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IL-17 and IL-22 enhance skin inflammation by stimulating the secretion of il-1β by keratinocytes via the ROS-NLRP3-caspase-1 pathway
- IL-17 and IL-22 enhance skin inflammation by stimulating the secretion of il-1β by keratinocytes via the ROS-NLRP3-caspase-1 pathway
- Cho K.-A.; Suh J.W.; Ho Lee K.; Kang J.L.; Woo S.-Y.
- Ewha Authors
- 이지희; 우소연; 조경아
- SCOPUS Author ID
- 이지희; 우소연; 조경아
- Issue Date
- Journal Title
- International Immunology
- vol. 24, no. 3, pp. 147 - 158
- SCI; SCIE; SCOPUS
- Background: The pathogenesis of inflammatory skin disease involves the release of cytokines from keratinocytes, and one of these, IL-1β, has been previously implicated in inflammatory skin disease. T h17 cells, a subset of T h cells involved in autoimmunity and inflammation, possess IL-1β receptors and secrete cytokines such as IL-17 and IL-22 in response to IL-1β stimulation. A mutation in the inflammasome protein NLRP3 (NACHT, LRR and PYD domains-containing protein 3) causes excess production of IL-1β, resulting in an augmentation of T h17-dominant pathology. Methods: To determine the feedback effect, if any, of IL-17 and/or IL-22 on the secretion of IL-1β from keratinocytes, we stimulated the human keratinocyte cell line HaCaT, as well as caspase-1-deficient mice, with IL-17 or IL-22. Results: We found that treatment with IL-17 and IL-22 causes an increase in IL-1β via the activation of NLRP3 by a process that involves the generation of reactive oxygen species. Moreover, skin inflammation induced by IL-17 and IL-22 was lower in caspase-1 knockout (KO) mice relative to that induced by IL-1β treatment. Additionally, skin inflammation induced by the drug imiquimod was lower in caspase-1 KO mice than in wild-type mice. Conclusion: These results indicate that cytokines from T h17 cells may potentiate IL-1β-mediated skin inflammation and result in phenotypic alterations of keratinocytes via a feedback mechanism. © The Japanese Society for Immunology. 2011. All rights reserved.
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