Figure 4.
Figure 4. The clonal architecture of the HLA-A2−granulocytes in case 3. (A) The changes in the VAF of LRCH1- and PRR5L-mutant clones during the 12-year observation period. (B) The clonal composition of HLA− granulocytes, as revealed by HLA-A–allelic sequencing. An HLA-A*02:06-mutant clone (nonsense mutation) accounted for 5% of HLA-A2− granulocytes. (C) The chronological changes in the percentage of GPI-AP− granulocytes and HLA-A2− granulocytes. (D) The genotypes of 27 colonies derived from PB non-T–nonadherent cells. Whether individual colonies are positive or negative for the amplified product of A*02:06, mutated LRCH1, and mutated PRR5L sequences (top panel) and the summary of the colony genotypes (bottom panel) are shown. (E) The results of HUMARA. The relatively low S score (0.56), of the HLA− granulocytes was compatible with the results of HLA-A*02:06 sequencing, which showed triclonality.

The clonal architecture of the HLA-A2−granulocytes in case 3. (A) The changes in the VAF of LRCH1- and PRR5L-mutant clones during the 12-year observation period. (B) The clonal composition of HLA− granulocytes, as revealed by HLA-A–allelic sequencing. An HLA-A*02:06-mutant clone (nonsense mutation) accounted for 5% of HLA-A2− granulocytes. (C) The chronological changes in the percentage of GPI-AP− granulocytes and HLA-A2− granulocytes. (D) The genotypes of 27 colonies derived from PB non-T–nonadherent cells. Whether individual colonies are positive or negative for the amplified product of A*02:06, mutated LRCH1, and mutated PRR5L sequences (top panel) and the summary of the colony genotypes (bottom panel) are shown. (E) The results of HUMARA. The relatively low S score (0.56), of the HLA− granulocytes was compatible with the results of HLA-A*02:06 sequencing, which showed triclonality.

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