NLRP3-ASC-Caspase-1轴参与炎性途径等细胞生物学过程，在恶性胸腔积液发生和发展中发挥重要作用。针对该通路的研究不仅有助于深入了解恶性胸腔积液的分子机制，也为早期诊断和治疗提供新的干预靶点。我们前期实验证实Toll样受体(Toll-like receptor，TLR)，特别是TLR2和TLR4在恶性胸腔积液中表达增高，进一步用LLC细胞沉默NLRP3基因表达模型研究，发现NLRP3和caspase-1的mRNA表达降低，提示，恶性胸腔积液的生成可能与NLRP3-ASC-Caspase-1轴有关，但其作用机制目前尚不清楚。本研究拟从临床标本、LLC细胞体外和小鼠体内水平，运用慢病毒载体、基因敲除手段，探讨TLR通过NLRP3-ASC-Caspase-1轴对恶性胸腔积液的调控机制。研究将以炎性小体为切入点揭示TLR调控恶性胸腔积液的分子机制。

NLRP3-ASC-Caspase-1 axis plays an important role in the pathogenesis and development of malignant pleural effusion. The study of this pathway not only helps to understand the molecular mechanism of malignant pleural effusion, but also provides a new intervention target for early diagnosis and treatment. Our previous studies found Toll-like receptors (TLR), especially TLR2 and TLR4, are increased in malignant pleural effusion. Recently, we found the mRNA expressions of NLRP3 and caspase-1 were downregulated within the model of silencing NLRP3 gene expression in LLC cells, suggesting that the formation of malignant pleural effusion may be related to NLRP3-ASC-Caspase-1 axis. However, the underline mechanisms are not fully understood. The aim of this study is to investigate the regulation of TLR on malignant pleural effusion through NLRP3-ASC-Caspase-1 axis in clinical specimens, LLC cells in vitro and mice in vivo by means of lentivirus vector and gene knockout. This project will reveal the molecular mechanism of TLR regulating malignant pleural effusion from inflammasome.