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Fas ligand expression in primary colon adenocarcinomas: evidence that the Fas counterattack is a prevalent mechanism of immune evasion in human colon cancer
Author(s) -
O'Connell Joe,
Bennett Michael W.,
O'Sullivan Gerald C.,
Roche Desmond,
Kelly Jacquie,
Collins Kevin,
Shanahan Fergus
Publication year - 1998
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199811)186:3<240::aid-path173>3.0.co;2-l
Subject(s) - fas ligand , immune privilege , immune system , cancer research , biology , apoptosis , immunology , programmed cell death , biochemistry
Fas ligand (FasL) kills sensitive Fas receptor (FasR)‐bearing cells by inducing apoptosis. FasL expressed by non‐lymphoid cells within the eye and the testis mediates immune privilege by inducing apoptosis of Fas‐sensitive infiltrating pro‐inflammatory immune effector cells. It has previously been demonstrated by the present authors that the colon cancer cell SW620 expresses FasL and can kill lymphoid cells by Fas‐mediated apoptosis in vitro . This ‘Fas counterattack’ was subsequently confirmed by others as a potential mechanism of immune privilege in various malignancies. The aim of the present study was to ascertain the prevalence of FasL expression in human colon cancer and to confirm that neoplastic colonic epithelial cells express FasL in vivo . The study of FasL expression by colon cancer cell lines was extended: it was shown that seven of eight colon adenocarcinoma cell lines expressed FasL mRNA, using reverse transcription‐polymerase chain reaction (RT‐PCR). Prevalent expression of FasL was confirmed in vivo : all the resected colonic tumours examined (31/31) were found to express FasL. In the tumours, FasL protein and mRNA were co‐localized to neoplastic colonic epithelial cells, using immunohistochemistry and in situ hybridization, respectively. FasL expression was independent of Dukes' stage, suggesting that it may occur throughout colon cancer progression. These results suggest that FasL is a common mediator of immune privilege in colon cancer. © 1998 John Wiley & Sons, Ltd.