Purpose:
To investigate the expression of major histocompatibility complexII (MHC-II) and co-stimulatory molecue B7.1/CD80 on retinalmicroglia after T cell factor interleukin-4 (IL-4) or advancedglycation end products (AGEs) stimulation. To further discussthe relationship between changes in microglial antigen presentingfunction and apoptotic cells in cultured rat retinal tissues.
Methods:
Retinal microglia harvested from mixed culture system were seededin Petri dishes in certain densities for different procedures.Culture medium of various IL-4 or AGEs levels were added intothe dishes as treating sample, with pure medium as controls.A portion of treated microglial cells were collected for MHC-IIand CD80 detection, while the others were washed and culturedin medium, subsequently co-cultured with rat retinas for another24 hours, followed by TUNEL analysis on the retinas.
Results:
Compared with controls, IL-4 elevated the expression of bothMHC-II and CD80, while AGEs supressed both. Western blottingdemonstrated the increase of MHC-II protein expression in microglialcells treated with IL-4, contrast to the AGEs group. However,the expression of CD80 protein in the IL-4 group, which markedlydecreased in the AGEs group, did not change markedly comparedto the controls. IL-4 treated microglia induced less apoptoticcells in co-cultured retinas than AGEs counterpats.
Conclusions:
Microglial behaviors depend on local microencironment. Appropriateregulation by IL-4 increase the antigen presenting functionof microglia, which is furtherly induced to be protective. Onthe other hand, AGEs renders microlgia destructive featuresby inhibiting its antigen presenting function.
Keywords: microglia • antigen presentation/processing • diabetic retinopathy