Figure 1
Figure 1. Function of NK cells expressing inhibitory KIR is altered immediately after TCD-HSCT. Shown is the percentage of IFN-γ–producing cells among KIR-expressing NK populations from the HLA-C1/C1, Bw6/Bw6 donor, the HLA-identical patient (patient no. 2) before transplantation, and the patient at day +30, day +60, and day +200 after HSCT after coincubation with the indicated target cells. (A) NK cells exclusively expressing the inhibitory KIR for self-HLA class I (S-KIR) KIR2DL3 after HSCT are hyperresponsive compared with the donor and patient pre-HSCT, normalizing to donor level by day +200, and reactivity is inhibited upon challenge with the cognate class I ligand HLA-Cw3. NK cells exclusively expressing the inhibitory KIR for the non-self HLA class I (NS-KIR) KIR2DL1 (B) or KIR3DL1 (C) are functionally competent compared with the donor and patient pre-HSCT, reacting to lack of ligand. Reactivity is inhibited upon challenge with the cognate class I ligands HLA-Cw4 or Bw4, respectively.

Function of NK cells expressing inhibitory KIR is altered immediately after TCD-HSCT. Shown is the percentage of IFN-γ–producing cells among KIR-expressing NK populations from the HLA-C1/C1, Bw6/Bw6 donor, the HLA-identical patient (patient no. 2) before transplantation, and the patient at day +30, day +60, and day +200 after HSCT after coincubation with the indicated target cells. (A) NK cells exclusively expressing the inhibitory KIR for self-HLA class I (S-KIR) KIR2DL3 after HSCT are hyperresponsive compared with the donor and patient pre-HSCT, normalizing to donor level by day +200, and reactivity is inhibited upon challenge with the cognate class I ligand HLA-Cw3. NK cells exclusively expressing the inhibitory KIR for the non-self HLA class I (NS-KIR) KIR2DL1 (B) or KIR3DL1 (C) are functionally competent compared with the donor and patient pre-HSCT, reacting to lack of ligand. Reactivity is inhibited upon challenge with the cognate class I ligands HLA-Cw4 or Bw4, respectively.

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