Abstract
Vogt-Koyanagi-Harada (VKH) syndrome is a systemic autoimmune disease. CD4+ T cells have been shown to be involved in autoimmune diseases including VKH syndrome. To screen aberrantly expressed membrane proteins in CD4+ T cell from patients with active VKH syndrome, blood samples were taken from five patients with active VKH syndrome and five healthy individuals. A label-free quantitative proteomic strategy was used to identify the differently expressed proteins between the two groups. The results revealed that the expression of 102 peptides was significantly altered (p<0.05) between two groups and matched amino acid sequences of proteins deposited in the international protein index (ipi.HUMAN.v3.36.fasta). The identified peptides corresponded to 64 proteins, in which 30 showed more than a 1.5-fold difference between the two groups. The decreased expression of CD18 and AKNA transcription factor (AKNA), both being three-fold lower than controls in expression identified by the label-free method, was further confirmed in an additional group of five active VKH patients and six normal individuals using the Western blot technique. A significantly decreased expression of CD18 and AKNA suggests a role for both proteins in the pathogenesis of this syndrome.
Highlights
Vogt-Koyanagi-Harada (VKH) syndrome is an autoimmune disorder mainly affecting systemic melanocytes including those in the eyes, meninges, ears, skin, and hair [1]
The mechanisms involved in VKH syndrome are not fully elucidated, previous reports have showed that CD4+ T cells sensitive to melanocytes are responsible for the development of VKH syndrome [3,4]
The obtained CD4+ T cells from both groups were subjected to label-free quantitative proteomic analysis followed by Western blot validation
Summary
Vogt-Koyanagi-Harada (VKH) syndrome is an autoimmune disorder mainly affecting systemic melanocytes including those in the eyes, meninges, ears, skin, and hair [1]. It is one of the most common uveitis entities in China as well as in the Far East of Asia. Recent studies have shown that molecules related to CD4+ T cell function, including Fas/FasL [5,6], T-bet [7], IFN-c, RORct and IL-17 [7,8], are involved in the pathogenesis of this syndrome. As CD4+ T cells exert their role principally through a variety of receptors, adhesion molecules,transport proteins and costimulatory molecules,which have been found mainly in the plasma membrane or endomembrane systems, our study focused on the differentially expressed proteins in the CD4+ T cell membrane of VKH patients
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