Peer-Reviewed Journal Details
Mandatory Fields
O'Connell, J.,Bennett, M. W.,O'Sullivan, G. C.,Collins, J. K.,Shanahan, F.
1999
Resistance to Fas (APO-1/CD95)-mediated apoptosis and expression of Fas ligand in esophageal cancer: the Fas counterattack
Validated
()
Optional Fields
12
22
83
8983
The mechanisms by which esophageal tumors escape immunologic recognition and clearance are only partly understood at the molecular level. Esophageal cancers hale been shown to evade host recognition by down-regulation of antigen presentation and production of immunosuppressive factors, Recently, two independent reports have shown that esophageal tumor cells abundantly express Fas ligand (FasL) in vivo, As the triggering agonist for Fas receptor (Fas or APO-1/CD95)-mediated apoptosis of lymphocytes, Fast normally plays immune down-regulatory roles, including activation-induced cell death of T and B cells, as well as maintaining immune privilege in certain organs. Fas ligand expressed by esophageal cell lines has been shown to induce apoptosis of cocultured Fas-sensitive lymphoid cells in vitro. Fast expression by esophageal carcinomas in vivo has been associated with significantly reduced tumor-infiltrating lymphocytes (TILs) in Fast-positive tumor nests, concomitant with significantly increased TIL apoptosis in these nests, These studies support a 'Fas counterattack' mechanism of immune escape in esophageal cancer. By expressing functional Fas Ligand, esophageal cancer cells can deplete antitumor lymphocytes by inducing apoptosis, To express functional Fast, esophageal carcinomas also acquire molecular mechanisms to resist autocrine Fas-mediated apoptosis of tumor cells.The mechanisms by which esophageal tumors escape immunologic recognition and clearance are only partly understood at the molecular level. Esophageal cancers hale been shown to evade host recognition by down-regulation of antigen presentation and production of immunosuppressive factors, Recently, two independent reports have shown that esophageal tumor cells abundantly express Fas ligand (FasL) in vivo, As the triggering agonist for Fas receptor (Fas or APO-1/CD95)-mediated apoptosis of lymphocytes, Fast normally plays immune down-regulatory roles, including activation-induced cell death of T and B cells, as well as maintaining immune privilege in certain organs. Fas ligand expressed by esophageal cell lines has been shown to induce apoptosis of cocultured Fas-sensitive lymphoid cells in vitro. Fast expression by esophageal carcinomas in vivo has been associated with significantly reduced tumor-infiltrating lymphocytes (TILs) in Fast-positive tumor nests, concomitant with significantly increased TIL apoptosis in these nests, These studies support a 'Fas counterattack' mechanism of immune escape in esophageal cancer. By expressing functional Fas Ligand, esophageal cancer cells can deplete antitumor lymphocytes by inducing apoptosis, To express functional Fast, esophageal carcinomas also acquire molecular mechanisms to resist autocrine Fas-mediated apoptosis of tumor cells.
1120-86941120-8694
://WOS:000083699700001://WOS:000083699700001
Grant Details