Fas counterattack in cholangiocarcinoma: a mechanism for immune evasion in human hilar cholangiocarcinomas.
OBJECTIVE
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.


CONCLUSIONS
Hilar cholangiocarcinomas may elude immunological surveillance by inducing, via Fas/FasL system, the apoptosis of activated lymphocytes.
Li
Z Y
ZY
Department of General Surgery of Tongji Hospital, Wuhan 430030, Hubei Province, China.
Zou
S Q
SQ
D017209:Apoptosis / Q000502:physiology; D018281:Cholangiocarcinoma / Q000276:immunology* / Q000503:physiopathology*; D046508:Culture Techniques; D053222:Fas Ligand Protein; D006801:Humans; D007157:Immunologic Surveillance; D008562:Membrane Glycoproteins / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D014407:Tumor Cells, Cultured
C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D012333:RNA, Messenger