Division of Molecular Pathology, Research Institute for Biological Sciences, Tokyo University of Science Noda, Japan.
Front Immunol. 2012 Aug 30;3:275. doi: 10.3389/fimmu.2012.00275. eCollection 2012.
Although the major role of the immune response is host defense from a wide range of potentially pathogenic microorganisms, excess immune responses can result in severe host damage. The host thus requires anti-inflammatory mechanisms to prevent reactivity to self. Interleukin-10 (IL-10) is a cytokine with broad anti-inflammatory properties involved in the pathogenesis of various diseases. IL-10 was originally described as a T helper (T(H)2) derived cytokine, but further studies indicated that IL-10 is expressed not only by many cells of the adaptive immune system, including T and B cells, but also by the innate immune cells, including dendritic cells (DCs), macrophages, mast cells, and natural killer (NK) cells. In addition, IL-10 can be induced in T(H)1 and T(H)17 cells by chronic inflammation as a system of feedback regulation. In this review, we focus on the molecular mechanisms underlying IL10 gene expression in adaptive immune cells and summarize the recent progresses in epigenetic and transcriptional regulation of the IL10 gene. Understanding the transcriptional regulatory events may help in the development of new strategies to control inflammatory diseases.
虽然免疫反应的主要作用是宿主防御来自各种潜在致病微生物的侵袭，但过度的免疫反应可能会导致宿主严重损伤。因此，宿主需要抗炎机制来防止对自身的反应。白细胞介素-10（IL-10）是一种具有广泛抗炎特性的细胞因子，参与多种疾病的发病机制。IL-10 最初被描述为 T 辅助细胞（T(H)2）衍生的细胞因子，但进一步的研究表明，IL-10 不仅由适应性免疫系统的许多细胞表达，包括 T 细胞和 B 细胞，而且还由固有免疫细胞表达，包括树突状细胞（DCs）、巨噬细胞、肥大细胞和自然杀伤（NK）细胞。此外，IL-10 可以在慢性炎症中作为反馈调节系统被 T(H)1 和 T(H)17 细胞诱导。在这篇综述中，我们重点关注适应性免疫细胞中 IL10 基因表达的分子机制，并总结了 IL10 基因的表观遗传和转录调控的最新进展。了解转录调控事件可能有助于开发控制炎症性疾病的新策略。
