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• W1488367272 abstract "The NKG2D activating receptor on human NK cells mediates altered self recognition, as its ligands (NKG2DLs) are upregulated on target cells in a variety of stress conditions. Evidence collected in the past years shows that, even though expression of NKG2DLs acts as a danger signal that renders tumor cells susceptible to cytotoxicity, chronic exposure to soluble or membrane-bound NKG2DLs can lead to down-modulation of receptor expression and impairment of NKG2D-mediated cell functions. Here, we evaluated whether different cell-bound NKG2DLs, namely MICA and ULBP2, are equivalently able to induce NKG2D down-modulation on human NK cells. We found that although both ligands reduce NKG2D surface expression, MICA promotes a stronger receptor down-modulation than ULBP2, leading to a severe impairment of NKG2D-dependent NK-cell cytotoxicity. We also provide evidence that the ubiquitin pathway and c-Cbl direct MICA-induced but not ULBP2-induced NKG2D internalization and degradation, thus identifying a molecular mechanism to explain the differential effects of MICA and ULBP2 on NKG2D expression. A better understanding of the molecular mechanisms employed by the different NKG2DLs to control NKG2D surface expression could be useful for the development of anti-tumor strategies to restore a normal level of NKG2D receptors on human NK cells." @default.
• W1488367272 created "2016-06-24" @default.
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• W1488367272 date "2014-06-17" @default.
• W1488367272 modified "2023-10-07" @default.
• W1488367272 title "c-Cbl regulates MICA- but not ULBP2-induced NKG2D down-modulation in human NK cells" @default.
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• W1488367272 doi "https://doi.org/10.1002/eji.201444512" @default.
• W1488367272 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24846123" @default.
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