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

Author:

Break Timothy J.1,Oikonomou Vasileios1,Dutzan Nicolas2,Desai Jigar V.1,Swidergall Marc34,Freiwald Tilo5,Chauss Daniel5,Harrison Oliver J.6,Alejo Julie7,Williams Drake W.2,Pittaluga Stefania7,Lee Chyi-Chia R.7,Bouladoux Nicolas6,Swamydas Muthulekha1,Hoffman Kevin W.8,Greenwell-Wild Teresa2,Bruno Vincent M.9,Rosen Lindsey B.10,Lwin Wint11,Renteria Andy1,Pontejo Sergio M.12,Shannon John P.13,Myles Ian A.14,Olbrich Peter10,Ferré Elise M. N.1,Schmitt Monica1,Martin Daniel15,Barber Daniel L.16,Solis Norma V.3,Notarangelo Luigi D.17,Serreze David V.18,Matsumoto Mitsuru19,Hickman Heather D.14,Murphy Philip M.12,Anderson Mark S.11,Lim Jean K.8,Holland Steven M.10,Filler Scott G.34,Afzali Behdad5,Belkaid Yasmine6,Moutsopoulos Niki M.2,Lionakis Michail S.1,

Affiliation:

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

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

3. Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.

4. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.

5. Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Bethesda, MD, USA.

6. Metaorganism Immunity Section, Laboratory of Immune System Biology, NIAID, Bethesda, MD, USA.

7. Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD, USA.

8. Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

9. Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, USA.

10. Immunopathogenesis Section, LCIM, NIAID, Bethesda, MD, USA.

11. Diabetes Center, University of California, San Francisco, CA, USA.

12. Molecular Signaling Section, Laboratory of Molecular Immunology, NIAID, Bethesda, MD, USA.

13. Viral Immunity and Pathogenesis Unit, LCIM, NIAID, Bethesda, MD, USA.

14. Epithelial Therapeutics Unit, LCIM, NIAID, Bethesda, MD, USA.

15. Genomics and Computational Biology Core, NIDCR, Bethesda, MD, USA.

16. T Lymphocyte Biology Section, Laboratory of Parasitic Diseases, NIAID, Bethesda, MD, USA.

17. Immune Deficiency Genetics Section, LCIM, NIAID, Bethesda, MD, USA.

18. The Jackson Laboratory, Bar Harbor, ME, USA.

19. Division of Molecular Immunology, Institute for Enzyme Research, Tokushima University, Tokushima, Japan.

Abstract

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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