Back to Search
Start Over
Inflammatory Skin Disease in K5.hTGF-β1 Transgenic Mice Is Not Dependent on the IL-23/Th17 Inflammatory Pathway.
- Source :
-
Journal of Investigative Dermatology . Oct2009, Vol. 129 Issue 10, p2443-2450. 8p. 1 Color Photograph, 3 Graphs. - Publication Year :
- 2009
-
Abstract
- In the presence of IL-6, transforming growth factor (TGF)-β1 induces differentiation of T helper (Th) 17 cells in mice. Interleukin (IL)-23, a heterodimeric cytokine composed of IL-23p19 and IL-12/23p40 subunits, stimulates the growth and expansion of Th17 cells, and has been implicated in psoriasis pathogenesis. To study the associations between TGF-β1, the IL-23/Th17 inflammatory pathway, and psoriasis, we investigated inflammatory skin disease in transgenic mice that constitutively overexpress human TGF-β1 in basal keratinocytes (K5.hTGF-β1 transgenic mice); these mice had previously been reported as having a psoriasis-like disease. K5.hTGF-β1 transgenic mice had high levels of TGF-β1 mRNA and protein in both skin and serum. Levels of cytokines involved in IL-23/Th17-mediated inflammation were not elevated in lesional skin compared with those in non-lesional and wild-type skin. It is noteworthy that IL-4 and IgE were markedly elevated in inflamed skin and serum, respectively, of transgenic mice. Monoclonal antibodies (mAbs) specifically directed against IL-23p19 or IL-12/23p40 had no clinical effect on established inflammatory skin disease in K5.hTGF-β1 transgenic mice, whereas the same mAbs were able to block the development of murine experimental autoimmune encephalomyelitis, an IL-23/Th17-mediated disease. In summary, the IL-23/Th17 inflammatory pathway is not responsible for the maintenance of inflammatory skin disease in K5.hTGF-β1 transgenic mice. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 0022202X
- Volume :
- 129
- Issue :
- 10
- Database :
- Academic Search Index
- Journal :
- Journal of Investigative Dermatology
- Publication Type :
- Academic Journal
- Accession number :
- 44151827
- Full Text :
- https://doi.org/10.1038/jid.2009.88