6533b837fe1ef96bd12a3159

RESEARCH PRODUCT

Autoimmune thyroid disease: new models of cell death in autoimmunity

Ruggero De MariaGiorgio Stassi

subject

endocrine systemHistoryProgrammed cell deathFas Ligand Proteinendocrine system diseasesImmunologyThyroid GlandApoptosisAutoimmunityDiseasemedicine.disease_causeThyroiditisEducationAutoimmunityPathogenesisAntigenSettore MED/04 - PATOLOGIA GENERALEHumansMedicinefas ReceptorMembrane Glycoproteinsbiologybusiness.industryThyroidThyroiditis Autoimmunemedicine.diseaseGraves DiseaseComputer Science Applicationsmedicine.anatomical_structureModels AnimalImmunologybiology.proteinAntibodybusinessT-Lymphocytes Cytotoxic

description

Autoimmunity to thyroid antigens leads to two distinct pathogenic processes with opposing clinical outcomes: hypothyroidism in Hashimoto's thyroiditis and hyperthyroidism in Graves' disease. The high frequency of these diseases and easy accessibility of the thyroid gland has allowed the identification of key pathogenic mechanisms in organ-specific autoimmune diseases. In early investigations, antibody- and T-cell-mediated death mechanisms were proposed as being responsible for autoimmune thyrocyte depletion. Later, studies on apoptosis have provided new insights into autoimmune target destruction, indicating the involvement of death receptors and cytokine-regulated apoptotic pathways in the pathogenesis of thyroid autoimmunity.

https://doi.org/10.1038/nri750