Yun-Sik Yang, (Icksan, South Korea), Song-Chul Balk, (Icksan, South Korea), Jeong-Un Jang, (Icksan, South Korea), Sook-Hee Lee, (Icksan, South Korea), Chang-Uk Choi, MD (Icksan, South Korea), Hun-Taeg Chung, MD, PhD (Icksan, South Korea)


Experimental Autoimmune Uveitis (EAU) is a prototypic T-cell mediated autoimmune disease in which the target tissue is the neural retina. EAU is induced in susceptible animals by immunization with evolutionarily conserved retinal proteins such as interphotoreceptor retinoid binding protein (IRBP) or their peptides.


There were prepared four test groups which were IRBP injected EAU induced group. EAU induced Hemin treated group, EAU induced SnPP treated group and normal control group. We analyzed the infiltration of proteins into vitreous bodies of rats with four groups using twodimensional electrophoresis and the spots were identified by MALDI-TOF or LC-MS/MS.


Forty-five spots were identified in the vitreous bodies of the rats. Thirty-four of these spots were members of the crystallin family. The truncated form of beta A4- and beta B2-crystallin were predominant in normal vitreous bodies, but there were more intact form of crystallins in EAU. However, alpha A- and B-crystallins were not truncated in normal.


These results suggest that crystalline family proteins are the major group of proteins involved in uveitic vitreous and C-terminal truncation of beta-crystlalllins may play a role in EAUrelated disease progression.