LXRα represses LPS-induced inflammatory responses by competing with IRF3 for GRIP1 in Kupffer cells
文摘

LPS-induced TNF-<alpha >, IFN-<beta > and IL-1 < beta > generation was reduced by pretreatment with LXR < alpha > agonist.

The LPS-TLR4 signalling pathway involves IRF3 and GRIP1 co-activation of NF-kB.

LXR < alpha > agonist, T0901317, has little effect on the expression of either IRF3 or GRIP1.

Agonist-activated LXR < alpha > competes with IRF3 for GRIP1 and this is the mechanism by which TLR4 signalling is inhibited.

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