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 journalArticleAcademicpeer-review

7 Citations (Web of Science)


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 languageEnglish
Pages (from-to)294-299
JournalOcular Immunology and Inflammation
Issue number4
Publication statusPublished - Aug 2014


  • Autoimmune disease
  • interleukin-25
  • Vogt-Koyanagi-Harada syndrome

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