Abstract
Purpose: :
To delineate the potential implication of Th17 cells versus Th1 cells in the pathophysiology of birdshot chorioretinopathy.
Methods: :
Single center cohort study of 95 subjects with birdshot chorioretinopathy seen in October 2007 at Hôpital Cochin, Paris, compared to 25 normal controls. Subjects were assessed for best-corrected visual acuity (BCVA), and inflammation was quantified by examination of the vitreous inflammation, by fluorescein angiography features, by optical coherence tomography and by recording the use of immunosuppressive therapy. Sera were collected for each patients and interleukin-17 (IL-17), IL-23 (IL-23) and interferon-γ (IFN-γ) were assayed by standard Elisa and correlated with clinical parameters.
Results: :
IL-17 was detected in the sera of 18 birdshot patients and in 5 sera from controls. The levels of IL-17 were higher in birdshot sera than in controls, but this difference didn’t reach statistical significance (p=0.085). IL-23 was detected in the sera of 37 patients versus in the 14 normal sera, but with a similar level of IL-23 in the two groups (p=0.150). No correlation was observed between IL-17 and IL-23 and the clinical inflammation outcomes. IFN-γ was detected in the sera of 39 patients and of 5 normal controls. Levels of IFN-γ were higher among birdshot sera than in control sera (p=0.033). In addition, IFN-γ positive birdshot patients, had more signs of inflammation on fluorescein angiography (macular leakage and/or vasculitis), and had more often a macular edema detected by optical coherence tomography (p=0.05).
Conclusions: :
Th17 has been recently described as playing a major role in the pathogenesis of experimental autoimmune uveoretinitis. However, based on the study of peripheral cytokine levels, our observations suggest a prominent role of Th1 over Th17 response in the pathophysiology of birdshot chorioretinopathy.
Keywords: retinochoroiditis • autoimmune disease • cytokines/chemokines