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Tumorigenicity of adenovirus-transformed cells: region E1A of adenovirus 12 confers resistance to natural killer cells.

Abstract：

:Sensitivity of a library of rat cells transformed in vitro with viable recombinant adenoviruses to natural killer (NK) cells and allogeneic cytotoxic T cells has been studied and correlated with their oncogenic potential in syngeneic rats. All cell lines transformed with the sub370-12E1AB virus (containing E1A and E1B regions of Ad12) and with the sub370-12E1A virions (containing the E1A region of Ad12 and the E1B region of Ad5) showed a high degree of resistance to NK cells. The cell lines transformed with the sub370-12E1B virus (containing the E1A region of Ad5 and the E1B region of Ad12) were highly sensitive to NK cytotoxicity. While all cell lines transformed with virions containing the E1A genes of Ad5 expressed high levels of class I MHC antigen, only three of eight cell lines containing the E1A region of Ad12 showed detectable levels by flow cytometric analysis after staining with specific antibodies. All cell lines containing E1A genes of Ad5 were killed by in vitro generated allogeneic cytolytic T cells. Only three of eight cell lines containing the E1A region of Ad12 were killed by such CTLs; the level of cytotoxicity, however, did not reach that seen with the cells containing the E1A genes of Ad5. All cell lines containing the E1A and E1B genes of Ad12 were highly tumorigenic. Only two of four cell lines transformed with virus containing the E1A genes of Ad12 and E1B region of Ad5 were tumorigenic. The efficiency of tumor induction was low and the latent period was long confirming the importance of the E1B region. None of the cell lines transformed with virus containing the E1A region of Ad5 and the E1B genes of Ad12 were tumorigenic, reflecting their high degree of sensitivity to both natural and induced cellular immunity. Expression of the E1A region of Ad12 in transformed cells modulates not only the level of class I MHC antigens, but also confers resistance to NK cell cytotoxicity.

journal_name

Virology

journal_title

Virology

authors

Sawada Y,Föhring B,Shenk TE,Raska K Jr

doi

10.1016/0042-6822(85)90143-6

subject

Has Abstract

pub_date

1985-12-01 00:00:00

pages

413-21

issue

2

eissn

0042-6822

issn

1096-0341

journal_volume

147

pub_type

杂志文章

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