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Involvement of Th17 cells and the effect of anti-IL-6 therapy in autoimmune uveitis
Rheumatology, 03/31/09
Yoshimura T et al. – Findings suggest that IL-6 is responsible for causing ocular inflammation, and it is, at least partially, due to IL-6-dependent Th17 differentiation. IL-6 may be a target for therapy of refractory endogenous uveitis in human
Methods- Study to investigate if IL-6-based biological therapies could be a choice for endogenous uveitis
- An increase of several inflammatory soluble factors including IL-6 in the vitreous fluids from pts was confirmed
- To investigate the role of IL-6 the mouse experimental autoimmune uveitis (EAU) model was used
- Both IL-6 and IL-23 are required for the development of IL-17-producing Th17 from naïve CD4+ T cells
- In EAU model, neither IL-6-deficient mice nor IL-23-deficient mice could induce Th17 cells
- EAU score was decreased in these mice in the entire time course
- Systemic administration of anti-IL-6 receptor Ab ameliorated EAU by suppressing both systemic and regional Th17 responses
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