Low Vγ9Vδ2 T-cell phenotype is associated with phenotypical changes. (A) Expression of surface Vγ9Vδ2 T-cell coreceptors in the FILO cohorts according to the frequency group of Vγ9Vδ2 T cells: percentage of cells positive for CD57 (n = 123), NKG2A (n = 116), DNAM-1 (n = 116), NKG2D (n = 115), and CD56 (n = 123). (B) Vγ9Vδ2 T cells from PBMCs of HVs and patients with AML from the HEMATOBIO cohort were manually pregated and exported in OMIQ for t-SNE analysis. Subsampling was performed for HVs and for each patient group with a fixed number of 100 000 Vγ9Vδ2 T cells for each group (HV, n = 8; patients with AML with low Vγ9Vδ2 T cells, n = 12; patients with AML with high Vγ9Vδ2 T cells, n = 7). Vγ9Vδ2 T cells were analyzed using t-the t-SNE dimensionality reduction algorithm. In the left panel, the density of Vγ9Vδ2 T-cell subsets in each patient group is projected (blue, low cell density; red, high cell density). The expression of markers of Vγ9Vδ2 T cells is projected onto t-SNE maps in the right panel (blue, low expression; red, high expression). (C-H) Maturation phenotype and expression of surface Vγ9Vδ2 T-cell coreceptors from PBMCs of HVs (n = 18) and patients with AML from the HEMATOBIO cohort (n = 40) according to the Vγ9Vδ2 T-cell frequency group (n = 20 in each group): (C) percentage of Vγ9Vδ2 T cells positive for NKG2A, CD57, DNAM-1, NKG2D, and CD56; (D) percentage of Vγ9Vδ2 T cells positive for CD16, CD69, CD8, CD28, and CD25; (E) maturation phenotype of Vγ9Vδ2 T cells according to the expression of CD45RA and CD27; (F) percentage of Vγ9Vδ2 T cells positive for OX40, 4-1BB, CD44, CCR7, and CD127; (G) percentage of Vγ9Vδ2 T cells positive for BTLA, TIGIT, PD-1, CTLA4, and TIM3; (H) percentage of Vγ9Vδ2 T cells positive for LAG3, HVEM, ICOS, PDL-1, CD95, and CD4. (I-J) BTN3A expression was assessed by flow cytometry on the surface of primary blasts from patients with AML (n = 27), the relative number of BTN3A molecules was quantified with MESF (molecules of equivalent soluble fluorochrome) method, using the anti-BTN3A 108.5 (I) and 20.1 epitopes (J). Results are presented as mean ± standard deviation (SD) (A, C-H) or as box plots (I-J), and statistical significance was established using a Mann-Whitney test (A), or a Kruskal-Wallis test followed by a Dunn's test (C-H), or a t test (I-J). ∗P < .5; ∗∗P < .01.

Low Vγ9Vδ2 T-cell phenotype is associated with phenotypical changes. (A) Expression of surface Vγ9Vδ2 T-cell coreceptors in the FILO cohorts according to the frequency group of Vγ9Vδ2 T cells: percentage of cells positive for CD57 (n = 123), NKG2A (n = 116), DNAM-1 (n = 116), NKG2D (n = 115), and CD56 (n = 123). (B) Vγ9Vδ2 T cells from PBMCs of HVs and patients with AML from the HEMATOBIO cohort were manually pregated and exported in OMIQ for t-SNE analysis. Subsampling was performed for HVs and for each patient group with a fixed number of 100 000 Vγ9Vδ2 T cells for each group (HV, n = 8; patients with AML with low Vγ9Vδ2 T cells, n = 12; patients with AML with high Vγ9Vδ2 T cells, n = 7). Vγ9Vδ2 T cells were analyzed using t-the t-SNE dimensionality reduction algorithm. In the left panel, the density of Vγ9Vδ2 T-cell subsets in each patient group is projected (blue, low cell density; red, high cell density). The expression of markers of Vγ9Vδ2 T cells is projected onto t-SNE maps in the right panel (blue, low expression; red, high expression). (C-H) Maturation phenotype and expression of surface Vγ9Vδ2 T-cell coreceptors from PBMCs of HVs (n = 18) and patients with AML from the HEMATOBIO cohort (n = 40) according to the Vγ9Vδ2 T-cell frequency group (n = 20 in each group): (C) percentage of Vγ9Vδ2 T cells positive for NKG2A, CD57, DNAM-1, NKG2D, and CD56; (D) percentage of Vγ9Vδ2 T cells positive for CD16, CD69, CD8, CD28, and CD25; (E) maturation phenotype of Vγ9Vδ2 T cells according to the expression of CD45RA and CD27; (F) percentage of Vγ9Vδ2 T cells positive for OX40, 4-1BB, CD44, CCR7, and CD127; (G) percentage of Vγ9Vδ2 T cells positive for BTLA, TIGIT, PD-1, CTLA4, and TIM3; (H) percentage of Vγ9Vδ2 T cells positive for LAG3, HVEM, ICOS, PDL-1, CD95, and CD4. (I-J) BTN3A expression was assessed by flow cytometry on the surface of primary blasts from patients with AML (n = 27), the relative number of BTN3A molecules was quantified with MESF (molecules of equivalent soluble fluorochrome) method, using the anti-BTN3A 108.5 (I) and 20.1 epitopes (J). Results are presented as mean ± standard deviation (SD) (A, C-H) or as box plots (I-J), and statistical significance was established using a Mann-Whitney test (A), or a Kruskal-Wallis test followed by a Dunn's test (C-H), or a t test (I-J). ∗P < .5; ∗∗P < .01.

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