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. 2016 Jan 7;12(1):e1005349. doi: 10.1371/journal.ppat.1005349

Fig 2. TIGIT expression on CD8+ terminal effector T cells and HIV-specific CD8+ T cells.

Fig 2

Cryopreserved PBMCs were thawed and surface phenotyped for TIGIT expression on CD8+ T cell compartments. (A) Graph shows compiled frequency (%) of TIGIT+ CD8+ T cell expression in differentiated compartments stratified by disease status. HIV-uninfected healthy donors (HD, X; n = 20), acute infected (AI, open diamond; n = 24), cART suppressed (AS, open triangle; n = 20), elite controller (EC, open square; n = 20), non-controllers (NC, open circle; n = 20). P values were calculated using one-way ANOVA, followed by Tukey’s multiple comparisons test (*p < 0.05; **p < 0.01; ***p < 0.001). PBMCs from HLA-A*02:01 or HLA-B*07:02 HIV chronically infected individuals were stained with matched HLA pentamers presenting HIV-1 and CMV epitopes and anti-TIGIT. (B) Representative flow cytometry plots of pentamer-specific CD8+ T cells using HLA-A*02:01 HIV-1 Gag SLYNTVATL (A2*SL9), HLA-A*02:01 HIV-1 Pol ILKEPVHGV (A2*IV9), HLA-B*07:02 HIV-1 Env IPRRIRQGL (B7*IL9), HLA-B*07:02 HIV-1 Nef TPGPGVRYPL (B7*TL10), and HLA-A*02:01 CMV pp65 NLVPMVATV (A2*NV9) (C) Compiled data of TIGIT expression frequency (%) on pentamer specific CD8+ T cells which was recalculated to 100% (left panel, n = 9) compiled data of TIGIT geometric mean fluorescence intensity (GMFI) on pentamer specific CD8+ T cells (right panel, n = 9).