Transgenic Mice Producing Major Histocompatibility Complex Class II Molecules on Thyroid Cells Do Not Develop Apparent Autoimmune Thyroid Diseases
Autor: | Kenji Moriyama, Takashi Akamizu, Yuji Hataya, Kazuwa Nakao, Yushu Li, Naotetsu Kanamoto, Hitomi Hiratani |
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Rok vydání: | 2004 |
Předmět: |
Genetically modified mouse
medicine.medical_specialty T-Lymphocytes Thyroid Gland Fluorescent Antibody Technique Mice Transgenic Lymphocyte Activation medicine.disease_cause Major histocompatibility complex Autoimmune Diseases MHC Class II Gene Autoimmunity Mice Endocrinology Internal medicine MHC class I medicine Animals Lymphocytes Promoter Regions Genetic Autoantibodies Autoimmune disease Mice Inbred C3H MHC class II biology Thyroid Histocompatibility Antigens Class II Receptors Thyrotropin Flow Cytometry medicine.disease Thyroid Diseases Thyroxine medicine.anatomical_structure Immunology biology.protein Cell Division |
Zdroj: | Endocrinology. 145:2524-2530 |
ISSN: | 1945-7170 0013-7227 |
DOI: | 10.1210/en.2003-1654 |
Popis: | 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. |
Databáze: | OpenAIRE |
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