Abstract
Agonistic antibodies that stimulate G protein-coupled receptors are accepted as causing diseases of the thyroid gland. Agonistic anti-thyrotropin receptor antibodies (TSAb) that mimic the action of thyrotropin (TSH) characterize Graves' disease. Nonetheless, the immunological mechanisms of TSAb production remain obscure. Autoantibodies directed against specific epitopes in the insulin receptor are rarely the cause of either recurrent hypoglycemia or a severe form of insulin resistance (type B insulin resistance). In cancer chemotherapy, antibodies against the death receptors DR4 and DR5 of tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL) are interesting therapeutic targets, since agonistic antibodies against DR5 and DR2 induce apoptosis in cancer cells. Furthermore, agonistic anti-CD40 antibodies profoundly suppress the immune response to infection with lymphocytic choriomeningitis virus.4 Thus agonistic antibodies directed against cell-surface receptors appear to have an in vivo functional capacity.
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