Open AccessRejection of Mouse Renal Cell Carcinoma Elicited by Local Secretion of Interleukin‐2
Author(s) -
Hara Isao,
Hotta Hak,
Sato Noriyuki,
Eto Hiroshi,
Arakawa Soichi,
Kamidono Sadao
Publication year - 1996
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1996.tb00284.x
Subject(s) - interleukin 2 , immune system , immunology , renal cell carcinoma , biology , cancer research , interleukin , secretion , immunotherapy , cellular immunity , interleukin 15 , natural killer cell , cytokine , medicine , pathology , endocrinology , cytotoxic t cell , in vitro , biochemistry
We introduced the interleukin‐2 (IL‐2) gene into mouse renal cell carcinoma (RenCa) in order to examine the mechanism of tumor rejection. IL‐2 gene‐transfected RenCa (RenCa/IL‐2Hi) exhibited marked retardation of tumor growth when implanted in a syngeneic host. Growth retardation of RenCa/IL‐2Hi was also observed in athymic nude mice even after depletion of natural killer (NK) cells by treatment with anti‐asialo GM1 antibody. Histological analysis of RenCa/IL‐2Hi tumors disclosed non‐specific inflammatory changes in syngeneic hosts. Co‐injection of Bacillus Calmette Guerin with RenCa/IL‐2Hi considerably enhanced the anti‐tumor effects. Taken together, these findings strongly suggest that in situ IL‐2 production leads to tumor rejection through non‐specific inflammatory responses without participation of T cells and NK cells. On the other hand, the syngeneic mice that had rejected RenCa/IL‐2Hi acquired immunity against parental RenCa, suggesting possible participation of memory T cells in the second rejection of the tumor.