Abstract

The term "microchimerism" indicates the coexistence, in the same organism, of genetically distinct populations of cells derived from two different individuals. The passage of cells from the fetus to the mother is called fetal cell microchimerism, whereas that occurring from the mother to the fetus is named maternal cell microchimerism. Microchimeric cells can persist in blood and tissues for decades. A literature search through the U.S. National Library of Medicine was used to identify and review studies on maternal and fetal microchimerism, focusing on endocrine diseases. According to the majority of reports, fetal cell microchimerism seems to have a detrimental role in autoimmune diseases and a positive effect on tumor burden in most human cancers studied. In autoimmune thyroid diseases, fetal microchimeric cells (fmcs) have been found to be significantly more represented within the thyroid gland of women with Hashimoto's thyroiditis and Graves' disease compared to those without thyroid autoimmunity, suggesting a pathogenic role. In thyroid cancer tissues, fmcs have been found to be present at higher levels than in contralateral normal tissues and have been shown to differentiate into epithelial and hematopoietic cells. Microchimeric cells with hematopoietic differentiation could have a role in destroying the tumor, whereas epithelial cells are believed to participate in the repairing processes. At the peripheral level, circulating fmcs were less frequently detected in patients with thyroid cancer than in healthy individuals, consistent with data obtained for breast cancer and other solid and hematological malignancies, indicating a protective role against cancer development. Finally, type 1 diabetes has been mostly related to maternal cell microchimerism. Indeed, the levels of circulating maternal cells were higher in type 1 diabetes patients than in controls. At the pancreas level, female β-cells were identified and hypothesized to be targets of autoimmunity or to regenerate diseased tissues.

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