Many, perhaps all, people harbor a small number of cells from genetically different individuals—from their mothers and, for women who have been pregnant, from their children. What in the world do these foreigners do in the body?
"Over the last decade, elevated levels of maternal cells have been reported in several autoimmune diseases (reviewed in , ) with several different hypotheses proposed; some suggest that MMc are effector cells of the immune response , others that semi-allogeneic MMc in specific host tissues may act as triggers of autoimmunity  while it has also been postulated that some MMc, like fetal microchimeric cells, may play a role in regeneration of damaged tissues . We previously observed increased levels of MMc in the pancreas and periphery of individuals with type 1 diabetes , . "
[Show abstract][Hide abstract] ABSTRACT: Maternal microchimeric cells (MMc) transfer across the placenta during pregnancy. Increased levels of MMc have been observed in several autoimmune diseases including type 1 diabetes but their role is unknown. It has been suggested that MMc are 1) effector cells of the immune response, 2) targets of the autoimmune response or 3) play a role in tissue repair. The aim of this study was to define the cellular phenotype of MMc in control (n = 14) and type 1 diabetes pancreas (n = 8).
Using sex chromosome-based fluorescence in-situ hybridization, MMc were identified in male pancreas and their phenotype determined by concomitant immunofluorescence.
In normal pancreas, MMc positive for endocrine, exocrine, duct and acinar markers were identified suggesting that these cells are derived from maternal progenitors. Increased frequencies of MMc were observed in type 1 diabetes pancreas (p = 0.03) with particular enrichment in the insulin positive fraction (p = 0.01). MMc did not contribute to infiltrating immune cells or Ki67+ islet cell populations in type 1 diabetes.
These studies provide support for the hypothesis that MMc in human pancreas are derived from pancreatic precursors. Increased frequencies of MMc beta cells may contribute to the initiation of autoimmunity or to tissue repair but do not infiltrate islets in type 1 diabetes.
PLoS ONE 01/2014; 9(1):e86985. DOI:10.1371/journal.pone.0086985 · 3.23 Impact Factor
"It is established that the fetal immune system has the ability to respond to antigens as early as by 18 weeks of gestation . A limited transfer of cells from the mother to the fetus and vice versa is the basis for the well recognized phenomenon of microchimerism , . Fetal Y-chromosome DNA was detected in the maternal circulation in cellular compartments beginning at 7 to 16 weeks , . "
[Show abstract][Hide abstract] ABSTRACT: We describe the distribution of indoleamine 2,3-dioxygenase 1 (IDO1) in vascular endothelium of human first-trimester and term placenta. Expression of IDO1 protein on the fetal side of the interface extended from almost exclusively sub-trophoblastic capillaries in first-trimester placenta to a nearly general presence on villous vascular endothelia at term, including also most bigger vessels such as villous arteries and veins of stem villi and vessels of the chorionic plate. Umbilical cord vessels were generally negative for IDO1 protein. In the fetal part of the placenta positivity for IDO1 was restricted to vascular endothelium, which did not co-express HLA-DR. This finding paralleled detectability of IDO1 mRNA in first trimester and term tissue and a high increase in the kynurenine to tryptophan ratio in chorionic villous tissue from first trimester to term placenta. Endothelial cells isolated from the chorionic plate of term placenta expressed IDO1 mRNA in contrast to endothelial cells originating from human umbilical vein, iliac vein or aorta. In first trimester decidua we found endothelium of arteries rather than veins expressing IDO1, which was complementory to expression of HLA-DR. An estimation of IDO activity on the basis of the ratio of kynurenine and tryptophan in blood taken from vessels of the chorionic plate of term placenta indicated far higher values than those found in the peripheral blood of adults. Thus, a gradient of vascular endothelial IDO1 expression is present at both sides of the feto-maternal interface.
PLoS ONE 07/2011; 6(7):e21774. DOI:10.1371/journal.pone.0021774 · 3.23 Impact Factor
"Bi-directional trafficking of maternal and fetal cells is now known to occur routinely during pregnancy with persistence of low levels of fetal cells in the mother and maternal cells in her offspring for decades after childbirth.(Bianchi et al. 1996; Lo et al. 2000; Maloney et al. 1999; Nelson 2008) Microchimerism (Mc) refers to a small population of cells or DNA in one individual that derives from a genetically distinct individual. The extent to which Mc is tolerated and whether dynamic changes occur over time are unknown, but observations from multiple disciplines implicate Mc in autoimmune disease pathogenesis decades after childbirth. "
[Show abstract][Hide abstract] ABSTRACT: Pregnancy has both short-term effects and long-term consequences on the maternal immune system. For women who have an autoimmune disease and subsequently become pregnant, pregnancy can induce amelioration of the mother's disease, such as in rheumatoid arthritis, while exacerbating or having no effect on other autoimmune diseases like systemic lupus erythematosus. That pregnancy also leaves a long-term legacy has recently become apparent by the discovery that bi-directional cell trafficking results in persistence of fetal cells in the mother and of maternal cells in her offspring for decades after birth. The long-term persistence of a small number of cells (or DNA) from a genetically disparate individual is referred to as microchimerism. While microchimerism is common in healthy individuals and is likely to have health benefits, microchimerism has been implicated in some autoimmune diseases such as systemic sclerosis. In this paper, we will first discuss short-term effects of pregnancy on women with autoimmune disease. Pregnancy-associated changes will be reviewed for selected autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus and autoimmune thyroid disease. The pregnancy-induced amelioration of rheumatoid arthritis presents a window of opportunity for insights into both immunological mechanisms of fetal-maternal tolerance and pathogenic mechanisms in autoimmunity. A mechanistic hypothesis for the pregnancy-induced amelioration of rheumatoid arthritis will be described. We will then discuss the legacy of maternal-fetal cell transfer from the perspective of autoimmune diseases. Fetal and maternal microchimerism will be reviewed with a focus on systemic sclerosis (scleroderma), autoimmune thyroid disease, neonatal lupus and type I diabetes mellitus.
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