Mechanism of HBD-3 deficiency in atopic dermatitis

Michael D. Howell, Mark Boguniewicz, Saveria Pastore, Natalija Novak, Thomas Bieber, Giampiero Girolomoni, D. Y M Leung

Research output: Contribution to journalArticlepeer-review


Extrinsic atopic dermatitis (EAD) and intrinsic atopic dermatitis (IAD) patients suffer from recurrent bacterial and viral infections. In this study, we demonstrate significantly decreased expression of human beta defensin (HBD)-3, a potent antimicrobial peptide (AMP), in lesional skin of both IAD (p <0.01) and EAD patients (p <0.01), as compared to psoriasis patients. Using primary keratinocytes from EAD and IAD patients, we determined that the deficiency in HBD-3 expression is an acquired rather than a constitutive defect. Furthermore, we demonstrate the down-regulatory effect of IL-4, IL-10, and IL-13 - which are over-expressed in the skin of AD patients - on HBD-3 expression in keratinocytes. Additionally, treatment of EAD skin explants with antibodies against IL-4, IL-10, and IL-13 augmented the expression of HBD-3. These studies suggest that neutralizing the Th2 cytokine milieu in AD skin may augment the innate immune response against bacterial and viral pathogens.

Original languageEnglish
Pages (from-to)332-338
Number of pages7
JournalClinical Immunology
Issue number3
Publication statusPublished - Dec 2006


  • Antimicrobial peptides
  • Cytokines
  • Extrinsic atopic dermatitis
  • Intrinsic atopic dermatitis

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy


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