Vogt-Koyanagi-Harada (VKH) disease is one of the most common forms of uveitis in Asians[1–4].It is an autoimmune disease characterized by a bilateral granulomatous uveitis, which mainly affects the eyes, ears, skin and central nervous system. Although the specific pathogenesis of VKH syndrome is still in the research stage, various types of immune cells have been found to play a vital role in the pathogenesis of VKH disease [6, 7]. Early studies confirmed that macrophages, dendritic cells, Th1 and Th17 cells were related to the pathogenesis of Vogt Koyanagi Harada (VKH) disease . In addition, a variety of inflammatory factors, such as IL-21, IL-27, IL-37, IL-35 and IL-12, have been found to be involved in the pathogenesis of VKH disease [8–12]. Previous studies of our research group showed that IL-25 may participate in the development of VKH disease by inhibiting the expression of proinflammatory cytokines .
Interleukin-25 is a newly discovered member of the IL-17 family, localized on chromosome 14q11, and was first reported by Lee et al . It has 3987 base pairs (bp), contains a 483 bp open reading frame, and encodes 161 amino acids . IL-25 has been proved to be produced by a variety of different cells and tissues and has the characteristics of wide distribution [16–25] .The IL-25 receptor (IL-25R) consists of IL-17RA and IL-17RB subunits. Mainly expressed on T cells, NKT cells, ILC2s, endothelial cells, dendritic cells, macrophages and so on [27–32]. Although IL-25 belongs to the IL-17 family, it has only 16% homology with IL-17A, and has a significantly different biological function from other IL-17 family cytokines . On the one hand, IL-25 can induce type 2 immune response and promote the secretion of cytokines such as IL-4, IL-5, IL-9 and IL-13 . On the other hand, it can also bind with IL-17A and its receptor il-17RA to inhibit the formation of pro-inflammatory factors and participate in autoimmune inflammatory diseases. A previous study showed that IL-25 can reduce the production of pro-inflammatory cytokines IL-12 and IL-23, thereby inhibiting DC driven Th1 inflammatory activity . Study has found that IL-25 primed mesenchymal stem cells can improve the symptoms of inflammatory bowel disease by inhibiting Th17 immune response and inducing T regulatory cell phenotype . In our previous study, we found that compared with the control group, the level of IL-25 in serum of VKH patients was significantly down-regulated. In addition, in vitro experiments have shown that rIL-25 can significantly inhibit the production of IL-1β, IL-6 and TNF-α in PBMC of active VKH patients .
The purpose of this study was to confirm the discovery of IL-25 in VKH disease and to further find out the changes of IL-25 expression in PBMC of VKH patients after the treatment with corticosteroid or CsA.