Crosstalk Between Apoptosis and Autophagy: Environmental Genotoxins, Infection, and Innate Immunity.
Crosstalk Between Apoptosis and Autophagy: Environmental Genotoxins, Infection, and Innate Immunity.
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DOI：
10.1177/1179670716685085
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Kemp MG
中科院分区：
文献类型：
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作者：
Kemp MG
自身免疫性疾病是一个主要的和日益严重的健康问题。然而，导致或加剧疾病症状的遗传和环境因素仍不清楚。已知I型干扰素（IFN）破坏免疫耐受并且在患有自身免疫性疾病如狼疮的患者的血清中升高。在过去的十年中，大量的工作已经表征了一种称为干扰素基因刺激因子或STING的蛋白质在介导IFN表达和激活以响应胞质DNA和环状二核苷酸中的作用。有趣的是，这种依赖STING的先天免疫途径既利用细胞的自噬机制，又被细胞的自噬机制靶向。鉴于细胞凋亡和自噬机制之间的异常相互作用有助于STING依赖性途径的失调，IFN调节的自身免疫表型可能受到环境致癌物和病原微生物和病毒的联合暴露的影响。因此，本综述总结了最近的数据，这些重要的问题，在该领域的自身免疫。
Autoimmune disorders constitute a major and growing health concern. However, the genetic and environmental factors that contribute to or exacerbate disease symptoms remain unclear. Type I interferons (IFNs) are known to break immune tolerance and be elevated in the serum of patients with autoimmune diseases such as lupus. Extensive work over the past decade has characterized the role of a protein termed stimulator of interferon genes, or STING, in mediating IFN expression and activation in response to cytosolic DNA and cyclic dinucleotides. Interestingly, this STING-dependent innate immune pathway both utilizes and is targeted by the cell’s autophagic machinery. Given that aberrant interplay between the apoptotic and autophagic machineries contributes to deregulation of the STING-dependent pathway, IFN-regulated autoimmune phenotypes may be influenced by the combined exposure to environmental carcinogens and pathogenic microorganisms and viruses. This review therefore summarizes recent data regarding these important issues in the field of autoimmunity.