SummaryIn vivoandin vitroparameters of tumour resistance were examined after immunization of mice with the attenuated 11RX strain ofS. enteritidis.During the bacterial carrier state produced by intraperitoneal (i.p.) or intravenous (i.v.) injection of 11RX the mice were resistant to i.p. tumour growth, could destroy i.p. injected125I‐ or131I‐labelled tumour cellsin vivoand had non‐specifically cytotoxic peritoneal cells (PC) which could lyse51Cr‐labelled tumour cellsin vitro.Most of thein vivoandin vitrocytotoxic activity could be attributed to activated macrophages (La Postaet al., 1982). The predominantly local nature of 11RX‐induced anti‐tumour activity was indicated by the superiority of the i.p. route of infection for induction of tumour resistance andin vivoandin vitrocytotoxicity.After i.v. injection of 11RX, none of the anti‐tumour effects outlasted the bacterial carrier state. However, after i.p. infection, a dichotomy was observed betweenin vitroandin vivoanti‐tumour effects.In vitroPC cytotoxicity lasted only for the length of the 11RX carrier state (approximately 30 days), whereas resistance to i.p. tumour growth lasted for 60 to 100 days and was correlated closely with cytotoxic activity measuredin vivo.Possible reasons for this dichotomy are discussed.