最新研究表明角质形成细胞来源的IL-36γ是银屑病皮损的生物学标记，其在银屑病皮损中的基因及蛋白质表达水平显著升高。标准长度的IL-36γ需要经过N末端蛋白酶切成缩短的IL-36γ才能发挥较强的生物学效应，但机制仍不明确。我们前期研究发现经PMA诱导使中性粒细胞形成胞外陷阱（NETs），可以处理标准长度的IL-36γ，进而使正常人角质形成细胞CXCL1和IL-8的mRNA表达显著增加，而CXCL1和IL-8具有趋化中性粒细胞作用。为此我们提出假说，IL-36γ和中性粒细胞在银屑病免疫网络中存在相互促进、放大炎症信号的作用。为了验证这一假说，我们将采用qRT-PCR, western blot, 蛋白质组学等手段，从分子、细胞、组织等多方面探讨IL-36γ与中性粒细胞在银屑病发病中的炎症信号放大机制。本研究将从IL-36γ/中性粒细胞促炎性正反馈回路这个新视点为银屑病发病机制研究提供新思路。

The latest study showed keratinocytes-derived IL-36γ was a biomarker for psoriasis skin lesions. IL-36γ mRNA and protein were confirmed to be highly expressed in psoriasis lesions. Full-length IL-36γ requires N-terminal proteolytic cleavage for highly active truncated IL-36γ, the mechanism of which remains unknown. Our preliminary experiment showed that neutrophils induced to form NETs by activation with PMA can process full-length IL-36γ, as evidenced by increased ability to induce keratinocytes expression of CXCL1 and IL-8 mRNA. CXCL1 and IL-8 could further recruit neutrophils. Herein, we propose a hypothesis that there might be interactional amplification of inflammatory signaling of IL-36γ with neutrophils in psoriasis immune network. To verify this hypothesis, we will use qRT-PCR, western blot, proteomics and other means to investigate the amplification mechanism of inflammatory signaling of IL-36γ with neutriphils in psoriasis pathogenesis from molecules, cells, tissues and other aspects. This study would provide new thought for pathogenesis study of psoriasis from the new viewpoint of positive proinflammatory feedback loop between IL-36γ and neutrophils.