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. 2001 Dec;7(6):860-3.
doi: 10.3748/wjg.v7.i6.860.

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

Affiliations

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

Z Y Li et al. World J Gastroenterol. 2001 Dec.

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.

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Figures

Figure 1
Figure 1
FasL positive in human hilar cholangiocarcinom as (brown). SABC × 200
Figure 2
Figure 2
Expression of FasL in cholangiocarcinoma cell line. QBC939 × 200
Figure 3
Figure 3
Expression of FasL mRNA in human cholangiocarcinoma cells QBC939. M: DL 2000 Marker; 1: FasL; 2: FasL+β-actin
Figure 4
Figure 4
CD45 positive cells (brown) of lymphoid morphology adjacent to carcinoma. × 200
Figure 5
Figure 5
Positive apoptotic TUNEL stainig in situ (brown) with apoptotic morphology.
Figure 6
Figure 6
Western blotting of FasL protein with mAb from QBC939 cell cultures clone 33 from QBC939 cell cultures

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