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Rejection of parental meth-a tumor on concomitant inoculation of meth-a cells infected retrovirally with the interferon-gamma gene into (balb/cxc57bl/6)f-1 mice
Authors:Harutsumi M  Aji T  Manki A  Hikida M  Omori H  Watanabe Y  Teramura Y  Kuribayashi K  Seino Y  Nakayama E
Institution:OKAYAMA UNIV,SCH MED,DEPT PARASITOL & IMMUNOL,OKAYAMA 700,JAPAN. OKAYAMA UNIV,SCH MED,DEPT PEDIAT,OKAYAMA 700,JAPAN. OKAYAMA UNIV,FAC ENGN,DEPT BIOTECHNOL,OKAYAMA 700,JAPAN. KYOTO UNIV,FAC MED,INST IMMUNOL,SAKYO KU,KYOTO 60601,JAPAN. KYOTO UNIV,FAC PHARMACEUT SCI,DEPT MOLEC MICROBIOL,SAKYO KU,KYOTO 60601,JAPAN.
Abstract:The IFN-gamma gene was introduced retrovirally into Meth A cells. IFN-gamma gene infected Meth A (K gamma) cells were highly antigenic and regressed in CB6F(1) mice. Concomitant immunization of CB6F(1), mice with IFN-gamma gene infected Meth A (K gamma) cells after inoculation of parental Meth A protected the mice from parental tumor growth. 1x10(6) infectant Meth A (K gamma) cells protected the mice from growth of 1x10(6) parental Meth A cells, but 2x10(6) infectant cells did not, suggesting that there was an optimal dose of infectant cells for rejection of the parental tumor. Specificity analysis revealed that growth of CMS13 tumor was slightly inhibited by Meth A (K gamma) cells but that of CMS5 was not inhibited. The findings are consistent to those obtained with parental Meth A cells and indicated that the relevant rejection antigen on Meth A (K gamma) cells was identical to the parental Meth A rejection antigen.
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