Current findings regarding the role of natural killer cells in adult-onset Still disease (AOSD) and systemic juvenile idiopathic arthritis (sJIA).
| Disease | Findings | Ref. |
|---|---|---|
| AOSD | Lower NK T cell counts | 4 |
| Defect in GalCer-mediated NK cytotoxicity | ||
| AOSD | Lower NK cell counts | 5 |
| Lower NK cytolytic function | ||
| sJIA | Lower NK cytolytic activity | 9 |
| Lower circulating CD56bright NK cell levels | ||
| sJIA | Impaired upregulation of cell-mediated perforin and IFN-γ in NK cells | 16 |
| Defect in IL-18 receptor β phosphorylation | ||
| sJIA | Lower cell counts, cytotoxicity, perforin, and granzyme B expression in NK cells | 13 |
| Lower frequency of KIR2DS4 | ||
| sJIA | Increased expression of innate genes and decreased expression of immune-regulating genes of NK cells | 12 |
| Alterations in inhibitory and excitatory receptors of NK cells | ||
| Decreased granzyme K expression in CD56bright | ||
| NK cells and defective IL-18–induced IFN-γ production | ||
| sJIA | Impaired NK cell activation by IL-18 | 21 |
NK: natural killer; IL: interleukin; KIR: killer cell immunoglobulin-like receptor; IFN: interferon; KIR2DS4: killer cell immunoglobulin-like excitatory receptors.