EBI3 is pivotal for the initiation of experimental autoimmune uveitis.

摘要: Murine experimental autoimmune uveitis (EAU) is a model for human uveitis, whose pathogenesis caused by both Th1 and Th17 cell responses. Epstein-Barr virus-induced gene 3 (EBI3) component of the heterodimeric cytokines: interleukin (IL)-27 IL-35. Although IL-27 was shown to initiate development, it also recognized as negative regulator fully activated CD4+ T cells, including cells. Recently, IL-35 has been reported play immunosuppressive roles in autoimmunity. To investigate EBI3 EAU, EBI3(-/-) mice were immunized with interphotoreceptor retinoid binding protein peptide 1-20 (IRBP) induce EAU. We observed that clinical score diminished compared EBI3(+/+) up day 22 after immunization, whereas reached same levels 28. Histological analysis revealed significant reduction cellular infiltration into retina on 16. responses IRBP-specific IL-10 production reduced mice, development unaffected 9. On 21, restored significantly increased mice. Furthermore, Foxp3 expression cells comparable between days 9 21. Therefore, these results indicate may be important EAU initiation suppress inhibition late/maintenance phase.