ArticleExperimental and therapeutic medicine2021
Antibodies against thyroid-stimulating hormone receptor cause maternal-neonatal transmission of Graves' Disease.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Insight Into Mouse Models of Hyperthyroidism.Frontiers in endocrinology · 2022Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate whether the thyroid-stimulating hormone receptor (TSHR) autoantibodies (Ab) from mothers with Graves' disease (GD) could cause neonatal thyroid disease and the underlying mechanisms of this. An adenovirus expressing the TSHR A-subunit and a control adenovirus expressing β-galactosidase was constructed by Beijing Sino Geno Max Co., Ltd. The sequences were subsequently verified and amplified via PCR. A GD model was established in female BALB/c mice (n=90) by three intramuscular injections of a TSHR-expressing adenovirus (Ad-TSHR). Mice injected with Ad-β-galactosidase served as a sham immunization group. The immunized females were paired with unimmunized males to generate offspring. The serum levels of TSHR-Ab and thyroxine (T4) of mothers and neonates were measured after delivery. Breast milk was collected from the stomachs of neonatal mice to determine the TSHR-Ab levels. The positive rate of serum TSHR-Ab (>0.3 IU/l) in the TSHR group was 99% (89/90) and 0% in the sham group. The mother mice in the TSHR group had elevated serum T4 levels and the thyroid pathological features of Graves' hyperthyroidism.GD mice gave birth to smaller newborns with thyroid pathological changes and higher serum levels of TSHR-Ab and T4, compared to the offspring in the sham group. The TSHR-Ab levels in breast milk from the GD mice declined with time. Mice immunized with Ad-TSHR exhibited the clinicopathological features of human GD and give birth to neonates with thyroid disease at birth.
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