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. 2016 Feb 25;12(2):e1005396. doi: 10.1371/journal.ppat.1005396

Fig 2. Possible activating receptor and NK cell subpopulation involvement in recognition of T. gondii-infected cells.

Fig 2

The subpopulation of NK cells important for IFNγ-dependent protection, defined by specific activating (immunoreceptor tyrosine-based activating motif [ITAM]) receptors, is unknown. A. Infection of a target cell by T. gondii could induce stress, resulting in expression of ULBPs (Rae1, Mult1, or others), or alter self (MICA/B), Ly49-specific ligands, and/or NCR1 ligands (NCR1L, possible molecules vimentin or heparan sulfate glycoproteins [HSGP]). B. ULBPs or altered self-molecules would be recognized by NKG2D. Parasite-produced Ly49 ligands would be recognized by Ly49H or Ly49D. Host-derived NCR1 ligands would be recognized by NKp46 (NCR1). MHC Class I (MHCI) could be recognized by immunoreceptor tyrosine-based inhibitory motif (ITIM) receptors and SHP1/SHIP1 could impact signaling. C. NK cell-activating ligands that are recognized would activate the NK cell to produce cytokines (IFNγ), be cytotoxic, proliferate, and promote survival via signaling from either NKG2D-associated DAP10 or DAP12-dependent activation of Vav2/3/Sos1/PI3K or Syk/ZAP70/PI3K-dependent pathways, respectively, Ly49-associated DAP12-dependent activation of Syk/ZAP70/PI3K or NKp46-associated FcγR, and CD3ζ chain-dependent activation of Syk/ZAP70/PI3K signaling. Additional receptors not shown in figure include CD94/NKG2C, 2B4, FcRγIII, TRAIL, and IL-12R.