Hoshino Katsuaki, Kaisho Tsuneyasu
Laboratory for Host Defense, Research Center for Allergy and Immunology, RIKEN, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa, Japan.
Curr Opin Immunol. 2008 Aug;20(4):408-13. doi: 10.1016/j.coi.2008.06.003. Epub 2008 Jul 1.
Dendritic cells (DCs) are crucial immune cells detecting microorganisms and linking innate and adaptive immunity. Various microorganism-derived components, including lipids, proteins, or nucleic acids, activate DCs through various pattern recognition receptors (PRRs). PRRs can principally detect non-self-components, but nucleic acid components are peculiar in that self-derived nucleic acids can also stimulate PRRs. Thus, nucleic-acid-sensing PRRs can potentially cause autoimmune responses. This potential danger comes out in certain situations, and especially nucleic-acid-induced type I interferon production contributes to the pathogenesis of autoimmune disorders. Here we review how DCs detect and respond to nucleic acid adjuvants and how self-derived nucleic acids can cause autoimmunity. Clarifying such mechanisms should contribute to the development of therapeutic manipulation for autoimmune diseases.
树突状细胞(DCs)是检测微生物并连接天然免疫和适应性免疫的关键免疫细胞。包括脂质、蛋白质或核酸在内的各种微生物衍生成分,通过各种模式识别受体(PRR)激活DCs。PRR主要可检测非自身成分,但核酸成分较为特殊,因为自身来源的核酸也能刺激PRR。因此,核酸传感PRR可能引发自身免疫反应。这种潜在危险在某些情况下会显现出来,尤其是核酸诱导的I型干扰素产生会导致自身免疫性疾病的发病机制。在此,我们综述DCs如何检测和响应核酸佐剂,以及自身来源的核酸如何引发自身免疫。阐明这些机制应有助于自身免疫性疾病治疗手段的发展。