Background: Interleukin (IL)-1 family cytokines have been proved to play a pathogenic role in psoriasis. Although receptor antagonists are a critical control mechanism of IL-1 system, their expression pattern in peripheral blood mononuclear cells (PBMCs) andregulation by inflammatory cytokines are still poorly characterized. Objectives: We investigated whether receptor antagonist IL-1 family members are increased in PBMCs of psoriatic patients. We also evaluated their regulation by various Th 1 and Th17 cytokines which are known to be critical in the pathogenesis of psoriasis. Methods: mRNA expression of receptor antagonist members of IL-1 family, IL-1Ra, IL-36Ra, and IL-38 was assessed in PBMCs from 10 psoriatic patients and 6 healthy controls by qRT-PCR. Primary keratinocyte (KC) culture was used to measure their gene expression with stimulation by Th1 and Th17 cytokines, such as interferon (IFN)-ャ, tumor necrosis factor (TNF)-メ, and IL-17A Results: IL-1Ra, IL-36Ra, and IL-38 mRNA levels were increased in PBMCs of patients with psoriasis patients, and IL-38 transcript level was positively correlated with the severity of psoriasis(PASI,BSA). Th1 and Th17 cytokines, IFN-ャ, TNF-メ, and IL-17A induced mRNA expression of receptor antagonist IL-1 family members by human KC. Conclusion: Icreased receptor antagonists of IL-1 family in PBMCs and their induction by Th1 and Th17 cytokines reflect the homeostatic balance between pro- and anti-inflammatory mediators in pathogenesis of psoriasis.
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