Massrali Aïcha, Adhya Dwaipayan, Srivastava Deepak P, Baron-Cohen Simon, Kotter Mark R
Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom.
Autism Research Centre, Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom.
Front Neurosci. 2022 Apr 12;16:834058. doi: 10.3389/fnins.2022.834058. eCollection 2022.
Maternal immune activation (MIA) is mediated by activation of inflammatory pathways resulting in increased levels of cytokines and chemokines that cross the placental and blood-brain barriers altering fetal neural development. Maternal viral infection is one of the most well-known causes for immune activation in pregnant women. MIA and immune abnormalities are key players in the etiology of developmental conditions such as autism, schizophrenia, ADHD, and depression. Experimental evidence implicating MIA in with different effects in the offspring is complex. For decades, scientists have relied on either MIA models or human epidemiological data or a combination of both. MIA models are generated using infection/pathogenic agents to induce an immunological reaction in rodents and monitor the effects. Human epidemiological studies investigate a link between maternal infection and/or high levels of cytokines in pregnant mothers and the likelihood of developing conditions. In this review, we discuss the importance of understanding the relationship between virus-mediated MIA and neurodevelopmental conditions, focusing on autism and schizophrenia. We further discuss the different methods of studying MIA and their limitations and focus on the different factors contributing to MIA heterogeneity.
母体免疫激活（MIA）是由炎症途径的激活介导的，导致细胞因子和趋化因子水平升高，这些因子穿过胎盘和血脑屏障，改变胎儿神经发育。母体病毒感染是孕妇免疫激活最知名的原因之一。MIA和免疫异常是自闭症、精神分裂症、注意力缺陷多动障碍（ADHD）和抑郁症等发育性疾病病因中的关键因素。涉及MIA对后代产生不同影响的实验证据很复杂。几十年来，科学家们要么依赖MIA模型，要么依赖人类流行病学数据，或者两者结合。MIA模型是通过使用感染/病原体在啮齿动物中诱导免疫反应并监测其影响而产生的。人类流行病学研究调查孕妇感染和/或高水平细胞因子与患病可能性之间的联系。在这篇综述中，我们讨论了理解病毒介导的MIA与神经发育疾病之间关系的重要性，重点关注自闭症和精神分裂症。我们进一步讨论了研究MIA的不同方法及其局限性，并关注导致MIA异质性的不同因素。
