Interleukin-10 downregulates anti-microbial peptide expression in atopic dermatitis

Michael D. Howell, Natalija Novak, Thomas Bieber, Saveria Pastore, Giampiero Girolomoni, Mark Boguniewicz, Joanne Streib, Cathy Wong, Richard L. Gallo, Donald Y M Leung

Research output: Contribution to journalArticlepeer-review


Recurrent skin infections in extrinsic atopic dermatitis (EAD) may be because of the suppression of anti-microbial peptide (AMP) expression by interleukin (IL)-4 and IL-13. Twenty to thirty percent of AD, however, are classified as intrinsic atopic dermatitis (IAD). They exhibit normal serum IgE levels, no allergen-specific sensitization, and lower levels of IL-4 and IL-13 than EAD. Both forms of AD have increased propensity to skin infection, suggesting a novel mechanism for infection in IAD. In this study, we observed significantly decreased human β-defensin (HBD)-2 gene expression in the skin of both IAD (p = 0.010) and EAD (p = 0.004), as compared with psoriasis patients. Conversely, IAD (p = 0.019) and EAD (p = 0.002) skin lesions exhibited elevated IL-10 gene expression when compared with psoriasis. Using primary keratinocytes, we found that the deficiency in AMP expression is an acquired rather than a constitutive defect. Interestingly, neutralizing antibodies to IL-10 augmented the production of tumor necrosis factor-α and interferon-γ by peripheral blood mononuclear cell from AD patients. Additionally, treatment of AD skin explants with anti-IL-10 augmented the expression of both HBD-2 and LL-37. Thus, increased levels of IL-10 may contribute to the AMP deficiency in both IAD and EAD by reducing cytokines that induce AMP.

Original languageEnglish
Pages (from-to)738-745
Number of pages8
JournalJournal of Investigative Dermatology
Issue number4
Publication statusPublished - Oct 2005


  • Anti-microbial peptides
  • Cytokines
  • Extrinsic atopic dermatitis
  • Intrinsic atopic dermatitis

ASJC Scopus subject areas

  • Dermatology


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