Fetal cell microchimerism develops through the migration of fetus-derived cells to the maternal organs early after implantation

Sunami, Rei; Komuro, Mayuko; Yuminamochi, Tsutomu; Hoshi, Kazuhiko; Hirata, Shuji

doi:10.1016/j.jri.2009.11.006

Cited by 40 publications

(40 citation statements)

References 25 publications

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“…Fetal cells can persist in maternal blood and tissue, and in some studies, association of fetal cells with autoimmune disease have been reported, perhaps indicating a pathological tolerance in the maternal immune system (Lambert et al 2002). However, recent data suggest that fetal cells may infiltrate injured maternal tissue as a repair mechanism (Khosrotehrani & Bianchi 2005, Sunami et al 2010.…”

Section: Systemic Strategiesmentioning

confidence: 99%

A balancing act: mechanisms by which the fetus avoids rejection by the maternal immune system

Warning¹,

McCracken²,

Morris³

2011

Reproduction

212

139

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Successful pregnancy requires strict temporal regulation of maternal immune function to accommodate the growing fetus. Early implantation is facilitated by inflammatory processes that ensure adequate vascular remodeling and placental invasion. To prevent rejection of the fetus, this inflammation must be curtailed; reproductive immunologists are discovering that this process is orchestrated by the fetal unit and, in particular, the extravillous trophoblast. Soluble and particulate factors produced by the trophoblast regulate maternal immune cells within the decidua, as well as in the periphery. The aim of this review is to discuss the action of recently discovered immunomodulatory factors and mechanisms, and the potential effects of dysregulation of such mechanisms on the maternal immune response that may result in pregnancy loss or preeclampsia.

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Section: Systemic Strategiesmentioning

confidence: 99%

A balancing act: mechanisms by which the fetus avoids rejection by the maternal immune system

Warning¹,

McCracken²,

Morris³

2011

Reproduction

212

139

View full text Add to dashboard Cite

show abstract

“…It is thought that these constant cycles of muscle degeneration-regeneration eventually lead to premature satellite cell exhaustion and consequent demise in this animal [37]. Since a local notexin insult is known to recruit bone marrow populations to aid in this repair process [38], we postulated that persistent FMCs (likely from the bone marrow compartment [8,29]) would be similarly recruited and participate in this repair process. Our results however cannot exclude the possibility that FMCs below detectable levels reside locally, proliferate, and become detectable in response to injury.…”

Section: Discussionmentioning

confidence: 98%

“…FMCs selectively home to damaged tissues where they are found in a higher frequency than in uninjured control tissues [6,7]. They can either be a part of the inflammatory infiltrate or integrated into the surrounding maternal tissue, displaying niche-appropriate phenotypes [4,8]. It is these end-point phenotypes that have been used to argue that FMCs have tissue regenerative properties.…”

mentioning

confidence: 99%

“…Transfer of a more primitive pluripotent progenitor, however, cannot be excluded [9], since transplacental traffic of fetal cells begins soon after implantation in both humans and mice [8,10]. There is evidence for the transfer and persistence of diverse multi-and unipotent fetal progenitors, including hematopoietic [1,3], endothelial [4,11], mesenchymal [12], and even neuronal [14] lineages.…”

mentioning

confidence: 99%

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Fetal Microchimeric Cells in a Fetus-Treats-Its-Mother Paradigm Do Not Contribute to Dystrophin Production in Serially ParousmdxFemales

Seppanen

Hodgson²,

Khosrotehrani³

et al. 2012

Stem Cells and Development

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Throughout every pregnancy, genetically distinct fetal microchimeric stem/progenitor cells (FMCs) engraft in the mother, persist long after delivery, and may home to damaged maternal tissues. Phenotypically normal fetal lymphoid progenitors have been described to develop in immunodeficient mothers in a fetus-treats-its-mother paradigm. Since stem cells contribute to muscle repair, we assessed this paradigm in the mdx mouse model of Duchenne muscular dystrophy. mdx females were bred serially to either ROSAeGFP males or mdx males to obtain postpartum microchimeras that received either wild-type FMCs or dystrophin-deficient FMCs through serial gestations. To enhance regeneration, notexin was injected into the tibialis anterior of postpartum mice. FMCs were detected by qPCR at a higher frequency in injected compared to noninjected side muscle (P = 0.02). However, the number of dystrophin-positive fibers was similar in mothers delivering wild-type compared to mdx pups. In addition, there was no correlation between FMC detection and percentage dystrophin, and no GFP + ve FMCs were identified that expressed dystrophin. In 10/11 animals, GFP + ve FMCs were detected by immunohistochemistry, of which 60% expressed CD45 with 96% outside the basal lamina defining myofiber contours. Finally we confirmed lack of FMC contribution to statellite cells in postpartum mdx females mated with Myf5-LacZ males. We conclude that the FMC contribution to regenerating muscles is insufficient to have a functional impact.

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“…These results suggest that most of the fetal cells capable of multilineage differentiation may have entered the maternal circulation early after implantation. 15 The biological significance of this physiological phenomenon is not yet known, however, many studies have demonstrated that fetal cells tend to concentrate in clinically affected tissues. 16,17 Therefore, fetal cell microchimerism may mediate tissue repair, have a beneficial effect on postnatal lifespan, and protect against some diseases during pregnancy.…”

mentioning

confidence: 99%

Migration of microchimeric fetal cells into maternal circulation before placenta formation

et al. 2010

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Fetal cell microchimerism develops through the migration of fetus-derived cells to the maternal organs early after implantation

Cited by 40 publications

References 25 publications

A balancing act: mechanisms by which the fetus avoids rejection by the maternal immune system

A balancing act: mechanisms by which the fetus avoids rejection by the maternal immune system

Fetal Microchimeric Cells in a Fetus-Treats-Its-Mother Paradigm Do Not Contribute to Dystrophin Production in Serially ParousmdxFemales

Migration of microchimeric fetal cells into maternal circulation before placenta formation

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