MicroRNA miR-223 as regulator of innate immunity.
MicroRNA miR-223 as regulator of innate immunity.
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DOI：
10.1002/jlb.3mr0218-079r
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发表时间：
2018-09
影响因子：
5.5
通讯作者：
Eltzschig H
中科院分区：
文献类型：
--
作者：
Yuan X;Berg N;Lee JW;Le TT;Neudecker V;Jing N;Eltzschig H
MicroRNAs是二十多年前发现的，对多种生物过程产生了深远的影响。特定的microRNAs在调节先天免疫反应中起着重要作用，它们的失调被证明与炎症性疾病有关。尤其是MIR-223，在造血细胞中高度表达，并受到严格调控。它是髓系细胞分化和激活的关键调节器。MiR-223在髓系细胞，特别是中性粒细胞和巨噬细胞的分化和激活中的中心作用已被广泛研究。MIR-223通过促进粒细胞生成而抑制巨噬细胞分化而促进髓系分化。在炎症性疾病中，不受控制的髓系激活会产生有害的后果。MIR-223作为一种负反馈机制，控制过度的先天性免疫反应，维持髓系细胞的动态平衡。本文综述了miR-223在髓系分化、中性粒细胞和巨噬细胞功能中的作用，以及在急性呼吸窘迫综合征和炎症性肠病等炎症性疾病中的作用。此外，本文还对miR-223的非髓系功能进行了讨论。MiR-223抑制炎症靶点的治疗增强也被强调为控制粘膜炎症期间过度先天免疫反应的潜在治疗方法。
MicroRNAs were discovered more than two decades ago and have profound impact on diverse biological processes. Specific microRNAs have important roles in modulating the innate immune response and their dysregulation has been demonstrated to contribute to inflammatory diseases. MiR-223 in particular, is very highly expressed and tightly regulated in hematopoietic cells. It functions as key modulator for the differentiation and activation of myeloid cells. The central role of miR-223 in myeloid cells, especially neutrophil and macrophage differentiation and activation has been studied extensively. MiR-223 contributes to myeloid differentiation by enhancing granulopoiesis while inhibiting macrophage differentiation. Uncontrolled myeloid activation has detrimental consequences in inflammatory disease. MiR-223 serves as a negative feedback mechanism controlling excessive innate immune responses in the maintenance of myeloid cell homeostasis. This review summarizes several topics covering the function of miR-223 in myeloid differentiation, neutrophil and macrophage functions, as well as in inflammatory diseases including acute respiratory distress syndrome and inflammatory bowel disease. In addition, non-myeloid functions of miR-223 are also discussed in this review. Therapeutic enhancement of miR-223 to dampen inflammatory targets is also highlighted as potential treatment to control excessive innate immune responses during mucosal inflammation.