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. 2019 Jan 24;10:412. doi: 10.1038/s41467-019-08311-0

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — HLA class I and II alleles and KIR genotype. a HLA class I A, B and C with corresponding allotype designations (non-Bw4, Bw6, Bw4-80TA, C1 and C2), and HLA class II DPB1, DQB1 and DRB1 alleles are indicated as allele 1 and 2. HLA B*44:03:01 has a threonine (T) at position 80 as part of the Bw4 epitope (NLRTALR) of the α1 helix 2 of the molecule—and therefore will bind to KIR3DL1 on NK cells. HLA- Cw*07:01:01 (allotype C1) and Cw*04:01:01 (C2) have a lysine (K) and asparagine (N) at position 80, respectively—allowing for interaction with both KIR2DL3 (C1) and 2DL1 (C2) on NK cells. b The presence (coloured box) or absence of 16 KIR genes (14 functional and 2 pseudogenes 2DP1 and 3DP1) is shown. The child has an AA1 genotype, which has 9 KIR genes, has 2 copies of KIR3DL1 and 2 copies of activating gene KIR2DS4 with one full-length (f) and one truncated (v) version (heterozygous f/v). 2D: 2-domain; 3D: 3-domain; L: long tail, inhibitory; S: short tail, activating