近年来，研究发现表观遗传修饰酶在机体生理及病理过程中都发挥着很重要的作用。但是，目前关于表观遗传修饰酶在先天免疫应答的研究还较少。Toll样受体（TLR）家族作为模式识别受体能诱导产生很多种炎症因子，并在先天免疫应答中扮演着重要角色，并且其异常与诸多炎症性疾病的发生发展皆有联系。为了系统研究在TLR通路中起重要调节作用的表观修饰酶并探索潜在的疾病治疗靶点，我们研究小组筛选了在表观遗传修饰中有重要作用的组蛋白甲基化酶，发现Suv4-20h2能够作为正向调节分子促进IL-6等炎症因子的产生。接下来我们拟利用co-IP、western blot、ChIP、蛋白质谱等分子生物学实验手段，研究Suv4-20h2正向调节炎症因子产生的分子机制，同时构建Suv4-20h2基因敲除小鼠进行LPS休克模型和胶原诱导的关节炎（CIA）等炎症性疾病模型的研究，进一步探讨Suv4-20h2在炎症性疾病中的作用。

In recent years, studies have shown that epigenetic modification enzymes are important regulators in multiple physiological and disease processes. However, their roles in innate immunity remain largely unknown. Toll-like receptors (TRLs) on innate immune cells can be recognized by foreign pathogens then induce production of varies inflammatory factors which are critical for immune responses and whose aberrant expression has been associated with various inflammatory diseases. In order to find novel epigenetic regulators in TLR signaling and potential therapeutic targets for inflammatory diseases, we screened lysine methyltransferases and found SUV4-20H2 as a positive regulator to promote the production of inflammatory cytokines like IL-6. Next, we will use molecular biological technologies like co-IP、western blot、ChIP and mass spectrum to study the mechanism of Suv4-20h2 positively regulating the production of inflammatory factors. And we also plan to establish LPS shock model and Collagen induced arthritis (CIA) model on Suv4-20h2 knockout mice to explore the function of Suv4-20h2 in inflammatory diseases.