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. 2022 May 31;13:840388. doi: 10.3389/fimmu.2022.840388

Figure 3.

Figure 3

CD43, CD45, and CD162/PSGL-1 are the counterreceptors of Siglec-7. (A) Effect of glycoprotein knockout (KO) on Siglec-7–Fc binding. The glycoprotein genes (SPN, PTPRC, and SELPLG – encoding CD43, CD45, and CD162/PSGL-1, respectively) in JVM-3 were disrupted with CRISPR–Cas9 technology, and the cells were subjected to staining with Siglec-7–Fc. The disruption of individual genes led to a small but reproducible reduction in Siglec-7–Fc binding. Data was normalized by the Siglec-7–Fc binding (in MFI) to control JVM-3 cells. *P < 0.05, and **P < 0.01, one-way ANOVA with Dunnett’s post hoc test. Bars represent mean ± SD of 6 independent experiments. (B) Effect of glycoprotein KO on NK cell cytotoxicity. Glycoprotein KO and control JVM-3 cells were subjected to NK cell cytotoxicity assay. Disruption of CD45 and CD162/PSGL-1 led to increased sensitivity to NK cytotoxicity. A trend toward increased sensitivity of CD43 KO cells to NK cytotoxicity was observed, but it was not statistically significant (*P < 0.05 and ***P < 0.001, repeated-measures one-way ANOVA with Dunnett’s post hoc test). Bars represent mean ± SD of 23 independent experiments.