title: Expression of adhesion molecules on infiltrating T cells in thyroid glands from patients with Graves' disease.
abstract: The present study was performed to elucidate the role of adhesion molecules in the pathogenesis of Graves' disease. Peripheral blood and intrathyroidal mononuclear cells were obtained from 14 patients with Graves' disease. The expression of adhesion molecules and HLA-DR antigen on CD4+ cells and CD4+ cell subpopulations was analysed by the two- or three-colour immunofluorescence method. The expression of adhesion molecules including LFA-1 alpha, LFA-1 beta, CD2, VLA-4 alpha and VLA-5 alpha on CD4+ cells in the thyroid gland was markedly higher than that in peripheral blood. In peripheral blood CD4+ cell subsets, the CD4+ CD45RO+ cell population had an enhanced expression of the adhesion molecules compared with the CD4+ CD45RA+ cell population. However, there was no significant difference in the expression of adhesion molecules by CD4+ cell populations and subsets between Graves' disease and healthy subjects. The thyroid gland from Graves' disease contained a higher percentage of CD4+ CD45RO+ cells and a lower percentage of CD4+ CD45RA+ cells. In intrathyroidal CD4+ cell subsets, the CD4+ CD45RO+ cell population had an increased expression of LFA-1 and CD2 compared with the CD4+ CD45RA+ cell population, but there was no significant difference in VLA-4 and VLA-5 expression between the two cell subsets. Furthermore, the expression of LFA-1 and CD2 on the CD4+ CD45RO+ cell population in the thyroid was significantly higher than that in matched peripheral blood. A similar finding was also observed for the CD4+ CD45RA+ cell population. The thyroid gland had an increased percentage of CD4+ HLA-DR+ cells compared with matched or healthy peripheral blood. However, there was no significant difference in the percentage of HLA-DR+ cells in the thyroid gland between CD4+ CD45RO+ cell and CD4+ CD45RA+ cell populations. These results suggest that increased expression of adhesion molecules on CD4+ cells may be responsible for the migration of these cells into thyroid glands and cellular interactions between these cells and thyroid epithelial cells.
authors.affiliation: Ito Hospital, Tokyo, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Ishikawa
authors.forename: K
authors.initials: K
authors.lastname: Eguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Ueki
authors.forename: M
authors.initials: M
authors.lastname: Nakashima
authors.forename: H
authors.initials: H
authors.lastname: Shimada
authors.forename: K
authors.initials: K
authors.lastname: Ito
authors.forename: S
authors.initials: S
authors.lastname: Nagataki
mesh_terms: D000328:Adult; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D018801:CD2 Antigens; D015704:CD4 Antigens / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005455:Fluorescent Antibody Technique; D015870:Gene Expression; D006111:Graves Disease / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D017493:Leukocyte Common Antigens / Q000378:metabolism; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D008297:Male; D017469:Receptors, Fibronectin / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism; D016029:Receptors, Very Late Antigen / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology; D013961:Thyroid Gland / Q000276:immunology* / Q000473:pathology
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D018801:CD2 Antigens; D015704:CD4 Antigens; D015815:Cell Adhesion Molecules; D006684:HLA-DR Antigens; D016169:Lymphocyte Function-Associated Antigen-1; D017469:Receptors, Fibronectin; D011971:Receptors, Immunologic; D016029:Receptors, Very Late Antigen; D017493:Leukocyte Common Antigens