IL-23 promotes CD4(+) T cells to produce IL-17 in Vogt-Koyanagi-Harada disease

W. Chi, P.Z. Yang, B. Li, C.Y. Wu, H.L. Jin, X.F. Zhu, L.N. Chen, H.Y. Zhou, X.K. Huang, A. Kijlstra

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Background: Vogt-Koyanagi-Harada (VKH) disease is a systemic refractory autoimmune disease. IL-23 has been thought to play a critical role in autoimmune disease through inducing the development of IL-17-producing CD4(+) T cells. Objective: To investigate the expression of IL-23 and IL-17 and the influence of IL-23 on IL-17 production in patients with VKH disease. Methods: Blood samples were taken from 25 patients with VKH disease and 16 healthy controls. Peripheral blood mononuclear cells (PBMCs) were subjected to analysis of IL-23p19 mRNA and IL-23 protein expression using RT-PCR and ELISA, respectively. The IL-17 levels in the supernatants of PBMCs and CD4(+) T cells cultured in the absence or presence of recombinant (r)IL-23, rIL-12, or anti-IFN-gamma were determined by ELISA. Results: The patients with VKH disease with active uveitis showed an elevated level of IL-23p19 mRNA in PBMCs, higher IL-23 in the serum and supernatants of PBMCs, and increased production of IL-17 by polyclonally stimulated PBMCs and CD4+ T cells. Recombinant IL-23 significantly enhanced IL-17 production, whereas rIL-12 and IFN-gamma inhibited IL-17 production. More importantly, IL-17 production was significantly increased in patients with active uveitis in the presence of rIL-23. Both rIL-23 and rIL-12 enhanced IFN-gamma production. Conclusion: The results suggest that IL-23-stimulated production of IL-17 by CD4+ T cells may be responsible for the development of uveitis seen in patients with VKH disease. Clinical implications: This study provides a new insight into the mechanism involved in the development of VKH disease.
Original languageEnglish
Pages (from-to)1218-1224
JournalJournal of Allergy and Clinical Immunology
Issue number5
Publication statusPublished - 2007


  • proinflammatory cytokine production
  • autoimmune inflammation
  • sympathetic ophthalmia
  • rheumatoid-arthritis
  • human keratinocytes
  • interferon-gamma
  • interleukin-17
  • expression
  • lymphocytes
  • distinct


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