Colorectal carcinoma in a rat model: suppression of tumour development and altered host immune status following treatment with anti B-lymphocyte serum.

The rate of colonic tumour development and immune capability in rats whose B-lymphocyte function was suppressed by injections of rabbit anti-rat IgM and also given the carcinogen dimethylhydrazine (DMH) were studied. Four rat groups were arranged to receive either DMH + anti-IgM, DMH + normal rabbit serum (NRS), saline + anti-IgM, or saline + NRS. Tumour weight, blood and mesenteric lymph node B-lymphocyte numbers, in vivo allograft response, in vitro lymphocytotoxicity, and leucocyte migration inhibition response (LMI) were recorded fortnightly. Tumour induction was delayed in the DMH + anti-IgM (treated tumour) group, which developed less tumour than the DMH + NRS (untreated tumour) group (p less than 0.001). Spleen cell lymphocytotoxicities were depressed in treated rats when compared to either the saline + anti-IgM (treated control) rats or the untreated rats (P less than 0.02), whereas anti-IgM treatment suppressed lymphocytotoxicity responses in control rats (p less than 0.05). The untreated tumour rats were tumour immune by LMI; however, the treated tumour rats did not express this in vitro tumour immunity. The B-lymphocyte levels in the mesenteric lymph nodes of untreated tumour rats increased with tumour induction (p less than 0.05), whereas in the treated tumour rats B-lymphocyte levels were not similarly stimulated.