| Project/Area Number |
08671198
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内分泌・代謝学
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
FUJIHIRA Takashi University of Occupational and Environmental Health, First Department of Internal Medicine, Assistant Professor, 医学部, 講師 (40159124)
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| Co-Investigator(Kenkyū-buntansha) |
ETO Sumiya University of Occupational and Environmental Health, First Department of Interna, 医学部, 教授 (90010347)
TANAKA Yoshiya University of Occupational and Environmental Health, First Department of Interna, 医学部, 講師 (30248562)
ZEKI Kazuya University of Occupational and Environmental Health, First Department of Interna, 医学部, 講師 (60183430)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | p53 / thyroid carcinoma / transfection / post-transcriptional regulation / cytotoxic T cell / MHC-class-II antigen / Class II主要組織適合抗原 |
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| Research Abstract |
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-lacking 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 :
1. expression of the major histocompatibility complex (MHC) class II antigen on 1F3, but not FRO ;
2. mRNA of class II gene was expressed in both 1F3 and FRO,but it was stable at post-transcriptional level in FRO,which restrained protein synthesis ;
3.1F3 induced MHC class II-specific CD4^+ cytotoxic T cell activity through alloantigen presentation and costimulation.
Although our novel results are limited to the wild-type p53-expressing clone from a p53-lacking 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.
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