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Series GSE184020 Query DataSets for GSE184020
Status Public on Sep 16, 2021
Title Human placental exosomes induce maternal systemic immune tolerance in a monocyte-dependent manner
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary Maternal immune tolerance toward to the semi-allograft fetus is a prerequisite condition for successful pregnancy. However, the role of maternal monocytes in the induction of systemic immune tolerance is poorly understood. Here we report that placenta facilitates maternal immune tolerance by extruding exosomes. Maternal monocytes were transformed into an immunosuppressive phenotype after taking up exosomes. Mechanistically, PD-L1 was significantly increased in pEXO-educated monocytes via miRNA-29a-3p/PTEN signaling pathway. In addition, pEXO-treated monocytes could increase Treg pool in maternal blood through a direct cell-cell interaction. Moreover, Th1 cytokines, IFNγ and TNF-α, in monocyte-T cell co-culture system were significantly decreased. Together, our results indicated that maternal monocyte is indispensable components in systemic immune tolerance establishment.
Overall design mRNA profiles of pEXO-treated monocyte (N=4) and Control monocyte (N=4)
Contributor(s) Chiu PC, Kunfeng B
Citation(s) 35180876
Submission date Sep 13, 2021
Last update date Feb 28, 2022
Contact name Jianlin Li
Organization name The university of Hong Kong
Street address L 7-08, Department of Obstetrics and Gynecology Laboratory block, 21th Sassoon Road, Hong Kong
City Hong Kong
ZIP/Postal code 999077
Country Hong Kong
Platforms (1)
GPL30209 MGISEQ-2000RS (Homo sapiens)
Samples (8)
GSM5576034 Control_monocyte_01
GSM5576035 Control_monocyte_02
GSM5576036 Control_monocyte_03
This SubSeries is part of SuperSeries:
GSE184195 Placental exosomes
BioProject PRJNA762864
SRA SRP336817

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Supplementary file Size Download File type/resource
GSE184020_Normalized_gene_counts_matrix.txt.gz 737.9 Kb (ftp)(http) TXT
GSE184020_Raw_gene_counts_matrix.txt.gz 332.5 Kb (ftp)(http) TXT
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