Department of Medicine, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
Trends Immunol. 2011 Mar;32(3):110-6. doi: 10.1016/j.it.2011.01.003. Epub 2011 Feb 18.
Interleukin-1β (IL-1β) and IL-18 contribute to host defense against infection by augmenting antimicrobial properties of phagocytes and initiating Th1 and Th17 adaptive immune responses. Protein complexes called inflammasomes activate intracellular caspase-1 autocatalytically, which cleaves the inactive precursors of IL-1β and IL-18 into bioactive cytokines. In this review, we discuss the controversies regarding inflammasome activation and the role of the inflammasome during infection. We highlight alternative mechanisms for processing IL-1β and IL-18 during infection, which involve extracellular cleavage of the inactive cytokines by neutrophil-derived serine proteases or proteases released from cytotoxic T cells.
白细胞介素-1β（IL-1β）和 IL-18 通过增强吞噬细胞的抗菌特性并启动 Th1 和 Th17 适应性免疫应答，有助于宿主抵抗感染。称为炎性体的蛋白质复合物通过自动催化激活细胞内半胱天冬酶-1，将 IL-1β 和 IL-18 的无活性前体切割成生物活性细胞因子。在这篇综述中，我们讨论了关于炎性体激活的争议以及在感染过程中炎性体的作用。我们强调了感染过程中 IL-1β 和 IL-18 加工的替代机制，其中包括中性粒细胞衍生的丝氨酸蛋白酶或来自细胞毒性 T 细胞的蛋白酶对无活性细胞因子的细胞外切割。
