Kaklamanis L, Townsend A, Doussis-Anagnostopoulou I A, Mortensen N, Harris A L, Gatter K C
Nuffield Department of Pathology, John Radcliffe Hospital, University of Oxford, United Kingdom.
Am J Pathol. 1994 Sep;145(3):505-9.
Presentation of endogenous antigenic peptides to cytotoxic T lymphocytes (CTLs) is mediated by the major histocompatibility complex (MHC) class I molecules. These antigenic peptides derived from the cytoplasmic protein pool are transported by the recently described MHC-encoded transporters (TAP1 and TAP2) into a pre-Golgi region where they take part in the assembly of MHC class I molecules. Using an affinity-purified polyclonal antibody (AK1.7) for TAP1, we analyzed 81 colorectal carcinomas, 32 adenomas, and the respective nonneoplastic mucosa. Loss of the transporter molecule (TAP1) was observed in 14% (11 of 81) of the carcinomas, either complete (7 of 11) or focal (4 of 11), whereas adenomas and normal mucosa were always positive. This study adds further information to the understanding of the mechanisms related to the defective presentation of the MHC class I molecules by tumor cells.
内源性抗原肽向细胞毒性T淋巴细胞(CTL)的呈递由主要组织相容性复合体(MHC)I类分子介导。这些源自细胞质蛋白池的抗原肽通过最近描述的MHC编码转运体(TAP1和TAP2)转运至高尔基前区,在那里它们参与MHC I类分子的组装。我们使用针对TAP1的亲和纯化多克隆抗体(AK1.7)分析了81例结直肠癌、32例腺瘤以及相应的非肿瘤性黏膜。在14%(81例中的11例)的癌组织中观察到转运体分子(TAP1)缺失,其中完全缺失(11例中的7例)或局灶性缺失(11例中的4例),而腺瘤和正常黏膜始终呈阳性。这项研究为理解肿瘤细胞MHC I类分子呈递缺陷相关机制提供了更多信息。