Laboratory of Tissue Engineering and Regenerative Medicine, Department of Embryology, Medical University of Gdansk, Gdansk, Poland.
Int Immunopharmacol. 2020 Apr;81:106262. doi: 10.1016/j.intimp.2020.106262. Epub 2020 Feb 8.
In recent years, epigenetic mechanisms became widely known due to their ability to regulate and maintain physiological processes such as cell growth, development, differentiation and genomic stability. When dysregulated, epigenetic mechanisms, may introduce gene expression changes and disturbance in immune homeostasis leading to autoimmune diseases. Systemic lupus erythematosus (SLE), the most extensively studied autoimmune disorder, has already been correlated with epigenetic modifications, especially in T cells. Since these cell rely on antigen presentation, it may be assumed that erroneous activity of antigen-presenting cells (APCs), culminates in T cell abnormalities. In this review we summarize and discuss the epigenetic modifications in SLE affected APCs, with the focus on dendritic cells (DCs), B cells and monocytes. Unravelling this aspect of SLE pathogenesis, might result in identification of new disease biomarkers and putative therapeutic approaches.
近年来，由于表观遗传机制能够调节和维持细胞生长、发育、分化和基因组稳定性等生理过程，因此备受关注。当表观遗传机制失调时，可能会导致基因表达变化和免疫稳态紊乱，从而引发自身免疫性疾病。系统性红斑狼疮（SLE）是研究最广泛的自身免疫性疾病，已经与表观遗传修饰相关，尤其是在 T 细胞中。由于这些细胞依赖于抗原呈递，因此可以假设抗原呈递细胞（APCs）的错误活性最终导致 T 细胞异常。在这篇综述中，我们总结并讨论了 SLE 相关 APCs 中的表观遗传修饰，重点关注树突状细胞（DCs）、B 细胞和单核细胞。阐明 SLE 发病机制的这一方面，可能会发现新的疾病生物标志物和潜在的治疗方法。
