IL-25 promotes Th2 bias by upregulating IL-4 and IL-10 expression of decidual γδT cells in early pregnancy
- Yuan Zhang
- Ying Wang
- Ming‑Qing Li
- Jie Duan
- Deng‑Xuan Fan
- Li‑Ping Jin
Published online on: December 15, 2017
Copyright: © Zhang et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Decidual immune cells (DICs), consisting of both innate and adaptive immune cells, have a pivotal role in maintaining immune tolerance for normal pregnancy. Our previous study demonstrated that interleukin (IL)‑25 stimulates the proliferation of decidual stromal cells (DSCs) in an autocrine manner. However, the role of IL‑25 in functional regulation of DICs is largely unknown. Flow cytometry was used to analyze the expression of IL‑25 and its receptor (IL‑17RB) in DICs, and the effect of IL‑25 on the expression of Ki‑67, IL‑4, IL‑10, interferon (IFN)‑γ and transforming growth factor (TGF)‑β in decidual γδT cells. In addition, ELISA assays were performed to detect the secretion of IL‑10 and TGF‑β in decidual γδT cells. The present findings indicated that decidual CD56 bright CD16‑natural killer (NK) cells, natural killer T (NKT) cells, regulatory T (Treg) cells, CD3+ T cells, macrophages and γδT cells co‑expressed IL‑25 and IL‑17RB, particularly γδT cells. Recombinant human (rh) IL‑25 protein upregulated the expression of Ki‑67, IL‑4, and IL‑10, but downregulated the expression of IFN‑γ in γδT cells; however, anti‑human IL‑25 or IL‑17RB neutralizing antibody reversed these effects. These data suggest that IL‑25 may promote IL‑10 production by γδT cells as well as the proliferation of γδT cells, and possibly forms a positive feedback loop to maintain a T helper 2 cell bias at the maternal‑fetal interface and further contributes to the maintenance of successful pregnancy.