You are currently viewing the editor's summary.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
Register for free to read this article
As a service to the community, this article is available for free. Existing users log in.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Distracting natural killer cells
Natural killer (NK) cells target virally infected and transformed cells for cytolysis. When sufficient activating receptors on the NK cell surface, such as NKG2D, are engaged by ligands on the target cell, such as ULBP proteins, the NK cell kills the target. Polymorphisms within ULBP-encoding genes are associated with immune dysfunction. Zuo et al. found that the affinity of a commonly occurring ULBP6 variant for NKG2D was greater than that of the wild-type protein, which impaired NK cell activation. A soluble form of this protein variant bound so tightly to NKG2D that it suppressed receptor activation and target cell killing in response to other NKG2D ligands. Together, these data suggest that targeting NK cell–ligand interactions may provide therapies to modulate the strength of immune responses.