CD56bright natural killer cells exhibit abnormal phenotype and function in severe aplastic anemia

IntroductionCD56(bright) NK cells have been highlighted to serve immunoregulatory functions. However, their roles in severe aplastic anemia (SAA) have not been elucidated. MethodsHere, we investigated the quantities, phenotypes, cytokine secretion abilities, and the cytotoxicities of peripheral CD56(bright) NK cells along with CD56(dim) NK cells obtained from patients with SAA, SAA in remission (R-SAA), and healthy controls (HC). ResultsWe observed the decreased quantities of CD56(bright) NK cells in SAA compared with in R-SAA and HC. In SAA, the quantities of CD56(bright) NK cells correlated with the disease severity. Activating receptors NKp46 and NKp44 on CD56(bright) NK cells were upregulated while inhibiting receptor NKG2A was downregulated in SAA. CD56(bright) NK cells obtained from SAA patients produced increased IL-10 and decreased IFN- in vitro compared with cells obtained from HC, while TNF- and IL-13 productions were not different between two groups. Under a 7-day prestimulation with IL-2 and IL-12, the serum concentrations of which were higher in SAA patients, CD56(bright) NK obtained from HC also produced increased IL-10 mRNAs. There were no differences of cytotoxicites between CD56(bright) NK cells in SAA and in HC. ConclusionWe discovered that CD56(bright) NK cells exhibited abnormal receptor expressions and cytokine production in SAA, and they were related with the severity of illness.