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. 2018 Apr 26;131(25):2803–2815. doi: 10.1182/blood-2017-09-808816

Figure 2.

Figure 2.

LGL leukemia cells are resistant to TRAIL-induced apoptosis and primarily express TRAIL receptor DcR2. (A) NKL, TL-1, and Jurkat cells were treated with either vehicle (normal saline) or rhTRAIL (10 ng/mL) for 48 hours. Cells were stained with Annexin-V and 7-AAD and analyzed by flow cytometry to identify apoptotic cells. Data are presented as mean ± SEM and representative of 3 separate experiments (ANOVA, *P < .0001 Jurkat cells vs TL-1 and NKL). (B) PBMCs isolated from normal donors (n = 4), NK-LGL patients (n = 4), and T-LGL patients (n = 9) were treated with either vehicle (normal saline) or rhTRAIL (10 ng/mL) for 48 hours. Cells were stained with Annexin-V and 7-AAD and analyzed by flow cytometry to identify apoptotic cells. Data represent mean ± SEM. (C) PBMCs from normal donors or LGL leukemia patients were assessed for their cell surface expression of TRAIL receptors using flow cytometry. Percentage of LGL cells from pathology flow cytometry report is shown below the horizontal axis. (D) PBMCs from normal donors, without or with activation (Act), or LGL leukemia patients were assessed for their cell surface expression of DcR2 receptor using flow cytometry to stratify samples based on CD3, CD8, and CD57 expression.