Signaling via MYD88 in the pancreatic tumor microenvironment
نویسندگان
چکیده
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 TH2-polarization of CD4+ T cells. TLR signaling appears to be central in pancreatic cancer-associated inflammation.
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