Abstract
Recent studies show that the aryl hydrocarbon receptor (AhR) is involved in immune responses. AhR is activated following interaction with its ligands, such as 6-formylindolo[3,2-b]carbazole (FICZ) and 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE). In this study, we investigated the role of AhR activation by its endogenous ligands in the pathogenesis of ocular Behcet's disease (BD). The expression of AhR was significantly decreased in active BD patients as compared to inactive BD patients and normal controls. Both FICZ and ITE inhibited Th1 and Th17 polarization and induced the expression of IL-22 by PBMCs and by CD4+T cells in active BD patients and normal controls. Stimulation of purified CD4+T cells with FICZ or ITE caused a decreased expression of RORC, IL-17, IL-23R, and CCR6 and an increased phosphorylation of STAT3 and STAT5. The present study suggests that a decreased AhR expression is associated with disease activity in BD patients. The activation of AhR by either FICZ or ITE was able to inhibit Th1 and Th17 cell polarization. Further studies are needed to investigate whether modulation of AhR might be used in the treatment of BD.
Highlights
Behcet’s disease (BD) is a chronic systemic inflammatory disease affecting the eye, skin, oral mucosa, gastrointestinal tract, and central nervous system [1]
The results showed that Aryl hydrocarbon receptor (AhR) mRNA expression was significantly decreased in active BD patients as compared to inactive BD patients (P = 0.006) and normal controls (P < 0.001)
Because an increased frequency of Th1 and Th17 cells has been shown to be associated with the inflammatory activity of BD and since AhR has been reported to be involved in T cell immune responses, we determined the effect of endogenous AhR ligands on the Th1 and Th17 cell response in active BD patients and normal controls
Summary
Behcet’s disease (BD) is a chronic systemic inflammatory disease affecting the eye, skin, oral mucosa, gastrointestinal tract, and central nervous system [1] It is a relatively common uveitis entity in China and the clinical ocular features have been described extensively elsewhere [2]. The pathogenesis of BD is still not completely understood, it is currently thought that environmental factors may trigger the development and recurrence of this disease in a genetically susceptible host [3]. It is classified as an example of an autoinflammatory disorder with marked involvement of both Th1 and Th17 lymphocyte subsets [4,5,6,7]. AhR plays a critical role in the normal physiological function
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