Studies on the poathogenesis of Graves' disease and new treatment using our recently established mouse model.

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(1)The effect of genetic background on development of Graves' hyperthyroidism : we found that non-MHC genes, but not MHC, play a major role in development of Graves' hyperthyroidism in our mouse model.(2)The effect of environmental factors : Neither environmental. microorganisms nor bacterial/yeast components appear to be involved in the pathogenesis of disease.(3)The effect of Th1/Th2 balance of anti-TSH receptor immune response: Th2-immune deviation at the time of antigen-presentation by co-injection of adenovirus expressing interleukin-4, Schistosoma mansoni infection or administration of a-galactosylceremaide prevent Graves' disease induction. However, anti-TSHR immune response is once activated, Th2-immune polarization has little effect on disease course, indicating this type of immune manipulation may be just preventive, not therapeutic.(4)Analysis of the epitopes on TSH receptor : N-terminus of TSH receptor extracellular domain is the major epitopes, for anti-TSH receptor antibodies recognizing conformational or linear epitopes.(5)The effect of B cell deletion : Existence of normal B cell. population is essential for establishment of anti-TSH receptor memory T lymphocytes.