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The atopic dermatitis-like symptoms induced by MC903 were alleviated in JNK1 knockout mice.

Authors
  • Choi, Jinhwan1
  • Kim, Jong Rhan
  • Kim, Heejeung
  • Kim, Yoon A
  • Lee, Hyong Joo
  • Kim, Jiyoung
  • Lee, Ki Won
  • 1 * WCU Biomodulation Major, Department of Agricultural Biotechnology and Center for Food and Bioconvergence, Seoul National University, Seoul 151-921, Republic of Korea; , (North Korea)
Type
Published Article
Journal
Toxicological Sciences
Publisher
Oxford University Press
Publication Date
Dec 01, 2013
Volume
136
Issue
2
Pages
443–449
Identifiers
DOI: 10.1093/toxsci/kft215
PMID: 24046278
Source
Medline
Keywords
License
Unknown

Abstract

Atopic dermatitis (AD) is a common allergic disease, imposing large social and economic burdens worldwide. Atopic dermatitis is characterized by eczematous skin lesions and immunoglobulin E (IgE) hypersecretion. We investigated the role of JNK1 on the development of AD in mice. The vitamin D3 analogue MC903, a psoriasis therapeutic drug, was used to induce AD-like symptoms in wild-type (WT) and JNK1-/- mice. The symptoms of AD were less severe in JNK1-/- mice compared with WT mice. JNK1-/- mice showed less ear thickening and infiltration of eosinophils and mast cells in AD-like lesions than did WT mice when treated with MC903. MC903-treated JNK1-/- mice also showed significantly lower level of serum IgE, which was elevated in MC903-treated WT mice. Splenocytes isolated from MC903-treated WT and JNK1-/- mice were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies. Splenocytes from JNK1-/- mice produced lower levels of T-helper (Th2) cytokines (interleukin-4 and -13) and transcription factor GATA-binding protein 3, and produced increased levels of the Th1 cytokines interferon-γ and transcription factor T-box expressed in T cells. Our results indicate that JNK1 plays an important role in the pathogenesis of AD and may be a useful target for therapies to ameliorate AD.

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