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. Author manuscript; available in PMC: 2009 Nov 1.
Published in final edited form as: J Immunol. 2008 Nov 1;181(9):6293–6300. doi: 10.4049/jimmunol.181.9.6293

Figure 2. Mutations at positions 82 and 83 in the Bw4 motif of HLA-B*5101 reduce the capacity to engage KIR3DL1 and inhibit NK cells.

Figure 2

(A) Shows flow cytometric analysis with the anti-KIR3DL1 monoclonal antibody DX9 of NK cells from donors expressing different KIR3DL1 allotypes. NK cells from the 3DL1*005:*01502 heterozygous donor form a bimodal distribution in which the cells binding DX9 at low level express 3DL1*005 and the cells binding DX9 at high level express 3DL1*01502. The latter cells also include the small fraction of cells expressing both 3DL1*01502 and 3DL1*005; to signify this they are labeled as 3DL1*01502† cells. (B) Shows the interferon-γ response of NK cells cultured with 221 cells or 221 cells expressing wild-type (WT) or mutant HLA-B*5101. Cultures were performed in the absence or presence of the anti-HLA class I antibody DX17. Data shown here are the means from seven experiments. Statistically significant differences between mutant and wild-type are indicated by ***(p < 0.001), ** (p < 0.01), * (p < 0.05) as determined by Student's t-test. Error bars shown are SEM The antibody-blocking experiment was performed twice with similar results and data from one of those experiments is shown. (C) Shows the results of cytotoxicity assays in which NK cell clones expressing KIR3DL1*005 or KIR3DL1*01502† were incubated with 221 target cells expressing wild-type or mutant B*5101. The data were obtained at an effector to target ratio of 5:1 and are representative of five experiments.