Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
J Immunol. 2013 Mar 1;190(5):1911-8. doi: 10.4049/jimmunol.1203162.
Recognition of microbial nucleic acids is one strategy by which mammalian hosts respond to infectious agents. Intracellular DNA that is introduced into cells during infection elicits potent inflammatory responses by triggering the induction of antiviral type I IFNs and the maturation and secretion of inflammatory cytokines, such as TNF-α, IL-1β, and IL-18. In addition, if nucleases, such as DNase II or DNase III (Trex1), fail to clear self-DNA, accumulated DNA gains access to intracellular compartments where it drives inflammatory responses leading to autoimmune disease. In this review, we discuss a rapidly evolving view of how cytosolic DNA-sensing machineries coordinate antimicrobial immunity and, if unchecked, lead to autoimmune disease.
识别微生物核酸是哺乳动物宿主对感染因子做出反应的一种策略。在感染过程中,进入细胞的细胞内 DNA 通过触发抗病毒 I 型 IFN 的诱导和炎症细胞因子(如 TNF-α、IL-1β和 IL-18)的成熟和分泌,引发强烈的炎症反应。此外,如果核酶(如 DNase II 或 DNase III(Trex1))不能清除自身 DNA,积累的 DNA 就会进入细胞内区室,在那里它会引发炎症反应,导致自身免疫性疾病。在这篇综述中,我们讨论了胞质 DNA 感应机制如何协调抗菌免疫的快速发展的观点,如果这种机制不受控制,就会导致自身免疫性疾病。