Wright P, Gill M, Murray R M
Department of Psychological Medicine, Institute of Psychiatry, London, United Kingdom.
Am J Med Genet. 1993 May 1;48(1):40-6. doi: 10.1002/ajmg.1320480110.
Thirty years ago, Eliot Slater suggested that the reason schizophrenia was not progressively eliminated from the population was that the responsible gene also conveyed a compensatory advantage in terms of increased resistance to infection. If this selective advantage lies in the antibody response to certain viral infections, this could explain recent studies suggesting that exposure to influenza in the second trimester of gestation increases the risk of later schizophrenia. We propose that prenatal exposure to influenza induces maternal antibodies which then cross-react with proteins in the developing foetal brain, becoming foetal autoantibodies. Thus an immunogenetic response by the mother results in aberrant foetal neurodevelopment, the biological substrate for a proportion of adult schizophrenia. Initial research strategies to test this hypothesis are proposed.
30年前，艾略特·斯莱特提出，精神分裂症未能在人群中逐渐消失的原因是，相关基因在增强抗感染能力方面也具有补偿优势。如果这种选择优势在于对某些病毒感染的抗体反应，那么这可以解释最近的研究结果，即孕期第二个三月期接触流感会增加日后患精神分裂症的风险。我们认为，孕期接触流感会诱导母体产生抗体，这些抗体随后会与发育中的胎儿大脑中的蛋白质发生交叉反应，从而成为胎儿自身抗体。因此，母亲的免疫遗传反应会导致胎儿神经发育异常，这是一部分成人精神分裂症的生物学基础。本文还提出了检验这一假设的初步研究策略。
