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Induction of expression of MHC‐class‐II antigen on human thyroid carcinoma by wild‐type p53
Author(s) -
Zeki Kazuya,
Tanaka Yoshiya,
Morimoto Isao,
Nishimura Yasuharu,
Kimura Akinori,
Yamashita Uki,
Eto Sumiya
Publication year - 1998
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/(sici)1097-0215(19980130)75:3<391::aid-ijc11>3.0.co;2-c
Subject(s) - cytotoxic t cell , biology , major histocompatibility complex , mhc class i , antigen , antigen presentation , thyroid carcinoma , cancer research , cell culture , immune system , antigen processing , microbiology and biotechnology , t cell , immunology , thyroid , endocrinology , in vitro , genetics
Mutation of the tumor‐suppressor gene p53 is involved in carcinogenetics. We investigated the role of p53 in the induction of anti‐tumor immune responses by establishing a thyroid carcinoma cell line (1F3) prepared by transfection of wild‐type human p53 gene into a p53 ‐deficient cell line (FRO). Our results showed for the first time the involvement of p53 in the induction of anti‐tumor immune responses, as demonstrated by: (i) expression of the major‐histocompatibility‐complex(MHC)‐class‐II antigen on 1F3, but not FRO; (ii) mRNA of class‐II gene was expressed both in 1F3 and in FRO, but was stable at post‐transcriptional level in FRO, which restrained protein synthesis; (iii) 1F3 induced MHC‐class‐II‐specific CD4 + cytotoxic‐T‐cell activity through allo‐antigen presentation and co‐stimulation. Although our novel results are limited to the wild‐type‐p53‐expressing clone from a p53 ‐deficient cell line, we suggest that the absence of p53 in carcinoma cells may reduce the induction of CD4 + cytotoxic‐T‐cell activity against carcinoma cells by diminishing the expression of class‐II antigen. Int. J. Cancer 75:391–395, 1998. © 1998 Wiley‐Liss, Inc.