Data from: Deciphering the preeclampsia-specific immune microenvironment and the role of pro-inflammatory macrophages at the maternal-fetal interface

Preeclampsia (PE), a major cause of maternal and perinatal mortality with
highly heterogeneous causes and symptoms, is usually complicated by
gestational diabetes mellitus (GDM). However, a comprehensive
understanding of the immune microenvironment in the placenta of
PE and the differences between PE and GDM is still lacking. In
this study, Cytometry by time of flight (CyTOF)
indicated that the frequencies of memory-like Th17 cells
(CD45RA-CCR7+IL-17A+CD4+), memory-like CD8+ T cells
(CD38+CXCR3-CCR7+Helios-CD127-CD8+) and pro-inflam Macs
(CD206-CD163-CD38midCD107alowCD86midHLA-DRmidCD14+) were increased, while
the frequencies of anti-inflam Macs
(CD206+CD163-CD86midCD33+HLA-DR+CD14+) and granulocyte myeloid-derived
suppressor cells (gMDSCs, CD11b+CD15hiHLA-DRlow) were decreased in the
placenta of PE compared with that of NP, but not in that of GDM or
GDM&PE. The pro-inflam Macs were positively correlated
with memory-like Th17 cells and memory-like CD8+ T cells but
negatively correlated with gMDSCs. Single-cell RNA sequencing revealed
that transferring the F4/80+CD206- pro-inflam Macs with a
Folr2+Ccl7+Ccl8+C1qa+C1qb+C1qc+ phenotype from the uterus of PE
mice to normal pregnant mice induced the production of memory-like
IL-17a+Rora+Il1r1+TNF+Cxcr6+S100a4+CD44+ Th17 cells via
IGF1-IGF1R, which contributed to the development and recurrence of PE.
Pro-inflam Macs also induced the production of
memory-like CD8+ T cells but inhibited the production of
Ly6g+S100a8+S100a9+Retnlg+Wfdc21+ gMDSCs at the maternal-fetal
interface, leading to PE-like symptoms in mice. In
conclusion, this study revealed the PE-specific immune cell network, which
was regulated by pro-inflam Macs, providing new ideas about the
pathogenesis of PE.