Rubinow Katya B, Rubinow David R
Diabetes Institute, Department of Medicine, University of Washington, Seattle, Washington, USA.
Department of Psychiatry, University of North Carolina, Chapel Hill, North Carolina, USA.
Dialogues Clin Neurosci. 2017 Mar;19(1):19-26. doi: 10.31887/DCNS.2017.19.1/drubinow.
The recognition of altered immune system function in many chronic disease states has proven to be a pivotal advance in biomedical research over the past decade. For many metabolic and mood disorders, this altered immune activity has been characterized as inflammation, with the attendant assumption that the immune response is aberrant. However, accumulating evidence challenges this assumption and suggests that the immune system may be mounting adaptive responses to chronic stressors. Further, the inordinate complexity of immune function renders a simplistic, binary model incapable of capturing critical mechanistic insights. In this perspective article, we propose alternative paradigms for understanding the role of the immune system in chronic disease. By invoking allostasis or systems biology rather than inflammation, we can ascribe greater functional significance to immune mediators, gain newfound appreciation of the adaptive facets of altered immune activity, and better avoid the potentially disastrous effects of translating erroneous assumptions into novel therapeutic strategies.
在过去十年中，认识到许多慢性疾病状态下免疫系统功能的改变已被证明是生物医学研究中的一项关键进展。对于许多代谢和情绪障碍而言，这种改变的免疫活动已被描述为炎症，随之而来的假设是免疫反应异常。然而，越来越多的证据对这一假设提出了挑战，并表明免疫系统可能正在对慢性应激源产生适应性反应。此外，免疫功能极其复杂，使得简单的二元模型无法捕捉到关键的机制性见解。在这篇观点文章中，我们提出了理解免疫系统在慢性疾病中作用的替代范式。通过引入稳态或系统生物学而非炎症，我们可以赋予免疫介质更大的功能意义，重新认识改变的免疫活动的适应性方面，并更好地避免将错误假设转化为新治疗策略可能带来的灾难性后果。
