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. 2022 Mar 31;13:830396. doi: 10.3389/fimmu.2022.830396

Figure 2.

Figure 2

Molecular factors govern adaptive NK cell function. Fc segment of Abs can take shape specific signal of adaptive NK cells to recognize target cells by binding to CD16. NKG2C, CD2, TIGIT, and other unknown molecules may act as crucial signaling pathway for the activation or inhibition of adaptive NK cells. IL-12, IL-18, and other cytokines together constitute the pro-inflammatory cytokine signal, which guides adaptive NK cell differentiation, expansion, and activation. Epigenetic programming promotes stochastic DNA methylation-dependent allelic silencing of FCER1G, SYK, and SH2D1B. These ultimately contribute to IFNG promoter hypomethylation and format heterogeneous adaptive NK cell repertoire. The up-regulation of ARID5B and its inducing UQCRB with low H3K9Me2 in the promoter region alter metabolic reprogramming, prolong survival, and motivate abundant IFN-γ secretion of adaptive NK cells. Abs, antibodies; CD, cluster of differentiation; TIGIT, T-cell immunoglobulin and ITIM domain; interleukin, IL; IFN-γ, Interferon-gamma; TNF-α, Tumor necrosis factor alpha; and ARID5B, AT-rich interaction domain 5.