0000000000398638

AUTHOR

Paola Montagna

showing 3 related works from this author

Possible Pathogenetic Relevance of Interleukin-1beta in "Destructive" Organ-specific Autoimmune Disease (Hashimoto's Thyroiditis)

1999

Thyroid follicular cells (TFC) abundantly express a variety of immunologically relevant surface molecules in Hashimoto's thyroiditis (HT), for example, MHC antigens and adhesion molecules such as ICAM-1. Cytokines produced by infiltrating type 1 helper and cytotoxic T cells are importantly involved in de novo expression or up-regulation of such molecules. We recently demonstrated that TFC from HT patients almost invariably bear on their surface two additive functional molecules: Fas/Apo1/CD95, an important participant in apoptosis, and B7.1, a member of a family of "co-stimulatory" molecules that are crucial for efficient antigen presentation. To date, 12 out of 14 surgical HT thyroid speci…

medicine.medical_specialtymedicine.medical_treatmentAntigen presentationThyroid Glandmedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyFas ligandAutoimmunityHistory and Philosophy of ScienceInternal medicinemedicineHumansCytotoxic T cellfas ReceptorChemistryGeneral NeuroscienceThyroiditis AutoimmuneInterleukinFas receptorMolecular biologyGraves DiseaseRecombinant ProteinsCytokineEndocrinologyApoptosisB7-1 AntigenCytokinesInterleukin-1Annals of the New York Academy of Sciences
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Differential regulation of Fas-mediated apoptosis in both thyrocyte and lymphocyte cellular compartments correlates with opposite phenotypic manifest…

2001

Several mechanisms are probably involved in determining the evolution of autoimmune thyroid disease (AITD) towards either hypothyroidism and the clinical syndrome known as Hashimoto's thyroiditis (HT) or toward hyperthyroidism and the symptoms of Graves' disease (GD). To gain further insight into such mechanisms we performed an exhaustive comparative analysis of the expression of key molecules regulating cell death (Fas, Fas ligand [FasL], Bcl-2) and apoptosis in both thyrocytes and thyroid infiltrating lymphocytes (TILs) from patients with either GD or HT. GD thyrocytes expressed less Fas/FasL than HT thyrocytes, whereas GD TILs had higher levels of Fas/FasL than HT TILs. GD thyrocytes exp…

AdultMaleendocrine systemmedicine.medical_specialtyProgrammed cell deathFas Ligand Proteinendocrine system diseasesEndocrinology Diabetes and MetabolismLymphocyteThyroid Glandchemical and pharmacologic phenomenaApoptosisThyroiditisFas ligandAutoimmune DiseasesEndocrinologyInternal medicinemedicineHumansLymphocytesRNA Messengerfas ReceptorCellular compartmentAgedMembrane GlycoproteinsChemistryReverse Transcriptase Polymerase Chain ReactionThyroidThyroiditis Autoimmunehemic and immune systemsMiddle Agedmedicine.diseasePhenotypeThyroid DiseasesGraves DiseaseEndocrinologymedicine.anatomical_structurePhenotypeGene Expression RegulationProto-Oncogene Proteins c-bcl-2ApoptosisFemaleThyroid : official journal of the American Thyroid Association
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Regulation of Apoptosis in Endocrine Autoimmunity

2002

Dysregulation of apoptosis is associated with the pathogenesis of organ-specific autoimmune diseases, through altered target organ susceptibility. Apoptosis signaling pathways can be initiated through activation of death receptors such as Fas. A comparative analysis of the expression of Fas and FasL, the antiapoptotic molecule Bcl-2, and apoptosis in both thyrocytes and thyroid-infiltrating lymphocytes (TILs) from patients with either Graves' disease (GD) or Hashimoto's thyroiditis (HT) was performed. GD thyrocytes expressed less Fas than HT thyrocytes, whereas GD TILs had higher levels of Fas and FasL than HT TILs. GD thyrocytes expressed higher levels of Bcl-2 compared with HT thyrocytes.…

medicine.medical_specialtybusiness.industryGeneral NeuroscienceGraves' diseaseThyroidhemic and immune systemschemical and pharmacologic phenomenamedicine.diseaseFas receptormedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyFas ligandAutoimmunityEndocrinologymedicine.anatomical_structureHistory and Philosophy of ScienceApoptosisHormone receptorInternal medicinemedicinebusinessCell damageAnnals of the New York Academy of Sciences
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