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Transplantation of major histocompatibility complex‐mismatched mouse neural precursor cells (NPCs) into mice persistently infected with the neurotropic JHM strain of mouse hepatitis virus (JHMV) results in rapid rejection that is mediated, in part, by T cells. However, the contribution of the innate immune response to allograft rejection in a model of viral‐induced neurological disease has not been well defined. Herein, we demonstrate that the natural killer (NK) cell‐expressing‐activating receptor NKG2D participates in transplanted allogeneic NPC rejection in mice persistently infected with JHMV. Cultured NPCs derived from C57BL/6 (H‐2 b ) mice express the NKG2D ligand retinoic acid early precursor transcript (RAE)‐1 but expression was dramatically reduced upon differentiation into either glia or neurons. RAE‐1 +  NPCs were susceptible to NK cell‐mediated killing whereas RAE‐1 −  cells were resistant to lysis. Transplantation of C57BL/6‐derived NPCs into JHMV‐infected BALB/c (H‐2 d ) mice resulted in infiltration of NKG2D + CD49b +  NK cells and treatment with blocking antibody specific for NKG2D increased survival of allogeneic NPCs. Furthermore, transplantation of differentiated RAE‐1 −  allogeneic NPCs into JHMV‐infected BALB/c mice resulted in enhanced survival, highlighting a role for the NKG2D/RAE‐1 signaling axis in allograft rejection. We also demonstrate that transplantation of allogeneic NPCs into JHMV‐infected mice resulted in infection of the transplanted cells suggesting that these cells may be targets for infection. Viral infection of cultured cells increased RAE‐1 expression, resulting in enhanced NK cell‐mediated killing through NKG2D recognition. Collectively, these results show that in a viral‐induced demyelination model, NK cells contribute to rejection of allogeneic NPCs through an NKG2D signaling pathway. S tem  C ells   2014;32:2690–2701

Activating Receptor NKG2D Targets RAE‐1‐Expressing Allogeneic Neural Precursor Cells in a Viral Model of Multiple Sclerosis