title: Autoimmune thyroiditis induced in mice depleted of particular T cell subsets. II. Immunohistochemical studies on the thyroiditis lesion.
abstract: The intravenous (i.v.) administration of Lyt-1dull T cells into syngeneic (C57BL/6 x C3H/He)F1 T cell-depleted B cell mice resulted in the induction of typical thyroiditis exhibiting massive cellular infiltration. The present study investigated which types of lymphoid cells infiltrate in the thyroiditis lesion and whether immunohistologic change takes place on epithelial cells of thyroid follicles. Both L3T4+ and Lyt-2+ T cells were found in the lesion, although the frequency of infiltration was higher in the former than in the latter. Thyroiditis was also induced by injection of Lyt-1dull L3T4+ but not of Lyt-1dull Lyt2+ T cells, indicating the critical role of a part of L3T4+ T cell subset (Lyt-1dull L3T4+ T cell subpopulation) in inducing thyroiditis. Only rare Lyt-2+ T cells were seen in such a thyroiditis lesion. Infiltrating T cells were predominantly of L3T4+, and these L3T4+ T cells formed cellular infiltrating lesion together with moderate number of B cells and relatively small number of macrophages. Importantly, class II MHC antigens were detected on epithelial cells of thyroid follicles. Such class II MHC expression was observed in coincidence with the area of cellular infiltration in the thyroid. These results demonstrate that: (1) a part of L3T4+ T cells which is required for the induction of thyroiditis by adoptive cell transfer infiltrates into the inflammatory lesion, (2) the induction of the thyroiditis lesion is formed by these L3T4+ T cells as well as B cells and macrophages, but does not necessarily depend on the participation of Lyt-2+ T cell subset, and (3) the aberrant expression of class II MHC antigens on thyroid epithelial cells coincides with cellular infiltration.
authors.affiliation: Biomedical Research Center, Osaka University Medical School, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Sugihara
authors.forename: S
authors.initials: S
authors.lastname: Maruo
authors.forename: T
authors.initials: T
authors.lastname: Tada
authors.forename: T
authors.initials: T
authors.lastname: Tsujimura
authors.forename: Y
authors.initials: Y
authors.lastname: Kohno
authors.forename: T
authors.initials: T
authors.lastname: Hamaoka
authors.forename: H
authors.initials: H
authors.lastname: Fujiwara
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D004848:Epithelium / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology*; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008809:Mice, Inbred C3H; D010641:Phenotype; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D013961:Thyroid Gland / Q000276:immunology / Q000378:metabolism; D013967:Thyroiditis, Autoimmune / Q000276:immunology* / Q000473:pathology
chemical_list: D000949:Histocompatibility Antigens Class II