ARDS抗炎治疗效果并不理想，免疫调控成为研究的新方向。Th17细胞兼具固有免疫应答和适应性免疫应答的特点，且有卓越的募集中性粒细胞的作用，其介导的免疫应答可能是潜在的发病机制。RORγt作为Th17细胞的特异性核转录因子，其转录活性决定了Th17细胞的分化。新近发现β-catenin分子核内积累可以促进RORγt的表达，可能是调控Th17细胞分化的重要上游分子。转录辅因子CBP/p300可作为β-catenin分子的核内伴侣调节这一过程。本课题拟通过siRNA干扰技术、双荧光素酶报告基因和cre-loxp基因工程技术明确β-catenin对Th17细胞分化的影响，并采用染色质免疫共沉淀结合高通量测序技术从表观遗传角度深入探讨可能的机制。这是对我们前期研究的深入和完善，对进一步阐明Th17细胞的精准调控机制有实际意义，为免疫治疗在ARDS中的应用提供理论依据。

The effect of treatment ARDS with anti-inflammatory is not satisfied. Immune regulation becomes a new direction of ARDS therapy. Th17 cell mediated immune response has a potential pathogenesis because of the role of recruitment neutrophils and characteristic of inducing both innate and adaptive immune response. The differention of Th17 cells determines by the activity of specific transcription factor RORγt. Recent studies found that nuclear accumulation of β-catenin promoted the expression of RORγt. It was suggested that β-catenin mightbe an important upstream molecular in regulation of RORγt expression. The transcriptional coactivators CBP/p300 as nucleus partners help β-catenin regulate this process. This study proposes to proof the effect of β-catenin on Th17 cell differentiation usingsiRNA, dual luciferase report gene , cre-loxP gene engineering technology, and CHIP-seq to further explore the possible epigenetic mechanism.This is an improvement to our previous studies. It helps to elucidate the precise regulatory mechanisms of Th17 cells and provides theoretical basis for application immune therapy in ARDS.