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Publication : An essential function for beta-arrestin 2 in the inhibitory signaling of natural killer cells.

First Author  Yu MC Year  2008
Journal  Nat Immunol Volume  9
Issue  8 Pages  898-907
PubMed ID  18604210 Mgi Jnum  J:272247
Mgi Id  MGI:6284222 Doi  10.1038/ni.1635
Citation  Yu MC, et al. (2008) An essential function for beta-arrestin 2 in the inhibitory signaling of natural killer cells. Nat Immunol 9(8):898-907
abstractText  The inhibitory signaling of natural killer (NK) cells is crucial in the regulation of innate immune responses. Here we show that the association of KIR2DL1, an inhibitory receptor of NK cells, with beta-arrestin 2 mediated recruitment of the tyrosine phosphatases SHP-1 and SHP-2 to KIR2DL1 and facilitated 'downstream' inhibitory signaling. Consequently, the cytotoxicity of NK cells was higher in beta-arrestin 2-deficient mice but was inhibited in beta-arrestin 2-transgenic mice. Moreover, beta-arrestin 2-deficient mice were less susceptible than wild-type mice to mouse cytomegalovirus infection, an effect that was abolished by depletion of NK cells. Our findings identify a previously unknown mechanism by which the inhibitory signaling in NK cells is regulated.
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