Table 1.
The clinical features of the investigated patients with VKH disease.
Figure 1.
Representative flow cytometric map of CD4+ T cells isolated from peripheral blood of active VKH patients.
The PBMC and freshly isolated CD4+ T cells were stained with the indicated markers using fluorescence-labeled mAb and analyzed by flow cytometry. Before sorting, the ratio of CD4+ T cells in PBMC was 38.11% (A). After microbeads based sorting, the purity of CD4+ T cells was as high as 98.06% (B).
Figure 2.
Decyder MS intensity graphs of CD18 derived from LC-MS/MS analysis of a total membrane protein extracted from both normal group (A) and VKH group (B).
The location of peptide ALNEITESGR in both samples was labeled with square frames in the total graphs and the magnified graphs (C and D). Statistical analysis showed that the different expression of peptide ALNEITESGR was significant between VKH group and normal group (E).
Table 2.
The differently expressed proteins identified based on two or more peptides in CD4+ T cells between active VKH patients and normal individuals.
Table 3.
The differently expressed proteins identified based on single peptides in CD4+ T cells between active VKH patients and normal individuals.
Figure 3.
Validation of CD18 and AKNA by the Western blot technique.
Antibodies were used at a dilution of 1∶1000 for the anti-human CD18 monoclonal antibody and anti-human AKNA monoclonal antibody. Proteins were detected using the Phototope-HRP Western blot detection system(A). The immunoreactive band intensities were quantitated and were presented as intensity volumes (vol%). The results showed that both CD18 and AKNA were significantly down-regulated in VKH patients as compared to normal controls (B). VKH: VKH patients, NC: normal controls.