Choe Jamie Y, Nair Maya, Basha Riyaz, Kim Byung-Jin, Jones Harlan P
Department of Microbiology, Immunology and Genetics, Graduate School of Biomedical Sciences, University of North Texas Health Science Center, Fort Worth, Texas 76107; Texas College of Osteopathic Medicine, University of North Texas Health Science Center, Fort Worth, Texas 76107.
Department of Microbiology, Immunology and Genetics, Graduate School of Biomedical Sciences, University of North Texas Health Science Center, Fort Worth, Texas 76107.
Crit Rev Immunol. 2019;39(5):329-342. doi: 10.1615/CritRevImmunol.2020033244.
Childhood exposure to traumatic events, termed early life stress (ELS), is now widely recognized for causing long-term negative health effects that may not manifest until adulthood. Allostatic load (AL) describes the cumulative "wear-and-tear" effects of chronic stress on the body that may adversely affect human health by accelerating other disease processes. Recent epidemiological studies have reported higher stress levels in industrialized countries and trends of increasing prevalence in autoimmune diseases during recent decades. To elucidate mechanisms of stress-related immune dysregulation, most animal studies up to now have focused on AL and stress-triggered events occurring in adults but have not explored ELS in the context of autoimmune disorders. We have identified a current gap in understanding the impact of ELS on immune system ontogeny and its potential for priming genetically susceptible individuals who are at increased risk for autoimmune diseases later in life, through mechanisms involving neuroendocrine-immune cross talk. In this review, we highlight the intersection between stress and immune function, with a focus on ELS as consequential for increased autoimmune disorder risks later in life.
童年时期遭受创伤性事件，即所谓的早期生活压力（ELS），如今已被广泛认识到会导致长期的负面健康影响，这些影响可能直到成年才会显现出来。应激负荷（AL）描述了慢性应激对身体的累积“磨损”效应，这种效应可能通过加速其他疾病进程对人类健康产生不利影响。最近的流行病学研究报告称，工业化国家的压力水平较高，且近几十年来自身免疫性疾病的患病率呈上升趋势。为了阐明应激相关免疫失调的机制，到目前为止，大多数动物研究都集中在成年期发生的应激负荷和应激触发事件上，而没有在自身免疫性疾病的背景下探讨早期生活压力。我们发现，目前在理解早期生活压力对免疫系统个体发育的影响及其通过涉及神经内分泌 - 免疫相互作用的机制引发晚年患自身免疫性疾病风险增加的遗传易感个体的潜力方面存在差距。在这篇综述中，我们强调了压力与免疫功能之间的交叉点，重点关注早期生活压力对晚年自身免疫性疾病风险增加的影响。
