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

Author

Listed:
  • Joshua D. Milner

    (Laboratory of Immunology,)

  • Jason M. Brenchley

    (Human Immunology Section, Vaccine Research Center, and,
    Present address: Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.)

  • 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,
    Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA)

  • 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,)

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.

Suggested Citation

  • 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 , 2008. "Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome," Nature, Nature, vol. 452(7188), pages 773-776, April.
    • Handle: RePEc:nat:nature:v:452:y:2008:i:7188:d:10.1038_nature06764
    DOI: 10.1038/nature06764
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