Figure 1.
The NK receptor KIR3DL2 is expressed by tumor cells in patients with acute-type ATL. (A) Heat map showing NK receptor expression (defined using FC) in PBMCs sampled from 5 healthy controls (HCs), 2 patients with enteropathy-associated T-cell lymphoma (EATL), 2 patients with T-cell prolymphocytic leukemia (T-LPL), 2 patients with Sezary syndrome (SS), 1 patient with peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS), and 21 patients with ATL. The heat map represents the ratio of fluorescence intensity, as regards the isotypic control (IgG1), expressed as an arbitrary unit, to scale the color code of the heat map using the cytobank software (https://www.cytobank.org). High protein expressions are shown in yellow, and negative protein expressions are shown in black. KIR3DL2 was the only NKR expressed on ATL tumor cells among those studied. (B) IHC assessment of KIR3DL2 protein expression on representative lymph node biopsy specimens (original magnification, ×200), showing that a patient with acute-type ATL (P25) expressed KIR3DL2, whereas a patient with lymphoma-type ATL (P57) did not. (C) Percentage of KIR3DL2+ cells among tumor cells in patients with ATL by FC or IHC, according to the ATL subtype (acute, lymphoma, and chronic type). (D) Example of a patient (P18) with KIR3DL2− chronic-type ATL, which became KIR3DL2+ at the time of the transformation into an acute-type ATL. After 12 months of evolution, the patient presented with lymphocytosis (38.3 × 103 μL) with 96% abnormal KIR3DL2+ lymphocytes, high levels of lactate dehydrogenase, and lymph node and central nervous system involvement, leading to a diagnosis of an acute-type ATL. (E) KIR3DL2 mRNA expression (assessed by qRT-PCR) in PBMCs from 48 patients with ATL, 5 HTLV-1 carriers, CD4+ T lymphocytes from 4 healthy donors, and Hut 78 cells (2-sided Mann-Whitney nonparametric test). Two patients (P13 and P36) with high KIR3DL2 mRNA expression levels were diagnosed as having chronic-type ATL at the time of mRNA analysis; subsequently, the diseased transformed into KIR3DL2+ acute-type ATL.

The NK receptor KIR3DL2 is expressed by tumor cells in patients with acute-type ATL. (A) Heat map showing NK receptor expression (defined using FC) in PBMCs sampled from 5 healthy controls (HCs), 2 patients with enteropathy-associated T-cell lymphoma (EATL), 2 patients with T-cell prolymphocytic leukemia (T-LPL), 2 patients with Sezary syndrome (SS), 1 patient with peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS), and 21 patients with ATL. The heat map represents the ratio of fluorescence intensity, as regards the isotypic control (IgG1), expressed as an arbitrary unit, to scale the color code of the heat map using the cytobank software (https://www.cytobank.org). High protein expressions are shown in yellow, and negative protein expressions are shown in black. KIR3DL2 was the only NKR expressed on ATL tumor cells among those studied. (B) IHC assessment of KIR3DL2 protein expression on representative lymph node biopsy specimens (original magnification, ×200), showing that a patient with acute-type ATL (P25) expressed KIR3DL2, whereas a patient with lymphoma-type ATL (P57) did not. (C) Percentage of KIR3DL2+ cells among tumor cells in patients with ATL by FC or IHC, according to the ATL subtype (acute, lymphoma, and chronic type). (D) Example of a patient (P18) with KIR3DL2− chronic-type ATL, which became KIR3DL2+ at the time of the transformation into an acute-type ATL. After 12 months of evolution, the patient presented with lymphocytosis (38.3 × 103 μL) with 96% abnormal KIR3DL2+ lymphocytes, high levels of lactate dehydrogenase, and lymph node and central nervous system involvement, leading to a diagnosis of an acute-type ATL. (E) KIR3DL2 mRNA expression (assessed by qRT-PCR) in PBMCs from 48 patients with ATL, 5 HTLV-1 carriers, CD4+ T lymphocytes from 4 healthy donors, and Hut 78 cells (2-sided Mann-Whitney nonparametric test). Two patients (P13 and P36) with high KIR3DL2 mRNA expression levels were diagnosed as having chronic-type ATL at the time of mRNA analysis; subsequently, the diseased transformed into KIR3DL2+ acute-type ATL.

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