Figure 7
Figure 7. Low-dose and long-term exposure to 5-aza-cytidine promotes NK-cell ontogeny. (A-B) 5-Aza-cytidine does not significantly alter the expression of KIR2DL1/S1/S4, KIR2DL2/L3/S2, and KIR3DL1 (A), or other inhibitory or activating NK-cell receptors (B), on BM-derived NK cells of huNSG mice. (C) 5-Aza-cytidine induces the expression of BM-residing NK-cell precursors. Frequencies of the indicated NK-cell subpopulations in the BM of 5-aza-cytidine–treated or control huNSG mice (as defined by Freud22): preNK (CD34+CD117+), iNK (CD34−CD117lowCD94−), CD94+ mNK cells (CD34−CD117−CD94+NKp46+), and CD94− mNK cells (CD34−CD117−CD94−NKp46+). Data represent 2 independent experiments with a total of 11 huNSG mice and 14 control NSG mice. n.s., not significant.

Low-dose and long-term exposure to 5-aza-cytidine promotes NK-cell ontogeny. (A-B) 5-Aza-cytidine does not significantly alter the expression of KIR2DL1/S1/S4, KIR2DL2/L3/S2, and KIR3DL1 (A), or other inhibitory or activating NK-cell receptors (B), on BM-derived NK cells of huNSG mice. (C) 5-Aza-cytidine induces the expression of BM-residing NK-cell precursors. Frequencies of the indicated NK-cell subpopulations in the BM of 5-aza-cytidine–treated or control huNSG mice (as defined by Freud22 ): preNK (CD34+CD117+), iNK (CD34CD117lowCD94), CD94+ mNK cells (CD34CD117CD94+NKp46+), and CD94 mNK cells (CD34CD117CD94NKp46+). Data represent 2 independent experiments with a total of 11 huNSG mice and 14 control NSG mice. n.s., not significant.

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