Decidual Macrophages and Their Roles at the Maternal-Fetal Interface

Stem Cell and Regenerative Biology Department, Harvard University, Boston, MA 02115, USA.
The Yale journal of biology and medicine 03/2012; 85(1):105-18.
Source: PubMed


The semi-allogeneic fetus, whose genome consists of maternally and paternally inherited alleles, must coexist with an active maternal immune system during its 9 months in utero. Macrophages are the second most abundant immune cell at the maternal-fetal interface, although populations and functions for these populations remain ill defined. We have previously reported two distinct subsets of CD14(+) decidual macrophages found to be present in first trimester decidual tissue, 20 percent CD11c(HI) and 68 percent CD11c(LO). Interestingly, CD11c(HI) decidual macrophages express genes associated with lipid metabolism, inflammation, and antigen presentation function and specifically upregulate CD1 molecules. Conversely, CD11c(LO) decidual macrophages express genes associated with extracellular matrix formation, muscle regulation, and tissue growth. The large abundance of CD11c(HI) decidual macrophages and their ability to process antigens more efficiently than CD11c(LO) macrophages suggests that CD11c(HI) macrophages may be important antigen processing and presenting cells at the maternal-fetal interface, while CD11c(LO) macrophages may perform necessary homeostatic functions during placental construction. Thus, macrophage heterogeneity may be an important and necessary division of labor that leads to both an induction of maternal immune cell tolerance to fetal antigens as well as basic homeostatic functions in human pregnancy.


Available from: Brandy Houser, Aug 18, 2014
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    • "Prenatal stress inducing an increase of inflammatory cytokines (i.e., TNF-α) has been suggested to modify the neonatal immune response through the expression of toll-like receptors (TLRs) and TLR-signaling pathways [146]. Although the interplay between the innate immune system and mood-related disorders is still obscure [145] [146], the study of interactions between the immune system, its active mediators [146] [147], and the brain [32] may reveal important pathophysiological mechanisms that are involved in the development of moodrelated disorders in pregnancy. "
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    • "Early in human pregnancies, a tolerogenic phenotype predominates in the decidua during implantation of the fetus, which because of its expression of major and minor histocompatibility antigens differing from that of the mother, can be considered an allograft. Uterine natural killer (uNK) cells (Zhao et al., 2011; Le Bouteiller, 2013) and M2 (alternative) macrophages help with the initial steps of this process by mediating uterine spiral artery remodeling, trophoblastic invasion, and immunomodulation (Nagamatsu and Schust, 2010b; Houser, 2012 ). For example , unlike circulating monocyte-derived macrophages after the uptake of apoptotic trophoblasts, placental M2 macrophages do not produce inflammatory mediators (Ben Amara et al., 2013), and hence may limit immune responses and promote immunotolerance . "
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    • "In pregnancy it is the uterine natural killer (uNK) cells, innate immune actors, that seem to be the primary cytokine secretors at the level of the trophoblast [2,17]. Decidual macrophages also secrete both types of cytokines [18]. Thus these patterns of cytokine secretion are now being referred to as type 1 and type 2 because of the multiple types of immune cells that are capable of producing these two patterns of immune response [19]. "
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