Response to Comments on “Aberrant type 1 immunity drives susceptibility to mucosal fungal infections”,Science

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Response to Comments on “Aberrant type 1 immunity drives susceptibility to mucosal fungal infections”
Science ( IF 44.7 ) Pub Date : 2021-09-17 , DOI: 10.1126/science.abi8835
Timothy J Break ₁ , Vasileios Oikonomou ₁ , Nicolas Dutzan ₂ , Jigar V Desai ₁ , Marc Swidergall _{3,

4} , Tilo Freiwald ₅ , Daniel Chauss ₅ , Oliver J Harrison ₆ , Julie Alejo ₇ , Drake W Williams ₂ , Stefania Pittaluga ₇ , Chyi-Chia R Lee ₇ , Nicolas Bouladoux ₆ , Muthulekha Swamydas ₁ , Kevin W Hoffman ₈ , Teresa Greenwell-Wild ₂ , Vincent M Bruno ₉ , Lindsey B Rosen ₁₀ , Wint Lwin ₁₁ , Andy Renteria ₁ , Sergio M Pontejo ₁₂ , John P Shannon ₁₃ , Ian A Myles ₁₄ , Peter Olbrich ₁₀ , Elise M N Ferré ₁ , Monica Schmitt ₁ , Daniel Martin ₁₅ , , Daniel L Barber ₁₆ , Norma V Solis ₃ , Luigi D Notarangelo ₁₇ , David V Serreze ₁₈ , Mitsuru Matsumoto ₁₉ , Heather D Hickman ₁₄ , Philip M Murphy ₁₂ , Mark S Anderson ₁₁ , Jean K Lim ₈ , Steven M Holland ₁₀ , Scott G Filler _{3,

4} , Behdad Afzali ₅ , Yasmine Belkaid ₆ , Niki M Moutsopoulos ₂ , Michail S Lionakis ₁

Affiliation

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.
Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Bethesda, MD, USA.
Metaorganism Immunity Section, Laboratory of Immune System Biology, NIAID, Bethesda, MD, USA.
Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD, USA.
Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, USA.
Immunopathogenesis Section, LCIM, NIAID, Bethesda, MD, USA.
Diabetes Center, University of California, San Francisco, CA, USA.
Molecular Signaling Section, Laboratory of Molecular Immunology, NIAID, Bethesda, MD, USA.
Viral Immunity and Pathogenesis Unit, LCIM, NIAID, Bethesda, MD, USA.
Epithelial Therapeutics Unit, LCIM, NIAID, Bethesda, MD, USA.
Genomics and Computational Biology Core, NIDCR, Bethesda, MD, USA.
T Lymphocyte Biology Section, Laboratory of Parasitic Diseases, NIAID, Bethesda, MD, USA.
Immune Deficiency Genetics Section, LCIM, NIAID, Bethesda, MD, USA.
The Jackson Laboratory, Bar Harbor, ME, USA.
Division of Molecular Immunology, Institute for Enzyme Research, Tokushima University, Tokushima, Japan.

Puel and Casanova and Kisand et al. 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 Aire-deficient mice, with strong corroborative evidence in patients.

中文翻译：

回应“异常的 1 型免疫导致对粘膜真菌感染的易感性”的评论

普埃尔、卡萨诺瓦和基桑德等人。挑战我们的结论，即干扰素病而非 IL-17/IL-22 自身抗体会促进自身免疫性多内分泌腺病-念珠菌病-外胚层营养不良中的念珠菌病。我们承认，在复杂的人类疾病中很难获得因果关系确凿的证据。然而，我们的研究清楚地记录了干扰素病驱动粘膜念珠菌病，并在艾尔缺陷小鼠中具有完整的 IL-17/IL-22 反应，并在患者中提供了强有力的确凿证据。

更新日期：2021-09-17

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