Mast cells are required for full expression of allergen/SEB-Induced skin inflammation

Tomoaki Ando, Kenji Matsumoto, Siavash Namiranian, Hirotaka Yamashita, Haley Glatthorn, Miho Kimura, Brandon R. Dolan, James J. Lee, Stephen J. Galli, Yuko Kawakami, Colin Jamora, Toshiaki Kawakami

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disease. We recently described an animal model in which repeated epicutaneous applications of a house dust mite extract and Staphylococcal enterotoxin B induced eczematous skin lesions. In this study we showed that global gene expression patterns are very similar between human AD skin and allergen/staphylococcal enterotoxin B-induced mouse skin lesions, particularly in the expression of genes related to epidermal growth/differentiation, skin barrier, lipid/energy metabolism, immune response, or extracellular matrix. In this model, mast cells and T cells, but not B cells or eosinophils, were shown to be required for the full expression of dermatitis, as revealed by reduced skin inflammation and reduced serum IgE levels in mice lacking mast cells or T cells (TCRβ -/- or Rag1 -/-). The clinical severity of dermatitis correlated with the numbers of mast cells, but not eosinophils. Consistent with the idea that T helper type 2 (Th2) cells play a predominant role in allergic diseases, the receptor for the Th2-promoting cytokine thymic stromal lymphopoietin and the high-affinity IgE receptor, FcεRI, were required to attain maximal clinical scores. Therefore, this clinically relevant model provides mechanistic insights into the pathogenic mechanism of human AD.

Original languageEnglish (US)
Pages (from-to)2695-2705
Number of pages11
JournalJournal of Investigative Dermatology
Issue number12
StatePublished - Dec 2013

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology


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