Human placental trophoblast cells contribute to maternal–fetal tolerance through expressing IL-35 and mediating iTR35 conversion

Jia Liu, Shengnan Hao, Xi Chen, Hui Zhao, Lutao Du, Hanxiao Ren, Chuanxin Wang and Haiting Mao ()
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Jia Liu: The Second Hospital of Shandong University
Shengnan Hao: The Second Hospital of Shandong University
Xi Chen: The Second Hospital of Shandong University
Hui Zhao: The Second Hospital of Shandong University
Lutao Du: The Second Hospital of Shandong University
Hanxiao Ren: The Second Hospital of Shandong University
Chuanxin Wang: The Second Hospital of Shandong University
Haiting Mao: The Second Hospital of Shandong University

Nature Communications, 2019, vol. 10, issue 1, 1-10

Abstract: Abstract During pregnancy, trophoblast cells sustain the maternal–fetal tolerance via expressing and secreting various chemokines and cytokines. Our previous study revealed the expression of interleukin-35 (IL-35) in human first-trimester trophoblasts. Here we show that IL-35 is expressed in both human first-trimester primary trophoblast cells and a trophoblast cell line. Trophoblast cells inhibit the proliferation of human naive conventional T cells (Tconv cells) and convert suppressed Tconv cells into iTR35 in an IL-35-dependent manner. Mechanistically, trophoblast cell derived IL-35 mediates its function through phosphorylation of STAT1 and STAT3. In vivo studies confirm that mice with immunologically spontaneous abortion have lower levels of IL-35 and iTR35 cells at the maternal–fetal interface, and neutralizing anti-IL-35 mAb enhances abortion rates. Meanwhile, exogenous IL-35 induces iTR35 and prevents immunological abortion. Our findings thus suggest that trophoblast cells have a critical function in preserving maternal–fetal tolerance via secreting IL-35 during pregnancy.

Date: 2019
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DOI: 10.1038/s41467-019-12484-z

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