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-1β, IL-6, and TNF-α 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-1β, IL-6, and TNF-α 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; Vogt-Koyanagi-Harada syndrome; interleukin-25.