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Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms

Koebner phenomenon refers to the emergence of new psoriatic lesions in the healthy skin regions following an injury/trauma to psoriatic patients. The occurrence of psoriatic lesions at unusual areas of the body regions such as on penis, around eyes and on keloids suggest that the Koebner phenomenon...

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Detalles Bibliográficos
Autores principales: Ji, Yong-Zhi, Liu, Shi-Rui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893164/
https://www.ncbi.nlm.nih.gov/pubmed/31710084
http://dx.doi.org/10.1042/BSR20193266
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author Ji, Yong-Zhi
Liu, Shi-Rui
author_facet Ji, Yong-Zhi
Liu, Shi-Rui
author_sort Ji, Yong-Zhi
collection PubMed
description Koebner phenomenon refers to the emergence of new psoriatic lesions in the healthy skin regions following an injury/trauma to psoriatic patients. The occurrence of psoriatic lesions at unusual areas of the body regions such as on penis, around eyes and on keloids suggest that the Koebner phenomenon may be responsible for these lesions. A number of agents/triggers have been reported to induce the development of new psoriatic lesions in healthy skin areas and these include, tattooing skin, radiations, skin incision, viral infections and striae etc. The different mechanisms that contribute in inducing the development of new psoriatic lesions as Koebernization include the involvement of mast cell-derived inflammatory mediators such as tryptase, IL-6, IL-8, IL-17, and IL-36γ. Moreover, an increased expression of nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) also contribute in Koebernization. Apart from these, there is a critical role of α 2 β1 integrins, S100A7 (psoriasin) and S100A15 (koebnerisin), change in the ratio of CD4(+)/CD8(+) T cells, down-regulation of mechanosensitive polycystin 1 protein, decrease in inflammation controlling atypical chemokine receptor 2 (ACKR2), reduced expression of N-methyl-d-aspartate (NMDA) receptors (NMDARs) on the keratinocytes and increase in levels of chemokines (CXCL8 and CCL20) in inducing formation of new psoriatic lesions. The present review discusses the role of Koebner phenomenon in the development of new psoriatic lesions. Moreover, it also describes the mechanisms involved in Koebernization in the form of discussion of different key targets that may be potentially modulated pharmacologically to attenuate/halt the development of new psoriatic lesions.
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spelling pubmed-68931642019-12-10 Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms Ji, Yong-Zhi Liu, Shi-Rui Biosci Rep Immunology & Inflammation Koebner phenomenon refers to the emergence of new psoriatic lesions in the healthy skin regions following an injury/trauma to psoriatic patients. The occurrence of psoriatic lesions at unusual areas of the body regions such as on penis, around eyes and on keloids suggest that the Koebner phenomenon may be responsible for these lesions. A number of agents/triggers have been reported to induce the development of new psoriatic lesions in healthy skin areas and these include, tattooing skin, radiations, skin incision, viral infections and striae etc. The different mechanisms that contribute in inducing the development of new psoriatic lesions as Koebernization include the involvement of mast cell-derived inflammatory mediators such as tryptase, IL-6, IL-8, IL-17, and IL-36γ. Moreover, an increased expression of nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) also contribute in Koebernization. Apart from these, there is a critical role of α 2 β1 integrins, S100A7 (psoriasin) and S100A15 (koebnerisin), change in the ratio of CD4(+)/CD8(+) T cells, down-regulation of mechanosensitive polycystin 1 protein, decrease in inflammation controlling atypical chemokine receptor 2 (ACKR2), reduced expression of N-methyl-d-aspartate (NMDA) receptors (NMDARs) on the keratinocytes and increase in levels of chemokines (CXCL8 and CCL20) in inducing formation of new psoriatic lesions. The present review discusses the role of Koebner phenomenon in the development of new psoriatic lesions. Moreover, it also describes the mechanisms involved in Koebernization in the form of discussion of different key targets that may be potentially modulated pharmacologically to attenuate/halt the development of new psoriatic lesions. Portland Press Ltd. 2019-12-04 /pmc/articles/PMC6893164/ /pubmed/31710084 http://dx.doi.org/10.1042/BSR20193266 Text en © 2019 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).
spellingShingle Immunology & Inflammation
Ji, Yong-Zhi
Liu, Shi-Rui
Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms
title Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms
title_full Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms
title_fullStr Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms
title_full_unstemmed Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms
title_short Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms
title_sort koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms
topic Immunology & Inflammation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6893164/
https://www.ncbi.nlm.nih.gov/pubmed/31710084
http://dx.doi.org/10.1042/BSR20193266
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