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Epigenetic patterns in systemic sclerosis and their contribution to attenuated CD70 signaling cascades

机译:系统性硬化的表观遗传模式及其对减弱的CD70信号级联反应的贡献

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摘要

With the exception of rare monogenic disorders, the patho-genesis of autoimmune diseases is influenced by genetic variability, resulting in increased disease susceptibility and acquired epigenetic modifications. However, the interplay between genetic and epigenetic contributors to autoimmune disease is complex. Regardless of a continuously growing amount of reports on specific epigenetic patterns and their contribution to autoimmune pathology, we are just beginning to understand the role of epigenetic mechanisms in immune (dys-)regulation.Systemic scleroderma is a rare condition of yet undetermined origin. It primarily affects women (female:male ratio = 4:1) and results in fibrosis of the skin and internal organs, such as the esophagus, intestinal tract, heart, lungs and kidneys. Even though peak onset is between 30 and 50 years of age, it can affect any age group, including children [1-3].
机译:除罕见的单基因疾病外,自身免疫性疾病的发病机理受遗传变异性的影响,导致疾病易感性增加和获得的表观遗传修饰。然而,自身免疫疾病的遗传和表观遗传因素之间的相互作用是复杂的。尽管关于特定表观遗传模式及其对自身免疫病理学的贡献的报告数量不断增加,但我们才刚刚开始了解表观遗传机制在免疫(dys)调节中的作用。系统性硬皮病是一种罕见的病因,但尚未确定。它主要影响女性(女性与男性的比例= 4:1),并导致皮肤和内脏器官(如食道,肠道,心脏,肺和肾脏)的纤维化。即使发病高峰在30至50岁之间,它也会影响任何年龄段,包括儿童[1-3]。

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