Abstract
Purpose:
Studies have shown that, in the pathogenesis of uveitis, the damage of the immune privilege machanisms of retinal pigment epithelium (retinal pigment epithelium, RPE) would play an important role. Therefore, to study the RPE immune privilege function in uveitis is important for searching new treatment options.
Methods:
In our work, the POMC gene (precursor of a-MSH) will be over-expression or knockdown with lenti-virus infection system to RPE cells, then to study the immune privilege function of the RPE cells. In vitro study, RPE cells were treated with different doses of IL-17A, the expression of POMC was detected by real-time PCR and western blot. Secretion levels of TGF-β, IFN-γ and IL-17 were detected by ELISA.
Results:
In vitro study, the POMC gene (precursor of a-MSH) level decreased 10% in the RPE cells when treated with 1ng/ul IL-17A after 24h.The protein level of POMC decreased at the same time. Secretion levels of TGF-β, IFN-γ and IL-17 were detected by ELISA when simulated an inflammatory microenvironment of RPE cells by IL-17A. After 24h, secretion levels of IFN-γ and IL-17 were 3 folds and 5 folds each, while after stimulation with 48h, secretion level of TGF-β was decreased 40%. And we found the secretion levels of TGF-β, IFN-γ and IL-17 were different while the POMC gene (precursor of a-MSH) was over expressed in RPE cells.
Conclusions:
This study describes the POMC gene (precursor of a-MSH) may play a role in ocular immune privilege in the formation and maintenance. POMC may be a promising therapeutic target endophthalmitis.
Keywords: 701 retinal pigment epithelium •
553 immune tolerance/privilege