Intrathyroidal fetal microchimerism in pregnancy and postpartum.
Intrathyroidal fetal microchimerism in pregnancy and postpartum.
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DOI：
10.1210/endo.143.1.8563
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发表时间：
2002
期刊：
影响因子：
4.8
通讯作者：
M. Imaizumi;A. Pritsker;P. Unger;T. Davies
中科院分区：
文献类型：
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作者：
M. Imaizumi;A. Pritsker;P. Unger;T. Davies
为了研究胎儿微嵌合体与自身免疫性甲状腺炎之间可能的关系，我们在小鼠实验性自身免疫性甲状腺炎（EAT）中寻找母体血液和甲状腺中胎儿细胞的存在。我们使用 Y 染色体上 SRY 基因座产物的定量 PCR-ELISA 来检测怀孕期间和产后期的胎儿男性细胞，灵敏度约为 1 个男性细胞/10(5) 个女性细胞。在甲状腺内，26 只 Tg 免疫的怀孕小鼠中有 12 只 (46%) 呈 SRY 阳性（范围为 1-1700 个细胞），而相比之下，在未免疫怀孕小鼠的对照甲状腺中检测到很少的 SRY 转录本 (P < 0.05)。产后 5 周时，尽管 40 只 Tg 免疫小鼠中的 12 只（30%）的甲状腺中仍检测到 SRY，但雄性细胞数量显着减少（范围为 1-30），到产后 10 周时 SRY 已消失。使用绿色荧光蛋白表达杂合的同种异体雄性小鼠，在怀孕小鼠的血液和骨髓中检测到绿色荧光胎儿细胞。然而，仅在具有绿色荧光蛋白转基因绿色胎儿的Tg免疫怀孕小鼠的甲状腺中发现了绿色细胞，而在对照未免疫怀孕小鼠中则没有发现绿色细胞。从细胞学角度来看，胎儿细胞似乎具有不同的来源。使用抗体介导的甲状腺消化物亲和纯化，我们证明该细胞群包括 T 细胞和树突状细胞谱系的胎儿细胞。因此，免疫来源的胎儿细胞在怀孕期间和产后早期在 EAT 小鼠的甲状腺内积聚。这些数据表明发炎的甲状腺能够积聚胎儿细胞，包括 T 细胞和树突状细胞。这种活跃的免疫细胞可能对妊娠期和产后的自身免疫性甲状腺炎具有深远的调节影响。
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.