NDLI: IL-17A enhances vitamin D3-induced expression of cathelicidin antimicrobial peptide in human keratinocytes.

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IL-17A enhances vitamin D3-induced expression of cathelicidin antimicrobial peptide in human keratinocytes.

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IL-17A enhances vitamin D3-induced expression of cathelicidin antimicrobial peptide in human keratinocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Koglin, Sarah Peric, Mark Gallo, Richard L. Kim, Song-Min Morizane, Shin Besch, Robert Ruzicka, Thomas Schauber, Jürgen Prinz, Jörg C.
Description	Country affiliation: Germany Author Affiliation: Peric M ( Department of Dermatology and Allergology, Ludwig-Maximilians-University, Munich, Germany.)
Abstract	Cathelicidin is strongly expressed in lesional skin in psoriasis and may play an important role as both an antimicrobial peptide and as an autoinflammatory mediator in this chronic skin disease. The mechanism of increased cathelicidin in psoriatic keratinocytes is not known, but recent observations have found that psoriasis has abundant Th17 cells that produce IL-17A and IL-22. We found that human keratinocytes stimulated with supernatants from T cells isolated from lesional psoriatic skin increased expression of cathelicidin when stimulated in the presence of 1,25-dihydroxyvitamin D(3) (1,25D(3)). This increase was signaled through the IL-17RA. In vitro, IL-17A, but not IL-22, enhanced cathelicidin mRNA and peptide expression in keratinocytes dependent on the presence of 1,25D(3). At the same time, coincubation with 1,25D(3) blocked induction of human beta-defensin 2 (HBD2), IL-6, and IL-8, which are other target genes of IL-17A. Act1, an adaptor associated with IL-17RA and essential for IL-17A signaling, mediated cathelicidin induction, as its suppression by small interfering RNA inhibited HBD2 and cathelicidin. Both, 1,25D(3) and IL-17A signaled cathelicidin induction through MEK-ERK. These results suggest that increased IL-17A in psoriatic skin increases cathelicidin through a vitamin D(3)-, Act1-, and MEK-ERK-dependent mechanism. Therapy targeting this cathelicidin-regulating system might be beneficial in patients suffering from psoriasis.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	12
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-12-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antimicrobial Cationic Peptides Biosynthesis Cholecalciferol Pharmacology Interleukin-17 Physiology Keratinocytes Immunology Metabolism Anti-bacterial Agents Genetics Cathelicidins Cell Line Cells, Cultured Inflammation Mediators Enzymology Map Kinase Signaling System Psoriasis Pathology Tumor Necrosis Factor Receptor-associated Peptides And Proteins Up-regulation Drug Effects Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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IL-17A Enhances Vitamin D3-Induced Expression of Cathelicidin Antimicrobial Peptide in Human Keratinocytes1

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IL-17A enhances vitamin D3-induced expression of cathelicidin antimicrobial peptide in human keratinocytes.

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IL-17A Enhances Vitamin D3-Induced Expression of Cathelicidin Antimicrobial Peptide in Human Keratinocytes1

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IL-17A enhances vitamin D3-induced expression of cathelicidin antimicrobial peptide in human keratinocytes.