Wilson C B, Lewis D B
Department of Pediatrics, University of Washington, Seattle 98195.
Rev Infect Dis. 1990 May-Jun;12 Suppl 4:S410-20. doi: 10.1093/clinids/12.supplement_4.s410.
The human neonate is unduly susceptible to infection with viruses and other pathogens, such as Toxoplasma and Listeria, that survive and replicate within cells. Cellular immunity is the major mechanism of host defense against these intracellular pathogens. Selective immaturity in certain functions of T lymphocytes appears to be a major factor in the neonate's susceptibility to these infections. Particularly striking is the deficiency in production of interferon-gamma. We review the data regarding the deficiency in the production of interferon-gamma by cells of healthy and infected neonates, discuss what is known regarding the cellular and molecular mechanisms for this deficiency, and review the unique role played by interferon-gamma in host defense against intracellular pathogens. The response of the neonate's effector cells to the immunoenhancing effects of interferon-gamma appears to be variable; diminished enhancement by interferon-gamma of cytotoxic cell function and the production of tumor necrosis factor by macrophages may further compound the effects of diminished production of interferon-gamma.
人类新生儿极易感染病毒及其他病原体，如弓形虫和李斯特菌等能在细胞内存活并复制的病原体。细胞免疫是宿主抵御这些细胞内病原体的主要防御机制。T淋巴细胞某些功能的选择性不成熟似乎是新生儿易患这些感染的主要因素。尤其显著的是γ干扰素产生不足。我们回顾了关于健康和感染新生儿细胞产生γ干扰素不足的数据，讨论了已知的导致这种不足的细胞和分子机制，并回顾了γ干扰素在宿主抵御细胞内病原体中的独特作用。新生儿效应细胞对γ干扰素免疫增强作用的反应似乎存在差异；γ干扰素对细胞毒性细胞功能增强作用的减弱以及巨噬细胞产生肿瘤坏死因子的减少，可能会进一步加重γ干扰素产生减少的影响。
