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. Author manuscript; available in PMC: 2009 Jul 21.
Published in final edited form as: Curr Immunol Rev. 2009 Feb;5(1):22–34. doi: 10.2174/157339509787314369

Fig. (2). Commonalities between the pathways that induce NKG2D ligand expression in cancer, viral infection, and healthy cells.

Fig. (2)

There is evidence that the pathways leading to expression of NKG2D ligands in “stressed cells” could be closely related to those involved in NKG2D ligand expression on healthy cells. A role for ATM/ATR mediated phosphorylation of checkpoint kinase-1(chk1) in NKG2D ligand induction was first reported to occur in response to DNA damage [22]. Subsequently it has been shown that RAE-1 expression in class switching B cells, and on infection with a transforming retrovirus (Abelson murine leukaemia virus), is dependant on activation-induced cytidine deaminase (AID) mediated chk1 phosphorylation; a pathway that implies a role for ATM [54]. ATM/ATR and chk1 have also been implicated in the expression of NKG2D ligands on activated T cells [39]. The precise mechanism by which chk1 induces NKG2D ligand gene expression is unknown. ATM/ATR and chk1 are known to be regulators of cell division. Therefore increased cellular proliferation could be the crucial commonality between these four scenarios that result in NKG2D ligand expression.