Abstract:
:The forkhead transcription factor Foxp3 is highly expressed in CD4+CD25+ regulatory T cells (Treg) and was recently identified as a key player in mediating their inhibitory functions. Here, we describe for the first time the expression and function of Foxp3 in pancreatic ductal adenocarcinoma cells and tumors. Foxp3 expression was induced by transforming growth factor-beta2 (TGF-beta2), but not TGF-beta1 stimulation in these cells, and was partially suppressed following antibody-mediated neutralization of TGF-beta2. The TGF-beta2 effect could be mimicked by ectopic expression of a constitutively active TGF-beta type I receptor/ALK5 mutant. Down-regulation of Foxp3 with small interfering RNA (siRNA) in pancreatic carcinoma cells resulted in the up-regulation of interleukin 6 (IL-6) and IL-8 expression, providing evidence for a negative transcriptional activity of Foxp3 also in these epithelial cells. Coculture of Foxp3-expressing tumor cells with naive T cells completely inhibited T-cell proliferation, but not activation, and this antiproliferative effect was partially abrogated following specific inhibition of Foxp3 expression. These findings indicate that pancreatic carcinoma cells share growth-suppressive effects with Treg and suggest that mimicking Treg function may represent a new mechanism of immune evasion in pancreatic cancer.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Hinz S,Pagerols-Raluy L,Oberg HH,Ammerpohl O,Grüssel S,Sipos B,Grützmann R,Pilarsky C,Ungefroren H,Saeger HD,Klöppel G,Kabelitz D,Kalthoff Hdoi
10.1158/0008-5472.CAN-06-3304subject
Has Abstractpub_date
2007-09-01 00:00:00pages
8344-50issue
17eissn
0008-5472issn
1538-7445pii
67/17/8344journal_volume
67pub_type
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