Panda Santosh K, Kolbeck Roland, Sanjuan Miguel A
Dept of Respiratory, Inflammation & Autoimmunity, MedImmune LLC, Gaithersburg, MD, USA.
Dept of Respiratory, Inflammation & Autoimmunity, MedImmune LLC, Gaithersburg, MD, USA.
Curr Opin Immunol. 2017 Feb;44:20-25. doi: 10.1016/j.coi.2016.10.006. Epub 2016 Nov 14.
Plasmacytoid dendritic cells (pDC) is a unique cell population that produces large amounts of type I interferon upon recognition of nucleic acids placing them at the crossroad of both innate and adaptive immunity. Their ability to produce interferon makes them central to anti-viral responses. They are also responsive to circulating autoantibodies bound to nuclear antigens and in that scenario the release of interferons initiate self-directed immune responses. There are now a growing number of autoimmune disorders where unabated activation of pDC is suspected to be pathogenic. Here, we discuss the different mechanisms responsible for breaking tolerance to self-nucleic acids by pDC, including the novel role of IgE autoantibodies in systemic lupus erythematosus. We also summarized the recent progress on therapies undergoing clinical testing that target either pDC or type I interferons.
浆细胞样树突状细胞（pDC）是一种独特的细胞群体，在识别核酸后会产生大量I型干扰素，使其处于固有免疫和适应性免疫的交叉点。它们产生干扰素的能力使其成为抗病毒反应的核心。它们也对与核抗原结合的循环自身抗体有反应，在这种情况下，干扰素的释放会引发自身导向的免疫反应。现在，越来越多的自身免疫性疾病被怀疑pDC的持续激活具有致病性。在此，我们讨论了pDC打破对自身核酸耐受性的不同机制，包括IgE自身抗体在系统性红斑狼疮中的新作用。我们还总结了针对pDC或I型干扰素的正在进行临床试验的疗法的最新进展。
