Intrathyroidal fetal microchimerism in pregnancy and postpartum.

To investigate a possible relationship between fetal microchimerism and autoimmune thyroiditis, we looked for the presence of fetal cells in the maternal blood and thyroid gland in murine experimental autoimmune thyroiditis (EAT). We used a quantitative PCR-ELISA for products of the SRY locus on the Y chromosome to detect fetal male cells during pregnancy and the postpartum period with a sensitivity of approximately 1 male cell/10(5) female cells. Within the thyroid glands, 12 of 26 (46%) Tg-immunized pregnant mice were SRY positive (range, 1-1700 cells), whereas, in contrast, few SRY transcripts were detected in control thyroids from nonimmunized pregnant mice (P < 0.05). At 5 wk postpartum, although SRY was still detected in the thyroids of 12 of 40 (30%) Tg-immunized mice, the number of male cells was markedly decreased (range, 1-30), and by 10 wk postpartum SRY had disappeared. Using allogeneic male mice heterozygous for green fluorescent protein expression, green fluorescent fetal cells were detected in the blood and bone marrow of pregnant mice. However, green cells were only found in thyroid glands from Tg-immunized pregnant mice that had green fluorescent protein-transgenic green fetuses and not in control nonimmunized pregnant mice. Cytologically, the fetal cells appeared to be of variable origin. Using antibody-mediated affinity purification of thyroid digests we showed this cell population to include fetal cells of T cell and dendritic cell lineage. Hence, fetal cells of immune origin were shown to accumulate within the thyroid glands of mice with EAT during pregnancy and the early postpartum. These data indicated that the inflamed thyroid gland was capable of accumulating fetal cells, including T cells and dendritic cells. Such active immune cells may have a profound regulatory influence on autoimmune thyroiditis in pregnancy and the postpartum period.