IL-4 and IL-13 Negatively Regulate TNF-α- and IFN-γ-Induced β-Defensin Expression through STAT-6, Suppressor of Cytokine Signaling (SOCS)-1, and SOCS-3

DOI PDF 被引用文献7件
  • Cristina Albanesi
    Laboratory of Immunologia and Allergology, Istituto Dermopatico dell’Immacolata-Instituti di Recovero e Cura a Carattere Scientifico , Roma ,
  • Heather R Fairchild
    Division of Allergy and Immunology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206; and Department of Pediatrics, University of Colorado Health Sciences Center , Denver, CO 80262
  • Stefania Madonna
    Laboratory of Immunologia and Allergology, Istituto Dermopatico dell’Immacolata-Instituti di Recovero e Cura a Carattere Scientifico , Roma ,
  • Claudia Scarponi
    Laboratory of Immunologia and Allergology, Istituto Dermopatico dell’Immacolata-Instituti di Recovero e Cura a Carattere Scientifico , Roma ,
  • Ornella De Pità
    Laboratory of Immunologia and Allergology, Istituto Dermopatico dell’Immacolata-Instituti di Recovero e Cura a Carattere Scientifico , Roma ,
  • Donald Y M Leung
    Division of Allergy and Immunology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206; and Department of Pediatrics, University of Colorado Health Sciences Center , Denver, CO 80262
  • Michael D Howell
    Division of Allergy and Immunology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206; and Department of Pediatrics, University of Colorado Health Sciences Center , Denver, CO 80262

書誌事項

公開日
2007-07
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.179.2.984
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>Human β-defensins (HBDs) are a major class of antimicrobial peptides that play an important role in the innate immune response, however, the induction and regulation of these antimicrobial peptides is not well understood. We demonstrate here that stimulation of keratinocytes with TNF-α/IFN-γ induces HBD-2 and HBD-3 by activating STAT-1 and NF-κB signaling. We further demonstrate that IL-4 and IL-13 activate STAT-6 and induce the suppressors of cytokine signaling (SOCS)-1 and -3. This interferes with STAT-1 and NF-κB signaling, thereby inhibiting TNF-α/IFN-γ-mediated induction of HBD-2 and HBD-3. These data suggest that targeting the STAT-1-signaling pathway or suppressor of cytokine signaling expression enhances β-defensin expression and represents a new therapeutic strategy for reduction of infection in human diseases associated with β-defensin deficiency.</jats:p>

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