Br J Ophthalmol 92:557-561 doi:10.1136/bjo.2007.128769
  • Original Article
    • Laboratory science

Leptin increases in Vogt–Koyanagi–Harada (VKH) disease and promotes cell proliferation and inflammatory cytokine secretion

  1. L Liu1,2,
  2. P Yang1,2,
  3. H He1,2,
  4. X Lin1,2,
  5. L Jiang1,2,
  6. W Chi1,2,
  7. C Zhao1,2,
  8. H Zhou1,2
  1. 1
    State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, PR China
  2. 2
    Uveitis Study Center, Sun Yat-sen University and International Uveitis Study Laboratory, Guangzhou, PR China
  1. Professor P Yang, Zhongshan Opthalmic Center, Sun Yat-sen University, 54 Xianlie Road, Guangzhou 510060, PR China; peizengy{at}
  • Accepted 26 December 2007
  • Published Online First 1 February 2008


Backgroud/aims: Leptin has recently been found to play an important role in the development of autoimmune diseases. Our study is designed to investigate the expression and possible role of leptin in the pathogenesis of Vogt–Koyanagi–Harada (VKH) disease, one of the common types of autoimmune uveitis in China.

Methods: Leptin levels in serums of 20 active, 16 inactive VKH patients and 20 healthy controls were measured using ELISA. Peripheral blood mononuclear cells (PBMCs) separated from active VKH patients and healthy controls were cultured with recombinant human leptin, and cell proliferation was assayed by [3H]-TdR incorporation. Cytokine levels in the supernatant of PBMCs cultured in mixed lymphocyte reaction (MLR) upon stimulation with leptin were assayed by ELISA.

Results: Our results showed that leptin was significantly increased in the serum of active VKH patients compared with that in inactive VKH patients and healthy controls. Leptin levels in active VKH patients remained markedly higher when divided by body mass index (BMI). PBMCs cultured with leptin induced a marked cell proliferation and profound secretion of IFN-γ and IL-17.

Conclusion: These findings suggest that leptin may be involved in the development of VKH disease possibly by promoting an immune response.


  • Funding: This study was supported by Project of International Cooperation in Science and Technology, Guangdong Province (2004B50301002, 2006A50107001), Project of Science and Technology of Guangdong Province (2005B60302009), Key Project of Natural Science Foundation (30630064).

  • Competing interests: None.

  • Patient consent: All patients and controls signed the informed consents.

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