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. Author manuscript; available in PMC: 2016 Mar 24.
Published in final edited form as: J Innate Immun. 2015 Mar 24;7(6):557–562. doi: 10.1159/000375494

Figure 1. Mechanisms of NK cell memory formation.

Figure 1

During MCMV infection, naïve NK cells that express the activating receptor Ly49H recognize the virally encoded glycoprotein m157 on the surface of MCMV-infected host cells, resulting in the robust activation and proliferation of antigen specific NK cells. This process is critically dependent on pro-inflammatory IL-12 signaling through STAT4 and Zbtb32, and co-stimulatory signaling through the activating receptor DNAM-1. During clonal proliferation, antigen specific NK cells maintain viability by increasing the expression of miR155 to antagonize the pro-death factors Noxa and SOCS1; however, at the peak of virus-driven expansion, effector NK cells undergo BIM-mediated cell death to form a stable pool of long lived memory NK cells in a process that depends on endogenous IL-15. MCMV-elicited memory NK cells can respond robustly to secondary challenge with MCMV, but are less responsive to heterologous infection.