeneic murine fibrosarcomas (H1 and H2). The tumours were found not to share major tumour-specific transplantation antigens. H2 appeared more immunogenic than H1. In contrast to H1, immunity induced by H2 was not affected by Cg, nor was its growth in Cg-treated normal mice augmented.Postoperative i.p. injections of Cg abolished the weak anti-H1 immunity produced by H1 tumour excision. Furthermore, the subsequent growth of the H1 tumour challenge in the Cg-treated immune mice was significantly greater than the augmented growth in Cg-treated normal mice. The Prior administration of the macrophage-stabilizing agent polyvinylpyrrolidone (PVP) to immune mice significantly reduced the augmenting effect of Cg. The growth-promoting effect of Cg on a secondary H1 tumour challenge in mice immunized by tumour excision was abolished by 10(6) MCT-H1 cells injected s.c. before Cg. In contrast to the immunity induced by tumour excision, Cg did not abolish the immunity induced by the injection of MCT-H1 cells.Passive administration of H1 tumour-bearer serum (TBS) did not enhance the growth of H1 cells in normal mice, nor did TBS abrogate the specific cell-mediated immunity (CMI) induced in vivo by MCT-H1 cells. However, TBS administered to Cg-treated, MCT-H1-immune mice abolished tumour immunity.We propose that TBS does not inhibit CMI in vivo provided that macrophages remain functional, but may do so when macrophages are rendered defective by antimacrophage agents or by products of neoplastic cells. Increasing the levels of specific effector cells can over-ride the inhibiting effects of TBS, even when defective macrophages are present.