イチキ ヨシノブ
ICHIKI Yoshinobu
市来 嘉伸 所属 埼玉医科大学 医学部 国際医療センター 呼吸器外科 職種 専任講師 |
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論文種別 | 学術雑誌(原著) |
言語種別 | 英語 |
査読の有無 | 査読なし |
表題 | Haplotype loss of HLA class I antigen as an escape mechanism from immune attack in lung cancer. |
掲載誌名 | 正式名:Cancer research ISSNコード:00085472 |
巻・号・頁 | 65(13),5945-52頁 |
著者・共著者 | Tetsuya So,Mitsuhiro Takenoyama,Makiko Mizukami,Yoshinobu Ichiki,Masakazu Sugaya,Takeshi Hanagiri,Kenji Sugio,Kosei Yasumoto |
発行年月 | 2005/07 |
概要 | One of tumor escape mechanisms from the host's immunosurveillance system (i.e., a haplotype loss of HLA class I antigens) has been detected in various tumor cells. We hypothesize that the majority of tumor cells with normal HLA class I expression were attacked and eradicated by CTLs, and only a minority with an abnormal expression of HLA class I antigens could escape the host's immunosurveillance system. Using HLA class I-transfected tumor variants as stimulators in A904L lung cancer cell line, which has a haplotype loss of HLA class I antigens, both the transfected HLA-A26 and HLA-B39-restricted CTL lines were induced from autologous lymphocytes. However, only one HLA-B39-restricted CTL clone (CTL G3b) was established, and it was then used to identify the antigen. SGT1B [suppressor of G2 allele of SKP1 (SGT1), suppressor of kinetochore protein (SKP1)]was identified as the antigen recognized by CTL G3b. Further experiments using 13 subclones from a primary culture of A904L were found to confirm our above-mentioned hypothesis. Tumor cells with a normal HLA class I expression may thus be killed by CTL at an early stage of carcinogenesis, and only tumor cells with a haplotype loss of |
PMID | 15994973 |