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Response to Comments on "Aberrant type 1 immunity drives susceptibility to mucosal fungal infections".
Break, Timothy J; Oikonomou, Vasileios; Dutzan, Nicolas; Desai, Jigar V; Swidergall, Marc; Freiwald, Tilo; Chauss, Daniel; Harrison, Oliver J; Alejo, Julie; Williams, Drake W; Pittaluga, Stefania; Lee, Chyi-Chia R; Bouladoux, Nicolas; Swamydas, Muthulekha; Hoffman, Kevin W; Greenwell-Wild, Teresa; Bruno, Vincent M; Rosen, Lindsey B; Lwin, Wint; Renteria, Andy; Pontejo, Sergio M; Shannon, John P; Myles, Ian A; Olbrich, Peter; Ferré, Elise M N; Schmitt, Monica; Martin, Daniel; Barber, Daniel L; Solis, Norma V; Notarangelo, Luigi D; Serreze, David V; Matsumoto, Mitsuru; Hickman, Heather D; Murphy, Philip M; Anderson, Mark S; Lim, Jean K; Holland, Steven M; Filler, Scott G; Afzali, Behdad; Belkaid, Yasmine; Moutsopoulos, Niki M; Lionakis, Michail S.
Affiliation
  • Break TJ; Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
  • Oikonomou V; Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
  • Dutzan N; Oral Immunity and Inflammation Section, National Institute of Dental and Craniofacial Research (NIDCR), Bethesda, MD, USA.
  • Desai JV; Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
  • Swidergall M; Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
  • Freiwald T; David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
  • Chauss D; Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Bethesda, MD, USA.
  • Harrison OJ; Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Bethesda, MD, USA.
  • Alejo J; Metaorganism Immunity Section, Laboratory of Immune System Biology, NIAID, Bethesda, MD, USA.
  • Williams DW; Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD, USA.
  • Pittaluga S; Oral Immunity and Inflammation Section, National Institute of Dental and Craniofacial Research (NIDCR), Bethesda, MD, USA.
  • Lee CR; Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD, USA.
  • Bouladoux N; Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD, USA.
  • Swamydas M; Metaorganism Immunity Section, Laboratory of Immune System Biology, NIAID, Bethesda, MD, USA.
  • Hoffman KW; Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
  • Greenwell-Wild T; Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
  • Bruno VM; Oral Immunity and Inflammation Section, National Institute of Dental and Craniofacial Research (NIDCR), Bethesda, MD, USA.
  • Rosen LB; Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, USA.
  • Lwin W; Immunopathogenesis Section, LCIM, NIAID, Bethesda, MD, USA.
  • Renteria A; Diabetes Center, University of California, San Francisco, CA, USA.
  • Pontejo SM; Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
  • Shannon JP; Molecular Signaling Section, Laboratory of Molecular Immunology, NIAID, Bethesda, MD, USA.
  • Myles IA; Viral Immunity and Pathogenesis Unit, LCIM, NIAID, Bethesda, MD, USA.
  • Olbrich P; Epithelial Therapeutics Unit, LCIM, NIAID, Bethesda, MD, USA.
  • Ferré EMN; Immunopathogenesis Section, LCIM, NIAID, Bethesda, MD, USA.
  • Schmitt M; Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
  • Martin D; Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
  • Solis NV; T Lymphocyte Biology Section, Laboratory of Parasitic Diseases, NIAID, Bethesda, MD, USA.
  • Notarangelo LD; Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
  • Serreze DV; Immune Deficiency Genetics Section, LCIM, NIAID, Bethesda, MD, USA.
  • Matsumoto M; The Jackson Laboratory, Bar Harbor, ME, USA.
  • Hickman HD; Division of Molecular Immunology, Institute for Enzyme Research, Tokushima University, Tokushima, Japan.
  • Murphy PM; Epithelial Therapeutics Unit, LCIM, NIAID, Bethesda, MD, USA.
  • Anderson MS; Molecular Signaling Section, Laboratory of Molecular Immunology, NIAID, Bethesda, MD, USA.
  • Lim JK; Diabetes Center, University of California, San Francisco, CA, USA.
  • Holland SM; Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
  • Filler SG; Immunopathogenesis Section, LCIM, NIAID, Bethesda, MD, USA.
  • Afzali B; Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA.
  • Belkaid Y; David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
  • Moutsopoulos NM; Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Bethesda, MD, USA.
  • Lionakis MS; Metaorganism Immunity Section, Laboratory of Immune System Biology, NIAID, Bethesda, MD, USA.
Science ; 373(6561): eabi8835, 2021 Sep 17.
Article in En | MEDLINE | ID: mdl-34529475
ABSTRACT
Puel and Casanova and Kisand et al. challenge our conclusions that interferonopathy and not IL-17/IL-22 autoantibodies promote candidiasis in autoimmune polyendocrinopathy­candidiasis­ectodermal 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.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Immunity, Mucosal / Mycoses Limits: Animals / Humans Language: En Journal: Science Year: 2021 Document type: Article Affiliation country: Estados Unidos
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Immunity, Mucosal / Mycoses Limits: Animals / Humans Language: En Journal: Science Year: 2021 Document type: Article Affiliation country: Estados Unidos