The Expression of Adhesion Molecules in Thyroid Glands from Patients with Graves' Disease

Abstract

We studied the potential role of adhesion molecules in the pathogenesis of Graves' disease. Thyroid specimens of Graves' thyroid glands and control thyroid glands were stained with monoclonal antibodies against adhesion molecules by an immunohistologic method. Thyroid tissues obtained from patients with Graves' disease had an enhanced expression of intercellular adhesion molecule-1 (ICAM-1) on capillary endothelial cells around the thyroid follicles and on postcapillary endothelial cells in lesions with aggregates of mononuclear cells. Positive staining for ICAM-1, lymphocyte function-associated antigen-1 (LFA-1), and very late antigen-4 (VLA-4) was found on the infiltrating mononuclear cells. The postcapillary vascular endothelial cells expressed increased endothelial-leukocyte adhesion molecule-1 (ELAM-1), but not vascular cell adhesion molecule-1 (VCAM-1). VCAM-1 and ELAM-1 were detected on the dendritic-like cells in the germinal centers of lymphoid follicle-like areas. No significant expression of these adhesion molecules was detected on normal thyroid glands. These results suggest that the LFA-l/ICAM-1 and ELAM-1 pathways may be responsible for the migration of mononuclear cells into the thyroid glands of patients with Graves' disease, and that the VLA-4/VCAM-1 pathway plays a critical role in the cellular interactions that lead to the formation of B-memory cells and the excess production of antibodies.