Original Research
Copyright ©The Author(s) 2001. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 2001; 7(6): 860-863
Published online Dec 15, 2001. doi: 10.3748/wjg.v7.i6.860
Fas counterattack in cholangiocarcinoma: A mechanism for immune evasion in human hilar cholangiocarcinomas
Zi-Yu Li, Sheng-Quan Zou
Zi-Yu Li, Sheng-Quan Zou, Department of General Surgery of Tongji Hospital, Wuhan, 430030, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Sheng-Quan Zou, Department of General Surgery of Tongji Hospital, 1095 Jiefang Road, Wuhan 430030, Hubei Province, China. Sqzou@tjh.tjmu.edu.cn
Telephone: +86-27-83662851
Received: February 28, 2001
Revised: June 9, 2001
Accepted: June 21, 2001
Published online: December 15, 2001
Abstract

AIM: To investigate FasL expression in hilar cholangiocarcinoma tissues and cultured cholangiocarcinoma cells, and to assess its ability to induce apoptosis.

METHODS: We studied the expression of FasL by human hilar cholangiocaroinomas tissues by immunohistochemistry, and the QBC939 cholangiocarcinoma cell line by RT-PCR, immunohistochemistry, and Western Blot. TUNEL and flow cytometry were used to detect apoptotic cells.

RESULTS: Prevalent expression of FasL was detected in 39 resected hilar cholangiocarcinoma tissues. TUNEL staining disclosed a high level of cell death among lymphocytes infiltrating FasL positive areas of tumor. FasL mRNA and protein expressions in cholangiocarcinoma cells could induce Jurkat cells.

CONCLUSION: Hilar cholangiocarcinomas may elude immunological surveillance by inducing, via Fas/FasL system, the apoptosis of activated lymphocytes.

Keywords: cholangiocarcinoma/immunology; tumor cells, cultured/immunology; membrane glycoproteins/biosynthesis; lymphocytes/immunology; apoptosis