β-catenin regulates innate and adaptive immunity in mouse liver ischemia-reperfusion injury.

ABSTRACT:

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Dendritic cells (DCs) are critical mediators of immune responses that integrate signals from the innate immune system to orchestrate adaptive host immunity. This study was designed to investigate the role and molecular mechanisms of STAT3-induced β-catenin in the regulation of DC function and inflammatory responses in vitro and in vivo. STAT3 induction in lipopolysaccharide (LPS)-stimulated mouse bone marrow-derived DCs (BMDCs) triggered β-catenin activation by way of GSK-3β phosphorylation. The activation of β-catenin inhibited phosphatase and tensin homolog delete on chromosome 10 (PTEN) and promoted the phosphoinositide 3-kinase (PI3K)/Akt pathway, which in turn down-regulated DC maturation and function. In contrast, knockdown of β-catenin increased PTEN/TLR4 (Toll-li

SUBMITTER: Ke B 

PROVIDER: S-EPMC3594407 | biostudies-literature | 2013 Mar

REPOSITORIES: biostudies-literature