Titlebook: ;

Somber

,The Genetics of Familial and Non-Familial Hyperthyroid Graves’ Disease,ntal factors (1). Pathologically, the thyroid gland is infiltrated by T cells and B cells reactive with thyroid antigens, including the thyrotropin receptor (TSHR). This infiltration is associated with the production of antibodies which stimulate the thyroid via the TSHR causing hyperthyroidism and

Seminar

,Thyroid Autoantibodies in Graves’ Disease, extreme is Hashimoto’s thyroiditis, in which autoantibodies to thyroid peroxidase (TPO) and sometimes to thyroglobulin (Tg), are associated with (but do not necessarily cause) destruction of thyroid follicular cells and hypothyroidism. Less commonly, atrophic thyroiditis can be caused by TSH recept

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institute

,Cytokines in Graves’ Disease,sponses. These molecules usually have pleiotropic actions and their effects can be synergistic or antagonistic. Many cytokines are produced by both immune and non-immune cells, often act in an autocrine or paracrine fashion, and thus they infrequently achieve detectable levels in the circulation. In

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,Co-Stimulatory Molecules in Graves’ Disease, the best characterized of which are helper and cytotoxic T cells. CD4+ helper T cells can be divided into two subtypes. Type 1 helper T cells (Th1) mainly synthesize interferon-γ and interleukin (IL)-2; type 2 helper T cells (Th2) principally secrete IL-1, IL-5, and IL-10 (1). The pathogenesis and

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Compass

,Animal Models of Graves’ Disease,es unravelling relevant pathogenic mechanisms exceedingly difficult. GD is very common but patients present when disease has advanced to the extent of causing clinical signs and symptoms, which is likely to be temporally removed from the initiating immune events. Thus it has long been recognized tha

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Thionamide Drug Therapy,oactive iodine (.I)(l–3). These treatments, all directed at the thyroid gland, are necessarily imperfect, because none stops production of stimulatory TSH receptor autoantibodies. It seems unlikely that therapy to interrupt the underlying process of thyroid autoimmunity will be available any time so

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,Radioiodine Therapy of Graves’ Disease,ton and Soley using 130I and 131I in 1940 were followed in 1941 by the first radioiodine therapy of Graves’ hyperthyroidism by Hertz and Roberts (1,2). Since this first successful use, 131I has now become the most common therapy for Graves’ disease in adult patients in the United States (3). However

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