{"title":"Decreased CXCL14 expression in psoriasis recovered by narrow-band ultraviolet B therapy","authors":"Kaori Nakajima MD, Tomomitsu Miyagaki MD, PhD, Miho Tanaka MD, Reo Komaki MD, Tatsuro Okano MD, PhD, Sora Takeuchi MD, PhD, Hidenori Watabe MD, PhD, Takafumi Kadono MD, PhD","doi":"10.1002/cia2.12332","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background</h3>\n \n <p>CXCL14 is a member of CXC chemokine family, constitutively expressed in various normal tissues unlike many other chemokines. Other than the capacity to recruit natural killer cells, macrophages, and dendritic cells, CXCL14 suppresses CXCL12-CXCR4 interactions by inducing CXCR4 internalization. Thus, CXCL14 can both promote and hinder immune responses. Psoriasis is a chronic skin inflammatory disorder in which various chemokines play an important role.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>To investigate possible roles of CXCL14 in psoriasis, we examined CXCL14 expression in lesional skin by immunohistochemistry and measured serum CXCL14 levels in psoriasis. We also assessed the effect of ultraviolet irradiation, one of the main therapies for psoriasis, on CXCL14 expression by HaCaT cells.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>CXCL14 expression was decreased in epidermal keratinocytes in lesional skin and serum CXCL14 levels were negatively correlated with Psoriasis Area and Severity Index scores in psoriasis patients. Serum CXCL14 levels were increased in nbUVB-treated psoriasis patients and UVB irradiation induced CXCL14 mRNA expression from HaCaT cells.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>Our results suggest that decreased CXCL14 expression may contribute to the exacerbation of psoriasis and that the amplification of CXCL14 can be a therapeutic option for psoriasis. One of the mechanisms of the efficacy of nbUVB therapy in psoriasis may be the upregulation of CXCL14.</p>\n </section>\n </div>","PeriodicalId":15543,"journal":{"name":"Journal of Cutaneous Immunology and Allergy","volume":null,"pages":null},"PeriodicalIF":1.1000,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cia2.12332","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cutaneous Immunology and Allergy","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cia2.12332","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ALLERGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background
CXCL14 is a member of CXC chemokine family, constitutively expressed in various normal tissues unlike many other chemokines. Other than the capacity to recruit natural killer cells, macrophages, and dendritic cells, CXCL14 suppresses CXCL12-CXCR4 interactions by inducing CXCR4 internalization. Thus, CXCL14 can both promote and hinder immune responses. Psoriasis is a chronic skin inflammatory disorder in which various chemokines play an important role.
Methods
To investigate possible roles of CXCL14 in psoriasis, we examined CXCL14 expression in lesional skin by immunohistochemistry and measured serum CXCL14 levels in psoriasis. We also assessed the effect of ultraviolet irradiation, one of the main therapies for psoriasis, on CXCL14 expression by HaCaT cells.
Results
CXCL14 expression was decreased in epidermal keratinocytes in lesional skin and serum CXCL14 levels were negatively correlated with Psoriasis Area and Severity Index scores in psoriasis patients. Serum CXCL14 levels were increased in nbUVB-treated psoriasis patients and UVB irradiation induced CXCL14 mRNA expression from HaCaT cells.
Conclusion
Our results suggest that decreased CXCL14 expression may contribute to the exacerbation of psoriasis and that the amplification of CXCL14 can be a therapeutic option for psoriasis. One of the mechanisms of the efficacy of nbUVB therapy in psoriasis may be the upregulation of CXCL14.