中文摘要：

Toll样受体4（Toll-1ike receptor4，TLR4）属于模式识别受体，可识别来自G-细菌细胞壁的脂多糖（lipopoly-saccharides，LPS），并通过MyD88依赖途径或MyD88非依赖途径进行信号转导，引发核因子-κB（NF-κB）和其他转录因子的表达，从而诱导细胞因子、化学趋化因子的产生，引起系统性炎症反应。选择性剪接是真核生物控制基因表达的一种重要机制，在TLR4通路中很多信号分子都存在着选择性剪接产生的异构体，且这些剪接异构体分子大都可负性调控TLR4信号转导通路。本文针对这方面的研究进展作一综述。

英文摘要：

Toll-like receptor4 （TLR4） is the primary recognition molecule for inflammatory responses initiated by bacterial lipopolysaccharides（LPS）. After LPS is recognized by TLR4, the transcription factors such as nuclear factor-κB （NF-κB） can be expressed through MyD88-dependent pathway or MyD88-independent pathway subsequently, which can induce the cytokines production provoking systematical inflammatory reaction. Alternative splicing plays important roles in the eucaryotic gene expression, and a great deal of signaling molecules in the TLR4 passageway can be alternative spliced naturally. Furthermore, a majority of the isomerides can negatively modulate TLR4 signal transduction.