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Postpartum Autoimmune Thyroid Disease: The Potential Role of Fetal Microchimerism

Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029

Address all correspondence and requests for reprints to: Takao Ando, M.D., Mount Sinai School of Medicine, Box 1055, 1 Gustave L. Levy Place, New York, New York 10029. E-mail: takao.ando{at}mssm.edu.

Fetal microchimerism is defined as the presence of fetal cells in maternal tissues established during pregnancy. Immune suppression of maternal immunity during pregnancy by the placenta may play an important role in allowing the establishment of such fetal microchimerism. However, peripheral blood fetal microchimerism that persists in the postpartum period is considered a natural event and implies the induction of tolerance during pregnancy. Identification of fetal cells that persist preferentially in maternal tissues subject to autoimmunity, such as skin and thyroid, has also suggested the possible immune modulation of the autoimmune response at the target tissue by fetal cells. Accumulating evidence suggests that fetal immune cells may be reactive to maternal antigens and, therefore, have the capacity to trigger graft vs. host reactions. This would provide a mechanism for the initiation and/or exacerbation of autoimmune disease.

The course and severity of autoimmune thyroid disease have long been known to be profoundly influenced by pregnancy, with disease suppression prepartum and exacerbation postpartum. However, the precise mechanisms involved have not been fully understood. Here we have reviewed recent information on the possible role of fetal microchimerism in autoimmune thyroid disease, focusing on the immunological consequences of intrathyroidal fetal cells and their contribution to postpartum exacerbations.

This work was supported by in part by NIH Grants DK-52464, DK-45011, and AI-24671 (to T.F.D.) and the David Owen Segal Endowment (to T.A.).

Abbreviations: AITD, Autoimmune thyroid disease; EAT, experimental autoimmune thyroiditis; FISH, fluorescent in situ hybridization; GFP, green fluorescent protein; GvHD, graft vs. host disease; HLA, human leukocyte antigen; MHC, major histocompatibility complex; PBC, primary biliary cirrhosis; SRY, sex-determining region Y; Tg, thyroglobulin; Th, T helper; TPO, thyroid peroxidase; TSHR, TSH receptor.

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