Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris

Psoriasis is a type I–deviated disease characterized by the presence of interferon (IFN)-γ and multiple IFN-related inflammatory genes in lesions. Because interleukin (IL)-23 is now recognized to play a role in the recruitment of inflammatory cells in a T helper cell (Th)1-mediated disease, we exami...

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Main Authors: Lee, Edmund, Trepicchio, William L., Oestreicher, Judith L., Pittman, Debra, Wang, Frank, Chamian, Francesca, Dhodapkar, Madhav, Krueger, James G.
Format: Online
Language:English
Published: The Rockefeller University Press 2004
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1887731/
id pubmed-1887731
recordtype oai_dc
spelling pubmed-18877312008-03-11 Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris Lee, Edmund Trepicchio, William L. Oestreicher, Judith L. Pittman, Debra Wang, Frank Chamian, Francesca Dhodapkar, Madhav Krueger, James G. Article Psoriasis is a type I–deviated disease characterized by the presence of interferon (IFN)-γ and multiple IFN-related inflammatory genes in lesions. Because interleukin (IL)-23 is now recognized to play a role in the recruitment of inflammatory cells in a T helper cell (Th)1-mediated disease, we examined psoriasis skin lesions for production of this newly described cytokine. IL-23 is composed of two subunits: a unique p19 subunit and a p40 subunit shared with IL-12. We found a reliable increase in p19 mRNA by quantitative reverse transcription polymerase chain reaction in lesional skin compared with nonlesional skin (22.3-fold increase; P = 0.001). The p40 subunit, shared by IL-12 and IL-23, increased by 11.6-fold compared with nonlesional skin (P = 0.003), but the IL-12 p35 subunit was not increased in lesional skin. IL-23 was expressed mainly by dermal cells and increased p40 immunoreactivity was visualized in large dermal cells in the lesions. Cell isolation experiments from psoriatic tissue showed strong expression of p19 mRNA in cells expressing monocyte (CD14+ CD11c+ CD83−) and mature dendritic cell (DC) markers (CD14− CD11c+ CD83+), whereas in culture, the mRNAs for p40 and p19 were strongly up-regulated in stimulated monocytes and monocyte-derived DCs, persisting in the latter for much longer periods than IL-12. Our data suggest that IL-23 is playing a more dominant role than IL-12 in psoriasis, a Th1 type of human inflammatory disease. The Rockefeller University Press 2004-01-05 /pmc/articles/PMC1887731/ /pubmed/14707118 http://dx.doi.org/10.1084/jem.20030451 Text en Copyright © 2004, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Lee, Edmund
Trepicchio, William L.
Oestreicher, Judith L.
Pittman, Debra
Wang, Frank
Chamian, Francesca
Dhodapkar, Madhav
Krueger, James G.
spellingShingle Lee, Edmund
Trepicchio, William L.
Oestreicher, Judith L.
Pittman, Debra
Wang, Frank
Chamian, Francesca
Dhodapkar, Madhav
Krueger, James G.
Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris
author_facet Lee, Edmund
Trepicchio, William L.
Oestreicher, Judith L.
Pittman, Debra
Wang, Frank
Chamian, Francesca
Dhodapkar, Madhav
Krueger, James G.
author_sort Lee, Edmund
title Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris
title_short Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris
title_full Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris
title_fullStr Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris
title_full_unstemmed Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris
title_sort increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris
description Psoriasis is a type I–deviated disease characterized by the presence of interferon (IFN)-γ and multiple IFN-related inflammatory genes in lesions. Because interleukin (IL)-23 is now recognized to play a role in the recruitment of inflammatory cells in a T helper cell (Th)1-mediated disease, we examined psoriasis skin lesions for production of this newly described cytokine. IL-23 is composed of two subunits: a unique p19 subunit and a p40 subunit shared with IL-12. We found a reliable increase in p19 mRNA by quantitative reverse transcription polymerase chain reaction in lesional skin compared with nonlesional skin (22.3-fold increase; P = 0.001). The p40 subunit, shared by IL-12 and IL-23, increased by 11.6-fold compared with nonlesional skin (P = 0.003), but the IL-12 p35 subunit was not increased in lesional skin. IL-23 was expressed mainly by dermal cells and increased p40 immunoreactivity was visualized in large dermal cells in the lesions. Cell isolation experiments from psoriatic tissue showed strong expression of p19 mRNA in cells expressing monocyte (CD14+ CD11c+ CD83−) and mature dendritic cell (DC) markers (CD14− CD11c+ CD83+), whereas in culture, the mRNAs for p40 and p19 were strongly up-regulated in stimulated monocytes and monocyte-derived DCs, persisting in the latter for much longer periods than IL-12. Our data suggest that IL-23 is playing a more dominant role than IL-12 in psoriasis, a Th1 type of human inflammatory disease.
publisher The Rockefeller University Press
publishDate 2004
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1887731/
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