The immune potential of decidua-resident CD16+CD56+ NK cells in human pregnancy
- PMID: 33583640
- DOI: 10.1016/j.humimm.2021.01.014
The immune potential of decidua-resident CD16+CD56+ NK cells in human pregnancy
Abstract
Human CD56+CD3- NK cells can be subdivided into two different subsets according to the expression pattern of CD56 and CD16. CD56+/brightCD16- (CD16-) NK cells are prominently cytokine producers with little cytotoxicity whereas CD56+/dimCD16+ (CD16+) NK cells are efficient killers with poorer cytokine production potential. In human pregnancy, CD56+ decidual (d)NK cells accumulate in the maternal fetal interface to regulate placental immunity and development. Unlike peripheral blood (pb)NK cells, the majority of dNK cells are CD56 positive with limited CD16 reactivity. Our results demonstrated that in normal and pathological pregnancies, CD16+ dNK cells are a unique population in comparison to CD16- dNK subset. The expression of NK activation receptors CD335, CD336, CD244 and CD314 on CD16+ dNK subpopulation was lower than that on CD16- dNK cells. Upon cytokine stimulation with rhIL-12/15/18 or TGFβ blockade, the CD16+ dNK subset exhibited more robust response on the expression of IFNG, IL-8 and CD107a, compared to that of the CD16- dNK subpopulation. Functions of the CD16+ dNK subset were shown to be independent of cellular interaction with trophoblast cells. Studies of preeclamptic patients revealed lower proportions of CD16+ dNK cells, suggesting potential protective roles of these cells during normal gestations.. Therefore, we suggest that the CD16+ dNK subset, through compensating CD16- dNK cell function, is an indispensable componentto regulate decidual immune response and to support placentation.
Keywords: Flow cytometry; IFNG; NK cells; Preeeclampsia; data analysis.
Copyright © 2021 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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