INDUCTION OF IMMUNE REJECTION OF TUMORS BY PROTEIN A IN MICE BEARING TRANSPLANTABLE SOLID TISSUE DALTONS LYMPHOMA TUMORS

In a transplantable solid tissue Dalton's lymphoma tumor model in mice we have studied the mode of antitumor action of protein A, a well known biological response modifier. Protein A (15 ug) was administered intravenously in normal and solid tissue Dalton's lymphoma tumor bearing mice on day 3 and 7 after tumor inoculation. Incidence of mortality was more in untreated tumor bearing group than that in PA treated tumor bearers. There was a significant decrease (p < 0.001) in tumor diameter in PA treated group compared to untreated group. Protein A treatment significantly enhanced the delayed type hypersensitivity (p < 0.01), T-cell number in spleens (p < 0.001) and lymph nodes (p < 0.05) as well as phagocytosis (p < 0.001) of opsonized SRBC by peritoneal macrophages of tumor bearing animals. Apart from the nonspecific immunopotentiation, Protein A also activates natural Killer (NK) cell activity and also splenic lymphocytes mediated killing of autologous tumor targets in a significant (p < 0.001) manner. These results suggest that PA treatment activates cellular arc of the immune system in general, and macrophage, T cells and NK cells specifically. In the present communication, we have attemted to provide the information that these immune activations appear to be related to antitumor response induced by Protein A.