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Immunological and non‐immunological influence of H‐2K b gene transfection on the metastatic ability of B16 melanoma cells
Author(s) -
De Giovanni C.,
Palmieri G.,
Nicoletti G.,
Landuzzi L.,
Scotlandi K.,
Bontadini A.,
Tazzari P.L.,
Sensi M.,
Santoni A.,
Nanni P.,
Lollini P.L.
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910480220
Subject(s) - transfection , clone (java method) , immunogenicity , melanoma , in vitro , antigen , cytotoxic t cell , in vivo , cancer research , metastasis , biology , immunology , immune system , microbiology and biotechnology , cell culture , gene , cancer , biochemistry , genetics
The H‐2 b ‐negative B78HI clone (derived from B16 melanoma) was transfected with the H‐2K b gene; 4 cell clones expressing membrane H‐2K b antigens and 2 control clones (transfected with pSV 2 neo alone) were used for studies of metastatic ability, immunogenicity, NK sensitivity and homo‐typic adhesion. The experimental metastatic capacity of H‐2K b transfectants In syngeneic mice was greatly diminished in comparison with control and parent cells. Both immune‐mediated and Intrinsic properties of transfectants correlated with their lower metastatic ability. A cell‐mediated cytotoxic response was induced by repeated in vivo immunizations of syngeneic mice followed by in vitro restimulation of effectors when transfectants (but not controls) were used as immunizers and as targets. Moreover, homotypic adhesion of H‐2K b transfectants was significantly lower than that of controls. Sensitivity to NK ceils of transfectants was not decreased in comparison to H‐2‐negative controls. It is known that In vitro treatment with IFN‐γ of H‐2‐positive B16 melanoma cells induces a simultaneous increase in H‐2 expression and in experimental metastasis; treatment of H‐2K b transfectants with IFN‐γ induced a higher K b expression, but no increase in metastatic ability, thus suggesting that the IFN‐sensitive component that mediates enhancement of metastasis is not H ‐ 2K b .