Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases

Psoriasis is a chronic skin disease caused by the excessive secretion of inflammatory cytokines. Available therapeutic options include biologic drugs such as tumor necrosis factor alpha inhibitors and interleukin 12/23 (IL-12/23) inhibitors. The recent discovery of IL-17, which contributes to develo...

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Autores principales: Wasilewska, Agnieszka, Winiarska, Marta, Olszewska, Małgorzata, Rudnicka, Lidia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2016
Materias:
Review Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5004212/
https://www.ncbi.nlm.nih.gov/pubmed/27605893
http://dx.doi.org/10.5114/ada.2016.61599
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author Wasilewska, Agnieszka
Winiarska, Marta
Olszewska, Małgorzata
Rudnicka, Lidia
author_facet Wasilewska, Agnieszka
Winiarska, Marta
Olszewska, Małgorzata
Rudnicka, Lidia
author_sort Wasilewska, Agnieszka
collection PubMed
description Psoriasis is a chronic skin disease caused by the excessive secretion of inflammatory cytokines. Available therapeutic options include biologic drugs such as tumor necrosis factor alpha inhibitors and interleukin 12/23 (IL-12/23) inhibitors. The recent discovery of IL-17, which contributes to development of psoriasis, opened new possibilities for further treatment modalities. Currently, one anti-IL17 biological agent is approved for the treatment – a fully human monoclonal antibody that targets IL-17A (secukinumab). Further clinical trials, including a humanized IgG4 specific for IL-17 (ixekizumab) and a fully human antibody that targets the IL-17 receptor A (brodalumab).
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spelling pubmed-50042122016-09-07 Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases Wasilewska, Agnieszka Winiarska, Marta Olszewska, Małgorzata Rudnicka, Lidia Postepy Dermatol Alergol Review Paper Psoriasis is a chronic skin disease caused by the excessive secretion of inflammatory cytokines. Available therapeutic options include biologic drugs such as tumor necrosis factor alpha inhibitors and interleukin 12/23 (IL-12/23) inhibitors. The recent discovery of IL-17, which contributes to development of psoriasis, opened new possibilities for further treatment modalities. Currently, one anti-IL17 biological agent is approved for the treatment – a fully human monoclonal antibody that targets IL-17A (secukinumab). Further clinical trials, including a humanized IgG4 specific for IL-17 (ixekizumab) and a fully human antibody that targets the IL-17 receptor A (brodalumab). Termedia Publishing House 2016-08-16 2016-08 /pmc/articles/PMC5004212/ /pubmed/27605893 http://dx.doi.org/10.5114/ada.2016.61599 Text en Copyright: © 2016 Termedia Sp. z o.o. http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle Review Paper
Wasilewska, Agnieszka
Winiarska, Marta
Olszewska, Małgorzata
Rudnicka, Lidia
Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases
title Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases
title_full Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases
title_fullStr Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases
title_full_unstemmed Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases
title_short Interleukin-17 inhibitors. A new era in treatment of psoriasis and other skin diseases
title_sort interleukin-17 inhibitors. a new era in treatment of psoriasis and other skin diseases
topic Review Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5004212/
https://www.ncbi.nlm.nih.gov/pubmed/27605893
http://dx.doi.org/10.5114/ada.2016.61599
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