about
Breaking tolerance to thyroid antigens: changing concepts in thyroid autoimmunityReview and hypothesis: does Graves' disease develop in non-human great apes?Thyroglobulin-thyroperoxidase autoantibodies are polyreactive, not bispecific: analysis using human monoclonal autoantibodies.Evidence that the complement control protein-epidermal growth factor-like domain of thyroid peroxidase lies on the fringe of the immunodominant region recognized by autoantibodies.Human monoclonal thyroglobulin autoantibodies: epitopes and immunoglobulin genes.Human autoantibodies modulate the T cell epitope repertoire but fail to unmask a pathogenic cryptic epitope.Directed mutagenesis in region 713-720 of human thyroperoxidase assigns 713KFPED717 residues as being involved in the B domain of the discontinuous immunodominant region recognized by human autoantibodies.Thyrotropin (TSH) receptor residue E251 in the extracellular leucine-rich repeat domain is critical for linking TSH binding to receptor activationThyroid antigens, not central tolerance, control responses to immunization in BALB/c versus C57BL/6 mice.Sex, genetics, and the control of thyroxine and thyrotropin in mice.Exceptional hyperthyroidism and a role for both major histocompatibility class I and class II genes in a murine model of Graves' disease.Antibodies to thyroid peroxidase arise spontaneously with age in NOD.H-2h4 mice and appear after thyroglobulin antibodies.Variable suppression of serum thyroxine in female mice of different inbred strains by triiodothyronine administered in drinking water.Novel information on the epitope of an inverse agonist monoclonal antibody provides insight into the structure of the TSH receptorImmunoglobulin heavy chain variable region and major histocompatibility region genes are linked to induced graves' disease in females from two very large families of recombinant inbred miceSubclinical nonautoimmune hyperthyroidism in a family segregates with a thyrotropin receptor mutation with weakly increased constitutive activity.Breaking tolerance in transgenic mice expressing the human TSH receptor A-subunit: thyroiditis, epitope spreading and adjuvant as a 'double edged sword'.Graves' hyperthyroidism is antibody-mediated but is predominantly a Th1-type cytokine disease.Distinct genetic signatures for variability in total and free serum thyroxine levels in four sets of recombinant inbred mice.Evidence that the thyroid-stimulating hormone (TSH) receptor transmembrane domain influences kinetics of TSH binding to the receptor ectodomain.The link between Graves' disease and Hashimoto's thyroiditis: a role for regulatory T cells.Crystal structure of a TSH receptor monoclonal antibody: insight into Graves' disease pathogenesis.Thyroid-stimulating autoantibodies in Graves disease preferentially recognize the free A subunit, not the thyrotropin holoreceptor.Relationship between thyrotropin receptor hinge region proteolytic posttranslational modification and receptor physiological functionAn attempt to induce "Graves' disease of the gonads" by immunizing mice with the luteinizing hormone receptor provides insight into breaking tolerance to self-antigens.The thyrotropin receptor autoantigen in Graves disease is the culprit as well as the victim.Insight into thyroid-stimulating autoantibody interaction with the thyrotropin receptor N-terminus based on mutagenesis and re-evaluation of ambiguity in this region of the receptor crystal structureA unique mouse strain that develops spontaneous, iodine-accelerated, pathogenic antibodies to the human thyrotrophin receptor.Evidence that TSH Receptor A-Subunit Multimers, Not Monomers, Drive Antibody Affinity Maturation in Graves' DiseaseDeleting the Redundant TSH Receptor C-Peptide Region Permits Generation of the Conformationally Intact Extracellular Domain by Insect Cells.Thyroid stimulating monoclonal antibodies: overcoming the road blocks and the way forward.Why measure thyroglobulin autoantibodies rather than thyroid peroxidase autoantibodies?Insight into Graves' hyperthyroidism from animal models.Role of self-tolerance and chronic stimulation in the long-term persistence of adenovirus-induced thyrotropin receptor antibodies in wild-type and transgenic miceThe thyrotropin receptor hinge region as a surrogate ligand: identification of loci contributing to the coupling of thyrotropin binding and receptor activationProbing structural variability at the N terminus of the TSH receptor with a murine monoclonal antibody that distinguishes between two receptor conformational formsShared and unique susceptibility genes in a mouse model of Graves' disease determined in BXH and CXB recombinant inbred mice.Thyrotropin-blocking autoantibodies and thyroid-stimulating autoantibodies: potential mechanisms involved in the pendulum swinging from hypothyroidism to hyperthyroidism or vice versa.The thyrotropin receptor hinge region is not simply a scaffold for the leucine-rich domain but contributes to ligand binding and signal transduction.Genetic linkages for thyroxine released in response to thyrotropin stimulation in three sets of recombinant inbred mice provide evidence for shared and novel genes controlling thyroid function
P50
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P50
name
Basil Rapoport
@ast
Basil Rapoport
@en
Basil Rapoport
@nl
type
label
Basil Rapoport
@ast
Basil Rapoport
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Basil Rapoport
@nl
prefLabel
Basil Rapoport
@ast
Basil Rapoport
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Basil Rapoport
@nl
P1006
P214
P5361
P1006
P214
P31
P5361
RapoportBasil1943-
P7859
lccn-n00120044