title: Transgenic mice producing major histocompatibility complex class II molecules on thyroid cells do not develop apparent autoimmune thyroid diseases.
abstract: The expression of major histocompatibility complex (MHC) class II molecules on thyrocytes has been demonstrated in autoimmune thyroid diseases. However, the role of this aberrant MHC class II in disease development is controversial. In particular, it remains unknown whether MHC class II expression on thyrocytes, which are nonprofessional antigenpresenting cells, plays a role in inducing autoimmune processes. To clarify this issue, we have produced transgenic mice harboring an MHC class II gene ligated to the promoter of the rat TSH receptor. We obtained three lines of transgenic mice, and the expression of MHC class II by the thyrocytes was demonstrated by immunofluorescence staining and flow cytometry. Our examination revealed no obvious abnormalities in thyroid histology or in thyroid autoantibody production in these transgenic mice. Although serum-free T(4) levels were slightly lower than those of their nontransgenic littermates, no transgenic mouse suffered from clinical hypothyroidism or hyperthyroidism. Furthermore, thyroid lymphocytic infiltration was absent, and MHC class II-expressing thyrocytes obtained from transgenic mice failed to stimulate the proliferation of autologous T cells in vitro. Taken together, these results show that transgenic mice with MHC class II molecules on their thyrocytes do not develop apparent autoimmune thyroid diseases, suggesting that aberrant MHC class II expression alone is not sufficient to induce thyroid autoimmunity.
authors.affiliation: Translational Research Center, Kyoto University School of Medicine, 54 Shogoin Kawaharacho Sakyo-ku, Kyoto 606-8507, Japan.
authors.forename: Yu-Shu
authors.initials: YS
authors.lastname: Li
authors.forename: Naotetsu
authors.initials: N
authors.lastname: Kanamoto
authors.forename: Yuji
authors.initials: Y
authors.lastname: Hataya
authors.forename: Kenji
authors.initials: K
authors.lastname: Moriyama
authors.forename: Hitomi
authors.initials: H
authors.lastname: Hiratani
authors.forename: Kazuwa
authors.initials: K
authors.lastname: Nakao
authors.forename: Takashi
authors.initials: T
authors.lastname: Akamizu
mesh_terms: D000818:Animals; D001323:Autoantibodies / Q000096:biosynthesis; D001327:Autoimmune Diseases / Q000276:immunology*; D002455:Cell Division; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis* / Q000235:genetics; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000473:pathology; D051379:Mice; D008809:Mice, Inbred C3H; D008822:Mice, Transgenic; D011401:Promoter Regions, Genetic / Q000235:genetics; D011989:Receptors, Thyrotropin / Q000235:genetics; D013601:T-Lymphocytes / Q000276:immunology; D013959:Thyroid Diseases / Q000276:immunology*; D013961:Thyroid Gland / Q000276:immunology* / Q000473:pathology; D013974:Thyroxine / Q000097:blood
chemical_list: D001323:Autoantibodies; D000949:Histocompatibility Antigens Class II; D011989:Receptors, Thyrotropin; D013974:Thyroxine