| First Author | Lindroos J | Year | 2011 |
| Journal | J Invest Dermatol | Volume | 131 |
| Issue | 5 | Pages | 1110-8 |
| PubMed ID | 21289639 | Mgi Jnum | J:182081 |
| Mgi Id | MGI:5314693 | Doi | 10.1038/jid.2010.432 |
| Citation | Lindroos J, et al. (2011) IL-23-mediated epidermal hyperplasia is dependent on IL-6. J Invest Dermatol 131(5):1110-8 |
| abstractText | Psoriasis is a chronic inflammatory skin disease primarily driven by Th17 cells. IL-23 facilitates the differentiation and induces complete maturation of Th17 cells. Lesional psoriatic skin has increased levels of IL-23 and recent studies show that intradermal injections of IL-23 induce a psoriasis-like skin phenotype in mice. We have now characterized the IL-23-induced skin inflammation in mice at the molecular level and found a significant correlation with the gene expression profile from lesional psoriatic skin. As observed in psoriasis, the pathogenesis of the IL-23-induced skin inflammation in mice is driven by Th17 cells. We demonstrate a dramatic upregulation of IL-6 mRNA and protein after intradermal injections of IL-23 in mice. Using IL-6(-/-) mice we show that IL-6 is essential for development of the IL-23-elicited responses. Despite producing high levels of IL-22, IL-6(-/-) mice were unable to express the high-affinity IL-22 receptor chain and produced minimal IL-17A in response to intradermal injections of IL-23. In conclusion, we provide evidence for the critical role played by IL-6 in IL-23-induced skin inflammation and show that IL-6 is required for expression of IL-22R1A. |
