The Skin–Liver Axis Modulates the Psoriasiform Phenotype and Involves Leucine-Rich α-2 Glycoprotein

Abstract Leucine-rich α-2 glycoprotein (LRG), one of the acute phase proteins mainly produced by liver, similar to C-reactive protein, has been recognized as an inflammatory biomarker for rheumatoid arthritis and bowel diseases. We recently demonstrated that LRG was also increased in sera psoriasis patients correlated well with disease activity a sensitivity specificity much higher than protein; however, whether mechanistically contributed pathogenesis remained unclear. In this study, we explored role psoriasiform inflammation using LRG-knockout (KO) mice imiquimod (IMQ)–mediated model. Following topical treatment IMQ, serum levels its expression liver were abruptly elevated. Similarly, surge proinflammatory cytokines observed including IL-1β, TNF-α, IL-6, although LRG-KO showed delayed responses. less skin IMQ model wild-type mice. K5.Stat3C developed psoriasis-like lesions following tape stripping, which induced liver. A deficiency Lrg mitigated stripping–induced lesions, These results indicate modulates both feed-forward feedback loops skin–liver axis involved inflammation.