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. 2018 Sep 25;115(41):10410–10415. doi: 10.1073/pnas.1804108115

Fig. 1.

Fig. 1.

GBS strain A909 (GBS A909) interacts with human NK cells through the cell wall-anchored β-protein and Siglec-7 receptor. (A) Images taken by confocal microscopy show even distribution of Siglec-7 (red) across the cell surface of human NK cells under normal conditions. When NK cells are infected with FITC-labeled GBS (green), Siglec-7 on NK cells clusters toward GBS. Infection with β-protein–deficient mutant GBS ΔBAC restores the even distribution of Siglec-7 across the surface of NK cells. (B) Flow cytometry histograms of WT GBS A909 and ΔBAC stained with recombinant chimeric Siglec-7-Fc protein or IgG-Fc control. GBS A909 stained with Siglec-7-Fc showed positive signals above IgG-Fc, but GBS ΔBAC did not display any positive signals.