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. 2019 Sep 11;10:2164. doi: 10.3389/fimmu.2019.02164

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Copyright © 2019 Segerberg, Lundtoft, Reid, Hjorton, Leonard, Nordmark, Carlsten and Hagberg.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Anti-KIR autoantibodies induce hyporesponsiveness in NK cells. (A) NK cell degranulation and (B) viability of IL-2-activated PBMCs from 3 HDs following incubation with K562 cells, rituximab (RTX, anti-CD20), or IgG as indicated. (C) K562-induced degranulation in NK cells from 6 HDs exposed to IgG from patient SLE3, SLE138, or HDs (IVIG) relative to no IgG. P-values from a repeated measures one-way ANOVA comparing the relative degranulation in IgG-treated cells to untreated cells are shown. (D) Correlation between the difference in degranulation and the difference in cytotoxicity of IgG-treated NK cells compared to non-treated NK cells. (E) Comparison of the education level and the inhibitory effect of SLE138-IgG on degranulation compared to no IgG. Education level was defined as the difference in degranulation in indicated NK cell subsets relative to KIR-negative NK cells (KIR2DL1/DS1⁻KIR2DL2/DL3/DS2⁻KIR3DL1/DS1⁻) in the absence of IgG. (A–E) Data from patient SLE3 and SLE138 are colored in red and blue, respectively.