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Characterizing the immune cell population in the human fetal membrane
Author(s) -
Jacobs Sara O.,
ShellerMiller Samantha,
Richardson Lauren S.,
UrrabazGarza Rheanna,
Radnaa Enkhtuya,
Me Ramkumar
Publication year - 2021
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.13368
Subject(s) - immune system , fetus , biology , decidua , fetal membrane , flow cytometry , innate immune system , population , immunology , andrology , microbiology and biotechnology , placenta , medicine , pregnancy , genetics , environmental health
Abstract Problem This study localized CD45 + immune cells and compared changes in their numbers between term, not in labor (TNIL) and term, labor (TL) human fetal membranes. Method of study Fetal membranes (amniochorion) from normal TNIL and TL subjects were analyzed by immunohistochemistry (IHC), immunofluorescence (IF), and flow cytometry for evidence of total (CD45 + ) immune cells as well as innate immune cells (neutrophils, macrophages and NK cells) using specific markers. Fetal origin of immune cells was determined using polymerase chain reaction (PCR) for SRY gene in Y chromosome. Results CD45 + cells were localized in human fetal membranes for both TNIL and TL. A threefold increase in CD45 + cells was seen in TL fetal membranes of (7.73% ± 2.35) compared to TNIL (2.36% ± 0.78). This increase is primarily contributed by neutrophils. Macrophages and NK cells did not change in the membranes between TNIL and TL. Leukocytes of fetal origin are present in the fetal membranes. Conclusion The fetal membranes without decidua contain a small proportion of immune cells. Some of these immune cells in the fetal membrane are fetal in origin. There is a moderate increase of immune cells in the fetal membranes at term labor; however, it is unclear whether this is a cause or consequence of labor. Further functional studies are needed to determine their contribution to membrane inflammation associated with parturition.