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. 2019 Dec 9;10:2730. doi: 10.3389/fimmu.2019.02730

Figure 2.

Figure 2

NK cell recognition of HLA-C. (A) Missing-self recognition leads to NK activation when the HLA-C group ligand for a KIR is absent (e.g., when HLA-C2 is absent in the presence of KIR2DL1 or HLA-C1 is absent in the presence of KIR2DL2/3); (B) Recognition of allogeneic HLA-C2 molecules (red) may occur through binding of KIR2DS1 to HLA-C2 molecules. Upon HLA-C2—KIR2DS1 interaction GM-CSF secretion by dNK has been shown; (C) Pathogen derived peptides (green) presented by HLA-C1 and HLA-C2 molecules can activate NK cells expressing the activating receptors KIR2DS1, KIR2DS2, and KIR2DS4 in processes that may enhance NK cytotoxicity, release of perforin (PRF) and granzymes (GZMs) and pathogen clearance; (D) HLA-C independent NK-EVT interactions include HLA-E and NKG2A/C as well as HLA-F and KIR3DS1 interactions that may lead to degranulation and release of perforin (PRF) and granzymes (GZMs). Interaction of HLA-G and KIR2DL4 was shown to inhibit dNK cytotoxicity and promote IFNɤ secretion.