Behcet’s disease (BD) and Vogt-Koyanagi-Harada (VKH) syndrome are two intraocular
inflammatory diseases that are caused by an aberrant T lymphocyte response. Th17 cells, mainly producing
the cytokine IL-17, and Th1 cells, characterized by the production of the index cytokine IFN-γ, are the CD4+ T
lymphocyte subsets implicated in the pathogenesis of both BD and VKH. Suppressing the excessive response
of these Th17 and Th1 cells has been reported to be an effective therapeutic approach to treat these patients
and continuous efforts are being undertaken to find new methods to modulate the function of these cells.
Evidence is emerging that the Liver X receptor (LXR) is an important regulator of inflammatory and immune
responses and the study reported here was designed to investigate the role of LXR activation in BD and VKH.
Here we demonstrate that the frequency of Th17 and Th1 cells along with the relevant cytokines IL-17, IFN-γ
and corresponding transcriptional factors RORC, T-bet were all decreased following LXR activation by the
agonist GW3965. LXR controlled the expression of inflammatory cytokines through an effect on NF-kappa B
(NFκb) phosphorylation. Data from our study provide evidence for an association between a decreased LXR
expression and disease activity in both BD and VKH, due to the fact that a lower LXR activation may result in
an enhanced Th1 and Th17 immune response. Our study suggests that enhancing LXR activation may offer a
potential therapeutic approach targeting aberrant immune responses by inhibiting Th1 and Th17 cell
Keywords: Behcet's disease, liver X receptor, NF-kappa B, Th1, Th17, Vogt-Koyanagi-Harada syndrome.
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