| First Author | Lin Z | Year | 2014 |
| Journal | Immunology | Volume | 141 |
| Issue | 3 | Pages | 401-15 |
| PubMed ID | 24708417 | Mgi Jnum | J:345280 |
| Mgi Id | MGI:6872900 | Doi | 10.1111/imm.12203 |
| Citation | Lin Z, et al. (2014) CD4(+) NKG2D(+) T cells induce NKG2D down-regulation in natural killer cells in CD86-RAE-1epsilon transgenic mice. Immunology 141(3):401-15 |
| abstractText | The binding of NKG2D to its ligands strengthens the cross-talk between natural killer (NK) cells and dendritic cells, particularly at early stages, before the initiation of the adaptive immune response. We found that retinoic acid early transcript-1epsilon (RAE-1epsilon), one of the ligands of NKG2D, was persistently expressed on antigen-presenting cells in a transgenic mouse model (pCD86-RAE-1epsilon). By contrast, NKG2D expression on NK cells, NKG2D-dependent cytotoxicity and tumour rejection, and dextran sodium sulphate-induced colitis were all down-regulated in this mouse model. The down-regulation of NKG2D on NK cells was reversed by stimulation with poly (I:C). The ectopic expression of RAE-1epsilon on dendritic cells maintained NKG2D expression levels and stimulated the activity of NK cells ex vivo, but the higher frequency of CD4(+) NKG2D(+) T cells in transgenic mice led to the down-regulation of NKG2D on NK cells in vivo. Hence, high levels of RAE-1epsilon expression on antigen-presenting cells would be expected to induce the down-regulation of NK cell activation by a regulatory T-cell subset. |
