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Circulating soluble LIGHT/TNFSF14 is increased and associated with IL-8 concentration in chronic spontaneous urticaria

LIGHT (homologous to lymphotoxins, exhibiting inducible expression, and competing with herpes simplex virus (HSV) glycoprotein D for herpes virus entry mediator (HVEM), a receptor expressed by T lymphocytes) has been involved in various autoimmune and inflammatory disorders. LIGHT induces the expres...

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Detalles Bibliográficos
Autores principales: Kasperska-Zając, Alicja, Damasiewicz-Bodzek, Aleksandra, Grzanka, Ryszard, Skrzypulec-Frankel, Agnieszka, Bieniek, Katarzyna, Sikora-Żydek, Agnieszka, Jochem, Jerzy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073820/
https://www.ncbi.nlm.nih.gov/pubmed/29952668
http://dx.doi.org/10.1177/2058738418784431
Descripción
Sumario:LIGHT (homologous to lymphotoxins, exhibiting inducible expression, and competing with herpes simplex virus (HSV) glycoprotein D for herpes virus entry mediator (HVEM), a receptor expressed by T lymphocytes) has been involved in various autoimmune and inflammatory disorders. LIGHT induces the expression of interleukin-8 (IL-8), which is up-regulated in chronic spontaneous urticaria (CSU). To determine circulating soluble LIGHT concentration and its relationship with IL-8 concentration in patients with CSU. Concentrations of LIGHT, IL-8, and C-reactive protein (CRP) were determined in plasma or serum of CSU patients by an enzyme-linked immunosorbent assay. LIGHT plasma concentration was significantly higher in moderate–severe CSU patients as compared with the healthy subjects, but not with mild CSU patients. There were significant correlations between increased LIGHT and IL-8 concentrations, but not with increased CRP in CSU patients. Enhanced plasma concentrations of soluble LIGHT and its association with IL-8 concentration suggest the role of LIGHT in systemic inflammatory activation in CSU patients. We hypothesize that LIGHT-mediated immune–inflammatory response plays a role in severe phenotypes of the disease.