24. Immunology of Atopic Dermatitis

  1. Alan D. Irvine MD, FRCPI, FRCP3,4,
  2. Peter H. Hoeger MD5,6 and
  3. Albert C. Yan MD, FAAP, FAAD7,8
  1. Aideen M. Byrne MRCPI1 and
  2. Donald Y. M. Leung MD, PhD2

Published Online: 24 MAY 2011

DOI: 10.1002/9781444345384.ch24

Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition

Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition

How to Cite

Byrne, A. M. and Leung, D. Y. M. (2011) Immunology of Atopic Dermatitis, in Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition (eds A. D. Irvine, P. H. Hoeger and A. C. Yan), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781444345384.ch24

Editor Information

  1. 3

    Trinity College, Dublin, Ireland

  2. 4

    Our Lady's Children's Hospital, Dublin, Ireland

  3. 5

    University of Hamburg, Hamburg, Germany

  4. 6

    Catholic Children's Hospital Wilhelmstift, Hamburg, Germany

  5. 7

    University of Pennsylvania School of Medicine, Philadelphia, PA, USA

  6. 8

    The Children's Hospital of Philadelphia, Philadelphia, PA, USA

Author Information

  1. 1

    University of Colorado Denver Medical School, Aurora, CO, USA

  2. 2

    Department of Pediatrics, National Jewish Health, Denver, CO, USA

Publication History

  1. Published Online: 24 MAY 2011
  2. Published Print: 3 JUN 2011

ISBN Information

Print ISBN: 9781405176958

Online ISBN: 9781444345384

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Keywords:

  • allergy;
  • antimicrobial peptides;
  • atopic dermatitis;
  • cytokines;
  • dendritic cells;
  • eczema;
  • immunoglobulin E;
  • innate immune response;
  • microbes;
  • T cells

Summary

Atopic dermatitis (AD) is a chronic inflammatory skin disease that often has its onset during early infancy and childhood. The majority of patients have evidence of immunological abnormalities including elevated serum IgE, recurrent skin infections and systemic allergen sensitization that predisposes to allergic rhinitis, food allergy or asthma. There is no single mechanism that can account for all aspects of AD. This common skin condition probably represents a final clinical phenotype that results from many factors including gene–environment interactions, defective skin barrier function, neuropharmacological abnormalities and immune dysfunction. This chapter will focus on the role that immunological mechanisms play in AD.