西塔
人类白细胞抗原
肺癌
癌症研究
交易激励
生物
癌症
免疫学
医学
T细胞
MHC II级
免疫系统
转录因子
抗原
肿瘤科
基因
遗传学
作者
Takuya Yazawa,Hiroshi Kamma,Masachika Fujiwara,Miwa Matsui,Hisashi Horiguchi,Hiroaki Satoh,Mitsuo Fujimoto,Kôichi Yokoyama,Takesaburo Ogata
标识
DOI:10.1002/(sici)1096-9896(199901)187:2<191::aid-path206>3.0.co;2-3
摘要
Small cell lung cancer (SCLC) is characteristically not associated with tumour-infiltrating lymphocytes. Since SCLC has been reported to show marked reduction of class I HLA, the reduced expression has been considered a means of escaping anti-cancer immunity. However, HLA-DR expressed in cancer cells is now known to contribute to anti-cancer immunity. To clarify the difference in HLA-DR expression between SCLC and non-small cell lung cancer (NSCLC), and the mechanism, the expression and the cis- and trans-acting factors involved were investigated. HLA-DR was not immunohistochemically detected in any SCLC and could not be induced by interferon gamma (IFN-γ) in any SCLC cell line, whereas HLA-DR was expressed to varying degrees and was easily induced in NSCLC. SCLC cell lines lacked class II transactivator (CIITA) even after IFN-γ induction, whereas NSCLC cell lines expressed CIITA. The other class II HLA-specific transcription factors were expressed and genomic DNA of HLA-DR, including the promoter, was conserved well both in SCLC and in NSCLC cell lines. CIITA transfection improved the expression of HLA-DR in SCLC. In conclusion, the lack of CIITA results in severe deficiency of HLA-DR expression in SCLC. Since CIITA has also been reported to induce class I HLA, CIITA transfection might make it possible to establish effective anti-cancer immunotherapy against SCLC through the up-regulation of class I and class II HLA. Copyright © 1999 John Wiley & Sons, Ltd.
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