NDLI: IL-22 is required for Th17 cell–mediated pathology in a mouse model of psoriasis-like skin inflammation

Content Provider	PubMed Central
Author	Ma, Hak-ling Liang, Spencer Li, Jing Lee, Napierata Brown, Tom Benoit, Stephen Senices, Mayra Gill, Davinder Dunussi-joannopoulos, Kyriaki Collins, Mary Cheryl, Nickerson-nutter Fouser, Lynette A. Young, Deborah A.
Copyright Year	2008
Abstract	Psoriasis is a chronic skin disease resulting from the dysregulated interplay between keratinocytes and infiltrating immune cells. We report on a psoriasis-like disease model, which is induced by the transfer of CD4+CD45RBhiCD25– cells to pathogen-free scid/scid mice. Psoriasis-like lesions had elevated levels of antimicrobial peptide and proinflammatory cytokine mRNA. Also, similar to psoriasis, disease progression in this model was dependent on the p40 common to IL-12 and IL-23. To investigate the role of IL-22, a Th17 cytokine, in disease progression, mice were treated with IL-22–neutralizing antibodies. Neutralization of IL-22 prevented the development of disease, reducing acanthosis (thickening of the skin), inflammatory infiltrates, and expression of Th17 cytokines. Direct administration of IL-22 into the skin of normal mice induced both antimicrobial peptide and proinflammatory cytokine gene expression. Our data suggest that IL-22, which acts on keratinocytes and other nonhematopoietic cells, is required for development of the autoreactive Th17 cell–dependent disease in this model of skin inflammation. We propose that IL-22 antagonism might be a promising therapy for the treatment of human psoriasis.
Related Links	http://dx.doi.org/10.1172/jci33263
Starting Page	597
File Format	PDF
ISSN	00219738
Journal	The Journal of Clinical Investigation
Issue Number	2
Volume Number	118
Language	English
Publisher	American Society for Clinical Investigation
Publisher Date	2008-01-01
Access Restriction	Open
Rights Holder	American Society for Clinical Investigation
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Medicine

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