Divisions of Geriatric Medicine and Rheumatology, Department of Internal Medicine, University of Michigan, Room 3023 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI, 48109-2200, USA.
Clin Rev Allergy Immunol. 2010 Aug;39(1):42-50. doi: 10.1007/s12016-009-8169-3.
The decline in immunocompetence with age is accompanied by the increase in the incidence of autoimmune diseases. Aging of the immune system, or immunosenescence, is characterized by a decline of both T and B cell function, and paradoxically the presence of low-grade chronic inflammation. There is growing evidence that epigenetics, the study of inherited changes in gene expression that are not encoded by the DNA sequence itself, changes with aging. Interestingly, emerging evidence suggests a key role for epigenetics in human pathologies, including inflammatory and neoplastic disorders. Here, we will review the potential mechanisms that contribute to the increase in autoimmune responses in aging. In particular, we will discuss how epigenetic alterations, especially DNA methylation and histone acetylation, are accumulated during aging and how these events contribute to autoimmunity risk.
随着年龄的增长，免疫能力下降伴随着自身免疫性疾病发病率的增加。免疫系统的衰老，或免疫衰老，其特征是 T 细胞和 B 细胞功能下降，同时存在低度慢性炎症。越来越多的证据表明，表观遗传学是研究基因表达的遗传变化，而这些变化不受 DNA 序列本身的编码，会随着年龄的增长而发生变化。有趣的是，新出现的证据表明，表观遗传学在人类病理学中，包括炎症和肿瘤性疾病中起着关键作用。在这里，我们将回顾导致衰老时自身免疫反应增加的潜在机制。特别是，我们将讨论表观遗传改变，特别是 DNA 甲基化和组蛋白乙酰化，如何在衰老过程中积累，以及这些事件如何导致自身免疫风险。
