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Hepatic ILC2s contribute to the progression of cholangiocarcinoma in extra hepatic bile ducts. Loss of E-cadherin on cholangiocytes and enhanced cellular necrosis favor activation of hepatic ILC2s in an IL-33-dependent manner, thereby promoting expression of IL-13 and AREG. IL-13 and AREG induce hyperproliferation in cholangiocytes and enhanced expression of IL-33, inducing the ongoing activity of ILC2s that favor malignant transformation and progression of cholangiocarcinoma.
