KLRK1 and infection: Since (i) both infection and damage were shown to upregulate NKG2DLs on myeloid cells, and (ii) factors produced in response to these events (by stroma, parenchymal, and immune cells) can induce or upregulate NKG2D on lymphocytes, an NKG2D-driven lymphocyte-myeloid cell crosstalk is expected to play an important role in these processes.