Inhibition of Proinflammatory Cytokine by IL-25 in Vogt-Koyanagi-Harada Syndrome

Mei Xu; Chaokui Wang; Yuan Tian; Aize Kijlstra; Peizeng Yang

doi:10.3109/09273948.2013.854391

Inhibition of Proinflammatory Cytokine by IL-25 in Vogt-Koyanagi-Harada Syndrome

Mei Xu, Chaokui Wang, Yuan Tian, Aize Kijlstra, Peizeng Yang^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

Purpose: Vogt-Koyanagi-Harada (VKH) syndrome is a multisystem disorder presumed to be mediated by an autoimmune response. Recent studies have shown that interleukin (IL) 25 was involved in the T-cell immune response. This study analyzed the expression and potential role of IL-25 in the pathogenesis of VKH syndrome. Methods: The IL-25 serum levels were determined by enzyme-linked immunosorbent assay (ELISA). The IL-1 beta, IL-6, and TNF-alpha level in supernatants of PBMCs cultured with LPS in the absence or presence of recombinant(r) IL-25 was detected by ELISA. Results: A significantly decreased serum IL-25 level was found in VKH patients. In vitro experiments showed that rIL-25 was able to significantly inhibit the production of IL-1 beta, IL-6, and TNF-alpha by PBMCs from active VKH patients. Conclusions: IL-25 may be involved in the development of VKH syndrome, possibly by inhibiting the expression of proinflammatory cytokines.

Original language	English
Pages (from-to)	294-299
Journal	Ocular Immunology and Inflammation
Volume	22
Issue number	4
DOIs	https://doi.org/10.3109/09273948.2013.854391
Publication status	Published - Aug 2014

Keywords

Autoimmune disease
interleukin-25
Vogt-Koyanagi-Harada syndrome

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10.3109/09273948.2013.854391

Cite this

@article{f0d8dfcc367344b7bbc6084824fe6158,

title = "Inhibition of Proinflammatory Cytokine by IL-25 in Vogt-Koyanagi-Harada Syndrome",

abstract = "Purpose: Vogt-Koyanagi-Harada (VKH) syndrome is a multisystem disorder presumed to be mediated by an autoimmune response. Recent studies have shown that interleukin (IL) 25 was involved in the T-cell immune response. This study analyzed the expression and potential role of IL-25 in the pathogenesis of VKH syndrome. Methods: The IL-25 serum levels were determined by enzyme-linked immunosorbent assay (ELISA). The IL-1 beta, IL-6, and TNF-alpha level in supernatants of PBMCs cultured with LPS in the absence or presence of recombinant(r) IL-25 was detected by ELISA. Results: A significantly decreased serum IL-25 level was found in VKH patients. In vitro experiments showed that rIL-25 was able to significantly inhibit the production of IL-1 beta, IL-6, and TNF-alpha by PBMCs from active VKH patients. Conclusions: IL-25 may be involved in the development of VKH syndrome, possibly by inhibiting the expression of proinflammatory cytokines.",

keywords = "Autoimmune disease, interleukin-25, Vogt-Koyanagi-Harada syndrome",

author = "Mei Xu and Chaokui Wang and Yuan Tian and Aize Kijlstra and Peizeng Yang",

year = "2014",

month = aug,

doi = "10.3109/09273948.2013.854391",

language = "English",

volume = "22",

pages = "294--299",

journal = "Ocular Immunology and Inflammation",

issn = "0927-3948",

publisher = "Routledge/Taylor & Francis Group",

number = "4",

}

TY - JOUR

T1 - Inhibition of Proinflammatory Cytokine by IL-25 in Vogt-Koyanagi-Harada Syndrome

AU - Xu, Mei

AU - Wang, Chaokui

AU - Tian, Yuan

AU - Kijlstra, Aize

AU - Yang, Peizeng

PY - 2014/8

Y1 - 2014/8

N2 - Purpose: Vogt-Koyanagi-Harada (VKH) syndrome is a multisystem disorder presumed to be mediated by an autoimmune response. Recent studies have shown that interleukin (IL) 25 was involved in the T-cell immune response. This study analyzed the expression and potential role of IL-25 in the pathogenesis of VKH syndrome. Methods: The IL-25 serum levels were determined by enzyme-linked immunosorbent assay (ELISA). The IL-1 beta, IL-6, and TNF-alpha level in supernatants of PBMCs cultured with LPS in the absence or presence of recombinant(r) IL-25 was detected by ELISA. Results: A significantly decreased serum IL-25 level was found in VKH patients. In vitro experiments showed that rIL-25 was able to significantly inhibit the production of IL-1 beta, IL-6, and TNF-alpha by PBMCs from active VKH patients. Conclusions: IL-25 may be involved in the development of VKH syndrome, possibly by inhibiting the expression of proinflammatory cytokines.

AB - Purpose: Vogt-Koyanagi-Harada (VKH) syndrome is a multisystem disorder presumed to be mediated by an autoimmune response. Recent studies have shown that interleukin (IL) 25 was involved in the T-cell immune response. This study analyzed the expression and potential role of IL-25 in the pathogenesis of VKH syndrome. Methods: The IL-25 serum levels were determined by enzyme-linked immunosorbent assay (ELISA). The IL-1 beta, IL-6, and TNF-alpha level in supernatants of PBMCs cultured with LPS in the absence or presence of recombinant(r) IL-25 was detected by ELISA. Results: A significantly decreased serum IL-25 level was found in VKH patients. In vitro experiments showed that rIL-25 was able to significantly inhibit the production of IL-1 beta, IL-6, and TNF-alpha by PBMCs from active VKH patients. Conclusions: IL-25 may be involved in the development of VKH syndrome, possibly by inhibiting the expression of proinflammatory cytokines.

KW - Autoimmune disease

KW - interleukin-25

KW - Vogt-Koyanagi-Harada syndrome

U2 - 10.3109/09273948.2013.854391

DO - 10.3109/09273948.2013.854391

M3 - Article

C2 - 24329541

SN - 0927-3948

VL - 22

SP - 294

EP - 299

JO - Ocular Immunology and Inflammation

JF - Ocular Immunology and Inflammation

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ER -