Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome

Joshua D. Milner, Jason M. Brenchley, Arian Laurence, Alexandra F. Freeman, Brenna J. Hill, Kevin M. Elias, Yuka Kanno, Christine Spalding, Houda Z. Elloumi, Michelle L. Paulson, Joie Davis, Amy Hsu, Ava I. Asher, John O’Shea, Steven M. Holland, William E. Paul and Daniel C. Douek ()
Additional contact information
Joshua D. Milner: Laboratory of Immunology,
Jason M. Brenchley: Human Immunology Section, Vaccine Research Center, and,
Arian Laurence: Lymphocyte Cell Biology Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases,
Alexandra F. Freeman: Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Brenna J. Hill: Human Immunology Section, Vaccine Research Center, and,
Kevin M. Elias: Lymphocyte Cell Biology Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases,
Yuka Kanno: Lymphocyte Cell Biology Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases,
Christine Spalding: Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Houda Z. Elloumi: Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Michelle L. Paulson: Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Joie Davis: Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Amy Hsu: Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Ava I. Asher: Human Immunology Section, Vaccine Research Center, and,
John O’Shea: Lymphocyte Cell Biology Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases,
Steven M. Holland: Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
William E. Paul: Laboratory of Immunology,
Daniel C. Douek: Human Immunology Section, Vaccine Research Center, and,

Nature, 2008, vol. 452, issue 7188, 773-776

Abstract: Hyper-IgE syndrome is an autosomal dominant immunodeficiency that has been linked to mutations in stat3. This paper shows that stat3 mutant subjects fail to generate TH17 cells, which may account for their susceptibility to recurrent infections.

Date: 2008
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DOI: 10.1038/nature06764

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