Meccamsmi cellulari della immunodepressione da tumore

Mocarelli, Paolo ; Villa, Maria Luisa ; Pessina, Augusto ; Bigi, Giuseppe ; Clerici, Enrico

Atti della Accademia nazionale dei Lincei. Rendiconti della Classe di scienze fisiche, matematiche e naturali, Série 8, Tome 49 (1970) no. 6, pp. 446-451

Résumé

Adult mice grafted i.p. with Ehrlich ascites-carcinoma cells and then exposed to sublethal X—irradiation developed a significantly smaller number of "endogenous" spleen colonies than X-irradiated controls not grafted with tumor cells. Similar results were obtained when bone marrow cells from tumor bearing mice were injected i.v. into lethally X-irradiated mice, so as to produce "exogenous" spleen colonies. In both experiments, the Ehrlich ascites-carcinoma inoculum necessary to reduce significantly the frequency of hemopoietic stem cells was found equal to 8,5x105 cells. This is the number of tumor cells which inhibits the immune reactivity of host mice [1]. These findings are consistent with our working hypothesis that the immunological hyporeactivity of tumor-bearing animals is mediated through a functional defect of primitive bone marrow cells. Such a mechanism of action, similar to that recently proposed by Bennet and Steeves [14] for Friend leukemia virus and by Rowland and Hurd [15] for a chemical carcinogen (dimethylbenzanthracene), may point to a common pathway for the immunosuppression caused by malignant tumors.