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Induction of animal model of Graves' disease in BALB/c mice
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作者 Zhu-fang Tian1,2,Bing-yin Shi1,Xiao-yan Wu1,Li Xu1 1.Department of Endocrinology,the First Affiliated Hospital,Medical School of Xi’an Jiaotong University,Xi’an 710061 2.Department of Endocrinology,Xi’an Central Hospital,Xi’an 710003,China 《Journal of Pharmaceutical Analysis》 SCIE CAS 2009年第4期211-214,221,共5页
Objective To construct an animal model of Graves’ disease(GD)by immunizing BALB/c mice with hM12 cells co-expressing major histocompatibility complex(MHC)class II molecules and human thyrotropin receptor(TSHR)molecul... Objective To construct an animal model of Graves’ disease(GD)by immunizing BALB/c mice with hM12 cells co-expressing major histocompatibility complex(MHC)class II molecules and human thyrotropin receptor(TSHR)molecules.Methods BALB/c mice in experimental group(H-2d)were immunized with hM12 cells intraperitoneally every 2 weeks for six times,while mice in control group were immunized with M12 cells.Five weeks later,the thyroids were histologically examined,and serum samples were tested for thyroid-stimulating antibodies(TSAb)and thyroid hormone levels.Results One BALB/c mouse in experimental group developed Graves’-like disease.Total T4 and T3 levels in this mouse were above the upper limit of normal,TSAb activity was displayed in its serum.The thyroid histologically showed the features of thyroid hyperactivity including thyrocyte hypercellularity and colloid ABSorption.None of control mice developed Graves’-like disease.Conclusion An animal model with some characteristics of human Graves’ disease was successfully induced and the model will facilitate studies aimed directly at understanding the pathogenesis of autoimmunity in Graves’ disease. 展开更多
关键词 major histocompatibility complex thyrotropin receptor M12 cell Graves' disease
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TSH RECEPTOR GENETIC ALTERATIONS IN THE AUTONOMOUSLY FUNCTIONING THYROID ADENOMAS
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作者 施秉银 李雪萍 +3 位作者 李社莉 薛明战 王毅 徐莉 《Journal of Pharmaceutical Analysis》 SCIE CAS 2004年第1期39-41,共3页
Objective To determine the relationship between TSH receptor gene mutations and autonomously functioning thyroid adenomas (AFTAs). Methods The thyroid samples from 14 cases of diagnosed AFTAs were analyzed, with nor... Objective To determine the relationship between TSH receptor gene mutations and autonomously functioning thyroid adenomas (AFTAs). Methods The thyroid samples from 14 cases of diagnosed AFTAs were analyzed, with normal thyroid specimens adjacent to the tumors as controls. The 155 base pairs DNA fragments which encompassed the third cytoplasmic loop and the sixth transmembrane segments in the TSH receptor gene exon 10 were amplified by Polymerase chain reaction (PCR) and analyzed by the single-strand conformation polymorphism (SSCP). Direct sequencing of the PCR products was performed with Prism Dye Terminator Cycle Sequencing Core Kit. Results 6 of 14 AFTA specimens displayed abnormal migration in SSCP analysis. In sequence analysis of 3 abnormally migrated samples, one base substitution at nucleotide 1957 (A to C) and two same insertion mutations of one adenosine nucleotide between nucleotide 1972 and 1973 were identified. No mutations were found in controls. Conclusion This study confirmed the presence of TSH receptor gene mutations in AFTAs; both one-point substitution mutation and one-base insertion mutation were found to be responsible for the pathogenesis of AFTAs. 展开更多
关键词 thyrotropin receptor autonomously functioning thyroid adenoma gene mutation
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Role of natural killer T cells in Graves' disease
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作者 雒文田 郭辉 +1 位作者 青才文江 矢野明彦 《Chinese Medical Journal》 SCIE CAS CSCD 2002年第8期1183-1185,共3页
OBJECTIVE: To explore the role of natural killer T (NK T) cells in the pathogenesis of Graves' disease. METHODS: NK T cell deficient mice and wild BALB/c mice were immunized with cells expressing TSH receptor once... OBJECTIVE: To explore the role of natural killer T (NK T) cells in the pathogenesis of Graves' disease. METHODS: NK T cell deficient mice and wild BALB/c mice were immunized with cells expressing TSH receptor once every two weeks 6 times. Two weeks after the final immunization, the mice were killed and serum thyroxine levels, anti-TSH receptor antibodies and thyroid pathological changes were examined. RESULTS: The mean levels of TT(4) and TRAb in the immunized NK T cell deficient group were slightly elevated but significantly different from those of the non-immunized control group, while comparable to those in the immunized wild group. There were no significant changes of the activity levels of TSAb or TSBAb in the immunized NK T cell deficient mice compared to those in immunized wild control mice. Thyroids from immunized NK T cell deficient mice showed mild hypertrophy of some follicles as compared with non-immunized control mice. This change was comparable to immunized wild control mice. CONCLUSION: NK T cells may not be involved in the pathogenesis of Graves' disease. 展开更多
关键词 Animals CHO Cells CRICETINAE Female Graves Disease IMMUNIZATION Killer Cells Natural MICE Mice Inbred BALB C receptors thyrotropin Research Support Non-U.S. Gov't Thyroid Gland
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