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An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
The alpha-galactosyl epitope on human normal and autoimmune thyroid cells
A Thall1, J Etienne-Decerf, R J Winand
1Department of Laboratory Medicine, University of California, San Francisco 94143.
Autoimmunity
|January 1, 1991
Summary
The natural anti-Gal antibody targets alpha-galactosyl epitopes found on thyroid cells. While these epitopes are present in normal and Graves
Area of Science:
- Immunology
- Endocrinology
- Glycobiology
Background:
- Circulating human IgG includes natural anti-Gal antibodies targeting the alpha-galactosyl epitope (Gal alpha 1-3Gal beta 1-4GlcNAc-R).
- This epitope is abundant in non-primate mammals and New World monkeys but diminished in humans and apes.
- Previous research suggested anti-Gal interaction with aberrant alpha-galactosyl epitopes on thyroid cells may initiate autoimmune thyroid disorders.
Purpose of the Study:
- To investigate the role of alpha-galactosyl epitopes in the development of autoimmune thyroid disorders, specifically Graves' disease.
- To assess the expression levels of alpha-galactosyl epitopes on thyroid cell membranes in normal individuals and patients with Graves' disease.
Main Methods:
- Utilized a sensitive radioimmunoassay to quantify alpha-galactosyl epitope expression on thyroid cell membranes.
- Assessed the activity of alpha 1-3-galactosyltransferase, the enzyme responsible for synthesizing the alpha-galactosyl epitope, in microsomal fractions.
Main Results:
- Alpha-galactosyl epitopes were detected on thyroid cells from both normal individuals and patients with Graves' disease.
- No significant difference was observed in the concentration of these epitopes between Graves' disease and normal thyroid membranes.
- Alpha 1-3-galactosyltransferase activity showed a non-significant increase in some Graves' disease patients compared to controls.
Conclusions:
- Under physiological conditions, anti-Gal antibody interaction with alpha-galactosyl epitopes does not appear to cause thyroid pathology.
- Aberrant expression or altered presentation of alpha-galactosyl epitopes on thyroid cells could potentially lead to effective anti-Gal binding.
- Further research is needed to elucidate the precise mechanisms linking alpha-galactosyl epitopes and autoimmune thyroid diseases.
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