Linked Life Data

21606249

Source:http://linkedlifedata.com/resource/pubmed/id/21606249

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pubmed-article:21606249pubmed:abstractTextIL-17 and IL-23 are known to be absolutely central to psoriasis pathogenesis because drugs targeting either cytokine are highly effective treatments for this disease. The efficacy of these drugs has been attributed to blocking the function of IL-17-producing T cells and their IL-23-induced expansion. However, we demonstrate that mast cells and neutrophils, not T cells, are the predominant cell types that contain IL-17 in human skin. IL-17(+) mast cells and neutrophils are found at higher densities than IL-17(+) T cells in psoriasis lesions and frequently release IL-17 in the process of forming specialized structures called extracellular traps. Furthermore, we find that IL-23 and IL-1? can induce mast cell extracellular trap formation and degranulation of human mast cells. Release of IL-17 from innate immune cells may be central to the pathogenesis of psoriasis, representing a fundamental mechanism by which the IL-23-IL-17 axis mediates host defense and autoimmunity.lld:pubmed
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pubmed-article:21606249pubmed:pagination490-500lld:pubmed
pubmed-article:21606249pubmed:dateRevised2011-9-2lld:pubmed
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pubmed-article:21606249pubmed:year2011lld:pubmed
pubmed-article:21606249pubmed:articleTitleMast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis.lld:pubmed
pubmed-article:21606249pubmed:affiliationDepartment of Dermatology, University of Michigan, Ann Arbor, MI 48109, USA.lld:pubmed
pubmed-article:21606249pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21606249pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:21606249pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:21606249pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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