作者: Lena Seifert , Michael Deutsch , Sara Alothman , Dalia Alqunaibit , Gregor Werba
DOI: 10.1016/J.CELREP.2015.10.058
关键词:
摘要: Dectin-1 is a C-type lectin receptor critical in anti-fungal immunity, but has not been linked to regulation of sterile inflammation or oncogenesis. We found that expression upregulated hepatic fibrosis and liver cancer. However, deletion exacerbates fibro-inflammatory disease accelerates hepatocarcinogenesis. Mechanistically, we protects against chronic by suppressing TLR4 signaling inflammatory stellate cells. Accordingly, Dectin-1(-/-) mice exhibited augmented cytokine production reduced survival lipopolysaccharide (LPS)-mediated sepsis, whereas activation was protective. showed inhibits mitigating CD14 expression, which are regulated Dectin-1-dependent macrophage colony stimulating factor (M-CSF) expression. Our study suggests an attractive target for experimental therapeutics neoplastic transformation. More broadly, our work deciphers cross-talk between pattern recognition receptors implicates role suppression inflammation, inflammation-induced oncogenesis, LPS-mediated sepsis.