6533b850fe1ef96bd12a84d8
RESEARCH PRODUCT
Potential involvement of fas and its ligand in the pathogenesis of Hashimoto's thyroiditis
Aldo GalluzzoGiorgio StassiMatilde TodaroMarcello BagnascoGiuliana PapoffGiovina RubertiPierina RichiusaRuggero De MariaRoberto TestiCarla Giordanosubject
medicine.medical_specialtyFas Ligand Proteinmedicine.medical_treatmentThyroid GlandApoptosisPolymerase Chain ReactionThyroiditisFas ligandPathogenesisImmunoenzyme TechniquesInternal medicinemedicineTumor Cells CulturedHumansRNA Messengerfas ReceptorCells CulturedNucleic Acid Synthesis InhibitorsProtein Synthesis InhibitorsMultidisciplinaryMembrane GlycoproteinsChemistryThyroidThyroiditis AutoimmuneInterleukinAntibodies Monoclonalmedicine.diseaseFas receptorRecombinant ProteinsCytokinemedicine.anatomical_structureEndocrinologyApoptosisCytokinesInterleukin-1description
The mechanisms responsible for thyrocyte destruction in Hashimoto's thyroiditis (HT) are poorly understood. Thyrocytes from HT glands, but not from nonautoimmune thyroids, expressed Fas. Interleukin-1β (IL-1β), abundantly produced in HT glands, induced Fas expression in normal thyrocytes, and cross-linking of Fas resulted in massive thyrocyte apoptosis. The ligand for Fas (FasL) was shown to be constitutively expressed both in normal and HT thyrocytes and was able to kill Fas-sensitive targets. Exposure to IL-1β induced thyrocyte apoptosis, which was prevented by antibodies that block Fas, suggesting that IL-1β-induced Fas expression serves as a limiting factor for thyrocyte destruction. Thus, Fas-FasL interactions among HT thyrocytes may contribute to clinical hypothyroidism.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1997-02-14 |