Abstract
We have recently shown that Toll-like receptor (TLR) signaling exacerbates pancreatic fibro-inflammation and promotes carcinogenesis in mice. Paradoxically, inhibition of the TLR-MYD88 signaling pathway is pro-tumorigenic owing to the dendritic cell-mediated T(H)2-polarization of CD4(+) T cells. TLR signaling appears to be central in pancreatic cancer-associated inflammation.