Expression of intracellular adhesion molecule-1 and vascular cell adhesionmolecule-1 and homing factor CD44 after engraftment of Graves' lymphocytesin xenotransplanted human thyroid tissue in athymic nude mice

Citation
K. Jungheim et al., Expression of intracellular adhesion molecule-1 and vascular cell adhesionmolecule-1 and homing factor CD44 after engraftment of Graves' lymphocytesin xenotransplanted human thyroid tissue in athymic nude mice, THYROID, 11(9), 2001, pp. 831-837
Citations number
64
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
THYROID
ISSN journal
10507256 → ACNP
Volume
11
Issue
9
Year of publication
2001
Pages
831 - 837
Database
ISI
SICI code
1050-7256(200109)11:9<831:EOIAMA>2.0.ZU;2-P
Abstract
The expression of adhesion molecules on thyrocytes and endothelium. cells p lays an important role in the pathogenesis of Graves' disease (GD). The int ercellular adhesion molecule-1 (ICAM-1), the vascular cell adhesion molecul e-1 (WAM-1), and the homing receptor CD44 are responsible for the specific migration of lymphocytes in autoimmune thyroid diseases (AITD) (homing). Ei ght weeks after transplantation of thyroid tissue from 26 patients with non autoimmune thyroid disease (nontoxic nodular goiter [NTG]) into nude mice, peripheral (PBL) and intrathyroidal lymphocytes (ITL) from 14 patients with NTG and 12 patients with GD were grafted into the animals. Two days after lymphocyte engraftment, the thyroid transplants were examined histologicall y (HE) and immunohistologically stained with monoclonal antibodies directed against ICAM-1, VCAM-1, and CD44. After injection of GD lymphocytes, thyro id transplants expressed significantly more ICAM-1, VCAM-1, and CD44 than a fter injection of NTG lymphocytes. This expression was even more pronounced after grafting of GD intrathyroidal lymphocytes. Our data demonstrate that only GD lymphocytes induce the expression of adhesion molecules and homing factor CD44, both of which play an important role in the migration of lymp hocytes and induction of the autoimmune process.