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

Abstract

CD56bright NK cells have been highlighted to serve immunoregulatory functions. However, their roles in severe aplastic anemia (SAA) have not been elucidated. Here, we investigated the quantities, phenotypes, cytokine secretion abilities, and the cytotoxicities of peripheral CD56bright NK cells along with CD56dim NK cells obtained from patients with SAA, SAA in remission (R-SAA), and healthy controls (HC). We observed the decreased quantities of CD56bright NK cells in SAA compared with in R-SAA and HC. In SAA, the quantities of CD56bright NK cells correlated with the disease severity. Activating receptors NKp46 and NKp44 on CD56bright NK cells were upregulated while inhibiting receptor NKG2A was downregulated in SAA. CD56bright NK cells obtained from SAA patients produced increased IL-10 and decreased IFN-γ in vitro compared with cells obtained from HC, while TNF-α 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, CD56bright NK obtained from HC also produced increased IL-10 mRNAs. There were no differences of cytotoxicites between CD56bright NK cells in SAA and in HC. We discovered that CD56bright NK cells exhibited abnormal receptor expressions and cytokine production in SAA, and they were related with the severity of illness.