肺炎支原体在社区获得性肺炎中的占比逐年增高，其致病机制复杂，但目前多认为与免疫炎症损伤相关。研究表明Toll样受体4(TLR4)通过TLR4-MyD88-NF-κB信号通路及自噬通路诱导炎症反应，白细胞介素35(IL-35)被证实也参与肺炎支原体肺炎的致病，且与TLR4有着密切的关系。本文就TLR4、IL-35在肺炎支原体致病过程中的作用及表达水平作一综述。“,”The proportion of Mycoplasma pneumoniae in community-acquired pneumonia is increasing year by year, its pathogenic mechanism is complex.At present, it is mostly believed to be related to inflammatory damage of immunity.Studies have shown that Toll-like receptor 4 (TLR4) induces inflammatory responses through TLR4-MyD88-NF-κB signaling pathway and autophagy pathway.Interleukin-35 has also been proved to be involved in the pathogenesis of Mycoplasma pneumoniae pneumonia, and is closely related to TLR4.This paper reviews the roles and expressions of TLR4 and interleukin-35 in the pathogenesis of Mycoplasma pneumoniae.