| First Author | Choi J | Year | 2013 |
| Journal | Toxicol Sci | Volume | 136 |
| Issue | 2 | Pages | 443-9 |
| PubMed ID | 24046278 | Mgi Jnum | J:207545 |
| Mgi Id | MGI:5559102 | Doi | 10.1093/toxsci/kft215 |
| Citation | Choi J, et al. (2013) The atopic dermatitis-like symptoms induced by MC903 were alleviated in JNK1 knockout mice. Toxicol Sci 136(2):443-9 |
| abstractText | 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-gamma 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. |
