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回应对“异常的 1 型免疫驱动黏膜真菌感染易感性”一文的评论。

Response to Comments on "Aberrant type 1 immunity drives susceptibility to mucosal fungal infections".

机构信息

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

Oral Immunity and Inflammation Section, National Institute of Dental and Craniofacial Research (NIDCR), Bethesda, MD, USA.

出版信息

Science. 2021 Sep 17;373(6561):eabi8835. doi: 10.1126/science.abi8835. Epub 2021 Sep 16.

Abstract

Puel and Casanova and Kisand . challenge our conclusions that interferonopathy and not IL-17/IL-22 autoantibodies promote candidiasis in autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy. We acknowledge that conclusive evidence for causation is difficult to obtain in complex human diseases. However, our studies clearly document interferonopathy driving mucosal candidiasis with intact IL-17/IL-22 responses in -deficient mice, with strong corroborative evidence in patients.

摘要

普尔、卡桑诺瓦和基桑德质疑我们的结论,即干扰素病而非白细胞介素-17/白细胞介素-22 自身抗体促进自身免疫性多内分泌腺病-念珠菌病-外胚层营养不良的念珠菌病。我们承认,在复杂的人类疾病中,很难获得因果关系的确凿证据。然而,我们的研究清楚地证明了在缺乏 - 的小鼠中,干扰素病驱动黏膜念珠菌病,同时伴有完整的白细胞介素-17/白细胞介素-22 反应,在患者中也有强有力的佐证。

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