TBK1小泛素化在TLR3/4訊號傳遞所扮演之功能角色

Abstract

先天性免疫(innate immunity) 是宿主抵抗外來病原體侵略的第一道防線。Toll-like receptors (TLRs) 透過辨識pathogen-associated molecular patterns (PAMPs) 引發下游訊息傳遞,並誘發前發炎細胞激素(pro-inflammatory cytokines)以及第一型干擾素(type I interferon)的產生。TLR4訊息傳遞透過MyD88-IKKα/β-NF-κB以及TRIF- TBK1-IRF3/7途徑，分別參與在前發炎細胞激素以及第一型干擾素的生成。然而，先前研究NF-

Toll-like receptors (TLRs) belongs to the pattern-recognition-receptors (PRRs) that sense a variety of pathogen-associated molecular patterns (PAMPs) derived from microbes to initiate the first line of host defense against invading pathogens. TLR4 engagement mediates activation of downstream MyD88-IKK-NF-κB and TRIF-TBK1-IRF3 signaling pathways leading to pro-inflammatory cytokines and type I interferon production, respectively. We previously found that TBK1 deficiency resulted in defective production of certain NF-