Low expression of the IL-23/Th17 pathway in atopic dermatitis compared to psoriasis

Emma Guttman-Yassky, Michelle A. Lowes, Judilyn Fuentes-Duculan, Lisa C. Zaba, Irma Cardinale, Kristine E. Nograles, Artemis Khatcherian, Inna Novitskaya, John A. Carucci, Reuven Bergman, James G. Krueger

Research output: Contribution to journalArticlepeer-review

295 Scopus citations


The classical Th1/Th2 paradigm previously defining atopic dermatitis (AD) and psoriasis has recently been challenged with the discovery of Th17 T cells that synthesize IL-17 and IL-22. Although it is becoming evident that many Th1 diseases including psoriasis have a strong IL-17 signal, the importance of Th17 T cells in AD is still unclear. We examined and compared skin biopsies from AD and psoriasis patients by gene microarray, RT-PCR, immunohistochemistry, and immunofluorescence. We found a reduced genomic expression of IL-23, IL-17, and IFN-γ in AD compared with psoriasis. To define the effects of IL-17 and IL-22 on keratinocytes, we performed gene array studies with cytokine-treated keratinocytes. We found lipocalin 2 and numerous other innate defense genes to be selectively induced in keratinocytes by IL-17. IFN-γ had no effect on antimicrobial gene-expression in keratinocytes. In AD skin lesions, protein and mRNA expression of lipocalin 2 and other innate defense genes (hBD2, elafin, LL37) were reduced compared with psoriasis. Although AD has been framed by the Th1/Th2 paradigm as a Th2 polar disease, we present evidence that the IL-23/Th17 axis is largely absent, perhaps accounting for recurrent skin infections in this disease.

Original languageEnglish (US)
Pages (from-to)7420-7427
Number of pages8
JournalJournal of Immunology
Issue number10
StatePublished - Nov 15 2008
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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