Mechanism of HBD-3 deficiency in atopic dermatitis

Clin Immunol. 2006 Dec;121(3):332-8. doi: 10.1016/j.clim.2006.08.008. Epub 2006 Oct 2.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cells, Cultured
  • Cytokines / metabolism
  • Dermatitis, Atopic / genetics
  • Dermatitis, Atopic / immunology
  • Dermatitis, Atopic / metabolism*
  • Dermatitis, Atopic / pathology
  • Down-Regulation
  • Gene Expression Regulation
  • Humans
  • Inflammation Mediators / immunology
  • Inflammation Mediators / metabolism
  • Keratinocytes / immunology
  • Keratinocytes / metabolism
  • Middle Aged
  • Psoriasis / genetics
  • Th2 Cells / immunology
  • Th2 Cells / metabolism
  • beta-Defensins / deficiency*
  • beta-Defensins / genetics
  • beta-Defensins / metabolism*


  • Cytokines
  • DEFB103A protein, human
  • Inflammation Mediators
  • beta-Defensins