Radhakrishnan Girish K, Yu Qiqi, Harms Jerome S, Splitter Gary A
Department of Pathobiological Sciences, University of Wisconsin, Madison, Wisconsin 53706, USA.
J Biol Chem. 2009 Apr 10;284(15):9892-8. doi: 10.1074/jbc.M805458200. Epub 2009 Feb 5.
Toll-like receptors (TLRs) play essential roles in the activation of innate immune responses against microbial infections. TLRs and downstream adaptor molecules contain a conserved cytoplasmic TIR domain. TIRAP is a TIR domain-containing adaptor protein that recruits the signaling adaptor MyD88 to a subset of TLRs. Many pathogenic microorganisms subvert TLR signaling pathways to suppress host immune responses to benefit their survival and persistence. Brucella encodes a TIR domain-containing protein (TcpB) that inhibits TLR2- and TLR4-mediated NF-kappaB activation. Sequence analysis indicated a moderate level of similarity between TcpB and the TLR adaptor molecule TIRAP. We found that TcpB could efficiently block TIRAP-induced NF-kappaB activation. Subsequent studies revealed that by analogy to TIRAP, TcpB interacts with phosphoinositides through its N-terminal domain and colocalizes with the plasma membrane and components of the cytoskeleton. Our findings suggest that TcpB targets the TIRAP-mediated pathway to subvert TLR signaling. In vivo mouse studies indicated that TcpB-deficient Brucella is defective in systemic spread at the early stages of infection.
Toll样受体(TLRs)在激活针对微生物感染的固有免疫反应中发挥着重要作用。TLRs和下游衔接分子含有保守的胞质TIR结构域。TIRAP是一种含TIR结构域的衔接蛋白,它将信号衔接蛋白MyD88招募至一部分TLRs。许多致病微生物会破坏TLR信号通路,以抑制宿主免疫反应,从而利于其生存和持续存在。布鲁氏菌编码一种含TIR结构域的蛋白(TcpB),该蛋白可抑制TLR2和TLR4介导的核因子κB激活。序列分析表明TcpB与TLR衔接分子TIRAP之间存在中等程度的相似性。我们发现TcpB能够有效阻断TIRAP诱导的核因子κB激活。随后的研究表明,与TIRAP类似,TcpB通过其N端结构域与磷酸肌醇相互作用,并与质膜和细胞骨架成分共定位。我们的研究结果表明,TcpB靶向TIRAP介导的途径以破坏TLR信号。体内小鼠研究表明,缺乏TcpB的布鲁氏菌在感染早期的全身播散存在缺陷。