Figure 2
Figure 2. Detection of circulatory hTERT461-469-specific CTL precursors in the periphery of ATL patients. (A) hTERT461-469-specific CTL precursors in PBMCs repetitively stimulated with hTERT461-469 peptide from HLA-A*24:02+ ATL patients were detected by using HLA-A*24:02/hTERT461-469 tetramer. A representative case is shown. HLA-A*24:02/HIV tetramer was used as a negative control. (B) In comparison with HLA-A*24:02− ATL patients (●) (n = 3) and HLA-A*24:02+ healthy individuals (▲) (n = 6), the frequency of hTERT461-469-specific CTL precursors in HLA-A*24:02+ ATL patients (▪) (n = 7) was significantly high (*P < .01; **P < .05). The frequency was 0.88% ± 0.55% for HLA-A*24:02+ ATL patients, 0.11% ± 0.1% for HLA-A*24:02− ATL patients, and 0.2% ± 0.04% for HLA-A*24:02+ healthy individuals (mean ± SD).

Detection of circulatory hTERT461-469-specific CTL precursors in the periphery of ATL patients. (A) hTERT461-469-specific CTL precursors in PBMCs repetitively stimulated with hTERT461-469 peptide from HLA-A*24:02+ ATL patients were detected by using HLA-A*24:02/hTERT461-469 tetramer. A representative case is shown. HLA-A*24:02/HIV tetramer was used as a negative control. (B) In comparison with HLA-A*24:02 ATL patients (●) (n = 3) and HLA-A*24:02+ healthy individuals (▲) (n = 6), the frequency of hTERT461-469-specific CTL precursors in HLA-A*24:02+ ATL patients (▪) (n = 7) was significantly high (*P < .01; **P < .05). The frequency was 0.88% ± 0.55% for HLA-A*24:02+ ATL patients, 0.11% ± 0.1% for HLA-A*24:02 ATL patients, and 0.2% ± 0.04% for HLA-A*24:02+ healthy individuals (mean ± SD).

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