Abstract
The placental barrier is not the impenetrable wall that it was once presumed to be. During pregnancy, fetal cells pass into the mother, where they persist for decades after the pregnancy, leading to fetal microchimerism (FMc). Maternal cells also pass into the fetus, where they can persist long after birth of the child into adulthood, leading to maternal microchimerism(MMc). FMc and MMc represent foreign cells, and thus have been implicated in the pathogenesis of autoimmune diseases that resemble graft-versus-host disease after stem cell transplantation. FMc, hypothesized to contribute to the high predisposition of autoimmune diseases in women, has been reviewed recently. In patients who have never been pregnant, (children, males, and nulliparous females), MMc may represent the foreign cells that initiate or perpetuate chronic inflammatory disease.
Highlights
Pediatric Rheumatology 2007, 5:9 http://www.ped-rheum.com/content/5/1/9 expand by an antigenic stimulus yet to be identified, leading to clonal over-representation in the total population
Whereas in severe combined immunodeficiency (SCID) infants maternal cells make up the majority of lymphocytes, maternal microchimerism (MMc) is found at lower levels in immunocompetent infants
The levels of MMc in these studies were only roughly estimated until Lo and Lambert, et al, developed a panel of real-time quantitative polymerase chain reaction (PCR) (Q-PCR) assays specific for highly polymorphic HLA alleles that could be used to accurately measure a low level of maternal DNA by targeting maternal HLA alleles not shared by the child [10,20]
Summary
MMc is commonly present in tissues and blood of patients with autoimmune disease. The original hypothesis was that chimeric maternal or fetal T lymphocytes responding to host antigens led to chronic inflammation in a manner similar to GVHD, where maternal lymphocytes reacted to host antigens. Chronic inflammation may occur by host T lymphocyte activation in response to maternal cells within tissues. Injury or infection may upregulate maternal HLA expression, allowing the antigen load to exceed the T cell activation threshold for the otherwise tolerized host. The loss of tolerance to maternal antigens may extend to self antigens through epitope spreading, as after hematopoietic stem cell transplantation. Studies into the functional capabilities of maternal cells will be essential in understanding the biological significance of MMc in health and autoimmune disease
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