Kim Bae-Hoon, Chee Jonathan D, Bradfield Clinton J, Park Eui-Soon, Kumar Pradeep, MacMicking John D
Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut, USA.
Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, Connecticut, USA.
Nat Immunol. 2016 May;17(5):481-9. doi: 10.1038/ni.3440.
Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however, suggests that the inflammasome machinery is also subject to 'tunable' or inducible signals that might accelerate its autocatalytic properties and dictate where inflammasome assembly takes place in the cell. Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators, including a new family of interferon-induced GTPases called 'guanylate-binding proteins' (GBPs). Here we investigate the critical roles of interferon-induced GBPs in directing inflammasome subtype-specific responses and their consequences for cell-autonomous immunity to a wide variety of microbial pathogens. We discuss emerging mechanisms of action and the potential effect of these GBPs on predisposition to sepsis and other infectious or inflammatory diseases.
炎性小体的传统观点强调,在感染或组织损伤后不久,预先存在的核心成分会组装起来。然而,新出现的研究表明,炎性小体机制也会受到“可调节”或诱导性信号的影响,这些信号可能会加速其自身催化特性,并决定炎性小体在细胞内的组装位置。其中许多信号在干扰素受体下游发挥作用,以引发炎性小体调节因子,包括一个名为“鸟苷酸结合蛋白”(GBPs)的新的干扰素诱导GTP酶家族。在这里,我们研究了干扰素诱导的GBPs在指导炎性小体亚型特异性反应中的关键作用,以及它们对针对多种微生物病原体的细胞自主免疫的影响。我们讨论了这些GBPs新出现的作用机制及其对败血症和其他感染性或炎性疾病易感性的潜在影响。