Clinical Reviews in Allergy & Immunology

, Volume 41, Issue 3, pp 272–281

Innate Immunity in Atopic Dermatitis

  • Andreas Wollenberg
  • Helen-Caroline Räwer
  • Jürgen Schauber
Article

DOI: 10.1007/s12016-010-8227-x

Cite this article as:
Wollenberg, A., Räwer, HC. & Schauber, J. Clinic Rev Allerg Immunol (2011) 41: 272. doi:10.1007/s12016-010-8227-x

Abstract

Atopic dermatitis (AD) is a clinically defined, highly pruritic, chronic inflammatory skin disease. In AD patients, the combination of a genetic predisposition for skin barrier dysfunction and dysfunctional innate and adaptive immune responses leads to a higher frequency of bacterial and viral skin infections. The innate immune system quickly mobilizes an unspecific, standardized first-line defense against different pathogens. Defects in this system lead to barrier dysfunction which results in increased protein allergen penetration through the epidermis and predisposes to secondary skin infections. Two loss-of-function mutations in the epidermal filaggrin gene are associated with AD. Also, inducible endogenous antibiotics such as the antimicrobial peptides cathelicidin and the beta-defensins may show defective function in lesional AD skin. Eczema herpeticum is a disseminated viral infection almost exclusively diagnosed in AD patients, which is based on unmasking of the viral entry receptor nectin-1, lack of cathelicidin production by keratinocytes, and depletion of Type I IFN-producing plasmacytoid dendritic cells from AD skin. Future therapeutic approaches to AD may include enhancement of impaired innate in addition to downregulation of dysfunctional adaptive immunity.

Keywords

Innate immunity Atopic dermatitis Viral skin infection Antimicrobial peptides Epidermal barrier dysfunction Plasmacytoid dendritic cells 

Abbreviations

AD

Atopic dermatitis

AMP

Antimicrobial peptides

APC

Antigen-presenting cell

DC

Dendritic cell

EH

Eczema herpeticum

EM

Eczema molluscatum

FcεRI

High-affinity IgE receptor

FPR-1

Formyl peptide receptor

HBD

Human beta-defensin

HSV

Herpes simplex virus

IDEC

Inflammatory dendritic epidermal cell

IFN

Interferon

IL18-BP

Interleukin-18 binding protein

iNOS

Inducible NO synthase

KVE

Kaposi’s varicelliform eruption

LC

Langerhans cell

MCV

Molluscum contagiosum virus

NK

Natural killer cell

PAMP

Pathogen-associated molecular pattern

PDC

Plasmacytoid dendritic cell

PRR

Pathogen recognition receptor

S. aureus

Staphylococcus aureus

TLR

Toll-like receptor

Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  • Andreas Wollenberg
    • 1
  • Helen-Caroline Räwer
    • 1
  • Jürgen Schauber
    • 1
  1. 1.Department of Dermatology and AllergyLudwig-Maximilian-University of MunichMunichGermany

Personalised recommendations