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Using a human TSH receptor (TSH-R) cDNA probe we investigated TSH-R expression levels in 20 human thyroid fragments by Northern blot analysis: 14 Graves' disease, 2 Hashimoto's disease, 3 endemic goiter and 1 healthy thyroid gland. TSH-R expression was low in those thyroids where expression of the major histocompatibility complex class I (MHC I), class II (MHC II) and intercellular adhesion molecule 1 (ICAM-1) was high, whereas expression of the endothelial leukocyte adhesion molecule 1 (ELAM-1) bore no relation to TSH-R expression. In situ hybridization showed that next to lymphocytes (MHC II), thyroid cells (MHC II, ICAM-1) and endothelial cells (ICAM-1, ELAM-1) were the source of transcripts of these T-cell activating antigens. We conclude that next to MHC I and II, the expression of additional T-cell activating antigens such as ICAM-1 and ELAM-1 play a role in the initiation of auto-immune thyroid disease.
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