Source:http://linkedlifedata.com/resource/pubmed/id/21172868
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2011-1-20
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pubmed:abstractText |
IL-23 and Th17 cells producing IL-17A and IL-22 are found in excess in skin affected by psoriasis. Previous studies showed that IL-22, but not IL-17A, mediates psoriasis-like epidermal hyperplasia following recombinant murine (rm)IL-23 injections into skin. To further investigate the role of IL-17A, ears of mice were injected with rmIL-23. Investigators blinded to treatment conditions and mouse genotypes measured ear swelling, epidermal thickness, and cytokine expression. In wild-type (WT) mice, rmIL-23 induced ear swelling (p < 0.001, all p values versus saline), epidermal hyperplasia by histology (p < 0.001) and confocal microscopy (p < 0.004), and expression of both IL-17A and IL-22. As expected, rmIL-23 injections into IL-22(-/-) mice resulted in relatively little ear swelling (p < 0.09) and epidermal hyperplasia (p < 0.51 by histology and p < 0.75 by confocal microscopy). Notably, rmIL-23 injections into IL-17A(-/-) mice produced little ear swelling (p < 0.001, versus IL-23-injected WT mice) and epidermal hyperplasia (p < 0.001 by histology and p < 0.005 by confocal microscopy), even though IL-22 was readily induced in these mice. Furthermore, systemic delivery of blocking Abs directed against either IL-22 or IL-17A completely inhibited IL-23-induced epidermal hyperplasia in WT mice. These results demonstrate that IL-17A, like IL-22, is a downstream mediator for IL-23-induced changes in murine skin and that both of these Th17 cytokines are necessary to produce IL-23-mediated skin pathology. IL-17A may represent an attractive therapeutic target in individuals with psoriasis by blocking downstream effects of IL-23.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Blocking,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-23,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/interleukin-22
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1550-6606
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
186
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1495-502
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pubmed:meshHeading |
pubmed-meshheading:21172868-Animals,
pubmed-meshheading:21172868-Antibodies, Blocking,
pubmed-meshheading:21172868-Epidermis,
pubmed-meshheading:21172868-Hyperplasia,
pubmed-meshheading:21172868-Injections, Intradermal,
pubmed-meshheading:21172868-Interleukin-17,
pubmed-meshheading:21172868-Interleukin-23,
pubmed-meshheading:21172868-Interleukins,
pubmed-meshheading:21172868-Mice,
pubmed-meshheading:21172868-Mice, Inbred C57BL,
pubmed-meshheading:21172868-Mice, Knockout,
pubmed-meshheading:21172868-Psoriasis
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pubmed:year |
2011
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pubmed:articleTitle |
IL-23-mediated psoriasis-like epidermal hyperplasia is dependent on IL-17A.
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pubmed:affiliation |
Department of Dermatology, Oregon Health & Science University, Portland, OR 97239, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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