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对"异常类型免疫驱动对粘膜真菌感染的易感性"的评论的回应

Timothy J Break¹, Vasileios Oikonomou¹, Nicolas Dutzan²

¹Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.

Science (New York, N.Y.)

|September 16, 2021

概括

干扰,而不是IL-17/IL-22自身抗体,驱动了自身免疫多胞体病的候群病. 对缺氧小鼠和患者的研究提供了强有力的证据.

科学领域:

免疫学
内分泌学
传染性疾病

背景情况:

自体免疫多胞膜病变 (candidiasis) 皮质缩 (APECED) 是一种罕见的自体免疫疾病.
细胞因子如IL-17/IL-22和I型干扰素在与APECED相关的候群病的作用受到争论.
之前的研究表明IL-17/IL-22自身抗体是原因,但这项研究调查了其他机制.

研究的目的:

挑战IL-17/IL-22自身抗体在APECED中促进候群病的假设.
在APECED中提供证据支持干扰症是粘膜腺候群的主要驱动因素.
研究空气缺乏在菌病的产生中的作用.

主要方法:

使用缺氧小鼠模型研究粘膜腺.
在小鼠模型中分析了干扰症标志物和IL-17/IL-22反应.
通过APECED患者的临床数据和免疫学评估证实了这些发现.

主要成果:

已经证明,干扰因子会导致缺氧小鼠的粘膜腺.
在受影响的小鼠中观察到完整的IL-17/IL-22反应,这与自身抗体假设相矛盾.
在APECED中发现了强有力的证据,将干扰症与候选症联系起来.

结论:

在APECED中,干扰是促进粘膜腺的主要机制.
在这种情况下,IL-17/IL-22自身抗体的作用可能是次要的或可以忽略不计的.
空气缺乏会通过干扰症导致候群病变.

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