049 PRELP negatively regulate IL-17A mediated proliferation and inflammatory in psoriasis

Psoriasis is a common immune-mediated skin disease. Blockade of IL-17A has much improved the clinical outcome for psoriasis. By data mining, an array differentially expressed genes in three anti-IL-17A biologics(secukinumab, ixekizumab and brodalumab) treated psoriasis have been identified. Among them, PRELP(proline/arginine-rich end leucine-rich repeat protein) was up-regulated after treatments by biologics low lesions compared to non-lesions. PRELP belongs class II subfamily small proteoglycan (SLRP) family, which binds type I collagen basement membranes cartilage. It involved several paghogenesis process including osteoclastogenesis, infection Moraxella catarrhalis respiratory tract, hepatocellular caicinoma so on. But it’s role had never explored. We confirmed that lowly imiquimod induced model mouse, HaCat cells as well from patients. Over expression inhibited proliferation promoted apoptosis cells. could inhibit mediated NF-κB MAPK signaling molecules, release cytokines contributing development, TNF-α IL-1β. Conversely, inhibition mouse psoriatic exacerbated symptoms. Datasets analysis also found when patients with brodalumab methotrexate, high level at baseline associated better therapeutic response, not response treatment etanercept ustekinumab .Mechanically, we decreased through induction STAT3, transcription factor negatively regulates PRELP. In conclusion, postulate than negative regulator signal potential target