Journal
IMMUNITY
Volume 18, Issue 1, Pages 41-51Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(02)00505-8
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Funding
- NCI NIH HHS [CA 89189] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA089189] Funding Source: NIH RePORTER
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Nonobese diabetic (NOD) mice, a model of insulin-dependent diabetes mellitus, have a defect in natural killer (NK) cell-mediated functions. Here we show impairment in an activating receptor, NKG2D, in NOD NK cells. While resting NK cells from C57BL/6 and NOD mice expressed equivalent levels of NKG2D, upon activation NOD NK cells but not C57BL/6 NK cells expressed NKG2D ligands, which resulted in downmodulation of the receptor. NKG2D-dependent cytotoxicity and cytokine production were decreased because of receptor modulation, accounting for the dysfunction. Modulation of NKG2D was mostly dependent on the YxxM motif of DAP10, the NKG2B-associated adaptor that activates phosphoinositide 3 kinase. These results suggest that NK cells may be desensitized by exposure to NKG2D ligands.
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