KIR2DS1 does not affect alloreactive NK-cell repertoires. (A) A total of 11 999 NK-cell clones were generated from 110 HLA-C1⁺ individuals (mean 109 clones/individual [30-302]) and were screened for cytotoxicity against HLA-C1–missing, HLA-C2/C2 PHA T-cell blasts. Frequencies (mean ± SD) of alloreactive NK-cell clones in the 65 individuals without the KIR2DS1 gene (open bar) and in the 45 individuals with the KIR2DS1 gene (closed bar) are shown (P = NS by unpaired Student t test). (B) The KIR2DS1^– and KIR2DS1⁺ individuals in (A) were grouped according to their KIR2DL2 or KIR2DL3 homozygous or KIR2DL2/3 heterozygous inhibitory genotypes. Frequencies of alloreactive NK-cell clones in KIR2DS1^– (open bar) and KIR2DS1⁺ (closed bar) individuals are shown (P = NS by unpaired Student t test). (C) A total of 2281 clones obtained from 20 HLA-C1⁺ individuals (randomly selected from the 110 in [A]) were screened for allocytotoxicity against HLA-C1–missing, HLA-C2C2 PHA T-cell blasts. The contribution of KIR2DS1 to lysis was evaluated in 127 allocytotoxic NK-cell clones that expressed KIR2DL2/L3 (as evaluated by phenotypic analyses). Lysis (mean ± SD) by the 92 clones that did not express KIR2DS1 (open bar) and the 35 clones that expressed KIR2DS1 (closed bar) is shown.