| First Author | Maroof A | Year | 2008 |
| Journal | Immunity | Volume | 29 |
| Issue | 2 | Pages | 295-305 |
| PubMed ID | 18701085 | Mgi Jnum | J:139146 |
| Mgi Id | MGI:3807368 | Doi | 10.1016/j.immuni.2008.06.012 |
| Citation | Maroof A, et al. (2008) Posttranscriptional regulation of il10 gene expression allows natural killer cells to express immunoregulatory function. Immunity 29(2):295-305 |
| abstractText | Natural killer (NK) cells play a well-recognized role in early pathogen containment and in shaping acquired cell-mediated immunity. However, indirect evidence in humans and experimental models has suggested that NK cells also play negative regulatory roles during chronic disease. To formally test this hypothesis, we employed a well-defined experimental model of visceral leishmaniasis. Our data demonstrated that NKp46(+)CD49b(+)CD3(-) NK cells were recruited to the spleen and into hepatic granulomas, where they inhibited host protective immunity in an interleukin-10 (IL-10)-dependent manner. Although IL-10 mRNA could be detected in activated NK cells 24 hr after infection, the inhibitory function of NK cells was only acquired later during infection, coincident with increased IL-10 mRNA stability and an enhanced capacity to secrete IL-10 protein. Our data support a growing body of literature that implicates NK cells as negative regulators of cell-mediated immunity and suggest that NK cells, like CD4(+) T helper 1 cells, may acquire immunoregulatory functions as a consequence of extensive activation. |
