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侵袭性真菌感染(IFI)是致ICU患者死亡的重要原因之一。机体通过天然免疫重要的模式识别受体(PRR)Toll样受体(TLR)及C型凝集素受体(CLR)与病原相关分子模式(PAMP)识别后启动抗真菌免疫反应。目前明确磷脂甘露聚糖(PLM)的识别主要依赖TLR2和TLR4;β-葡聚糖经TLR2/树突状细胞相关性C型凝集素-1(Dectin-1)或只经Dectin-1识别。PLM和β-葡聚糖被识别后及经Dectin-1驱动获得性免疫后产生一系列下游细胞因子,一些下游细胞因子的免疫作用对不同组织有所不同、不确定或存在争议,一些免疫反应在细节上还没有详尽描述。因此,深入研究PAMP与PRR相互作用及其细胞因子对免疫调节影响,对IFI的预防治疗有重要意义。
Invasive fungal infection (IFI) is one of the major causes of death in ICU patients. The body starts anti-fungal immune response by recognizing TLRs and CLRs associated with pathogen-associated molecular patterns (PAMPs), which are important pattern-recognizing receptors (PRRs) of innate immunity. It is now clear that recognition of phospholipid mannan (PLM) depends primarily on TLR2 and TLR4; β-glucan is recognized by TLR2 / dendritic cell-associated Dectin-1 or Dectin-1 alone. A series of downstream cytokines are produced after PLM and β-glucan are recognized and deimmunized by Dectin-1-driven immunity. The immunogenicity of some downstream cytokines is different, uncertain or controversial to some tissues. Some immune responses There is no detail in the description. Therefore, in-depth study of PAMP and PRR interactions and cytokines on immune regulation, the prevention and treatment of IFI is of great significance.