Intra‐tumour host cells of transplanted rat neoplasms of different immunogenicity

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Abstract
The nature of host‐derived cells present in serial transplants of five tumours of variable immunogenicity in syngeneic NW rats was investigated. Single‐cell suspensions obtained by tumour disaggregation in papain‐collagenase‐DNase (PCD) mixture were quantitatively analysed for cells with Fc receptors by formation of erythrocyte‐antibody (EA) rosettes; for cells with receptors for the third component of complement (C3) by formation of erythrocyte‐antibody‐complement (EAC) rosettes; for macrophages by the uptake of polystyrene particles and/or phagocytosis of membrane‐bound EA rosettes and for T cells by means of rabbit anti‐rat thymocyte serum (ATS). In addition, the total host cell content of two neoplasms (MC40A and SP22) was determined by immunofluorescence analysis of tumours grown in (NWxPVG/c) F1 hybrids, using NW anti‐PVG/c antiserum. There was close correspondence between the host cell content of these tumours as determined by immunofluorescence and summation of total EA‐RFC and T lymphocytes, indicating the probability that EA‐RFC were of host, rather than tumour, origin. This latter population consisted of macrophages and non‐phagocytic Fc+ cells and these, together with T cells, constituted the major infiltrative components. Host cells were most evident in the two neoplasms (MC40A, MC57) which were immunogenic, where macrophages, non‐phagocytic Fc+ cells and T lymphocytes were present in approximately equivalent proportions. (Total host cells: 42% and 45% respectively.) For the nonimmunogenic tumours (AAF 57, SP1 and SP22) host cells accounted for ± 15% of the enzyme‐dispersed suspension. However, analysis of cellular infiltration as a function of time after injection of cultured tumour cells revealed that the macrophage content of MC40A, AAF 57 and SP22 was greatest when the tumours first became clinically manifest and thereafter rapidly declined to the levels observed in serial transplants. EA‐RFC were represented almost wholly by macrophages in AAF 57 and SP22, whereas in MC40A the declining macrophage population was replaced by non‐phagocytic Fc+ cells, the precise identity of which was not established. The results indicate that cellular infiltration of established neoplasms correlates with their immunogenicity; that this host cell component comprises non‐phagocytic Fc+ cells and T cells as well as macrophages; but that the macrophage content is significantly greater when tumours are first palpable than at later stages of development, even in neoplasms which evoke no transplantation immunity.