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Label-Free Proteomics Reveals Decreased Expression of CD18 and AKNA in Peripheral CD4(+) T Cells from Patients with Vogt-Koyanagi-Harada Syndrome

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 f...

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Detalles Bibliográficos
Autores principales: Mao, Liming, Yang, Peizeng, Hou, Shengping, Li, Fuzhen, Kijlstra, Aize
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030555/
https://www.ncbi.nlm.nih.gov/pubmed/21297967
http://dx.doi.org/10.1371/journal.pone.0014616
Descripción
Sumario: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.