Divergent Frequencies of IGF-I Receptor-Expressing Blood Lymphocytes in Monozygotic Twin Pairs Discordant for Graves’ Disease: Evidence for a Phenotypic Signature Ascribable to Nongenetic Factors

AUTOR(ES)

Douglas, Raymond S.

FONTE

The Endocrine Society

RESUMO

Context: Graves’ disease (GD) is an autoimmune process of the thyroid and orbital connective tissues. The fraction of T and B cells expressing IGF-I receptor (IGF-IR) is increased in GD. It is a potentially important autoantigen in GD. Susceptibility to GD arises from both genetic and acquired factors.

Documentos Relacionados

• Poliovirus variants selected on mutant receptor-expressing cells identify capsid residues that expand receptor recognition.
• Monoclonal antibody to the type I insulin-like growth factor (IGF-I) receptor blocks IGF-I receptor-mediated DNA synthesis: clarification of the mitogenic mechanisms of IGF-I and insulin in human skin fibroblasts.
• Granulosa cell-derived insulin-like growth factor (IGF) binding proteins are inhibitory to IGF-I hormonal action. Evidence derived from the use of a truncated IGF-I analogue.
• Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplasia in skeletal muscle
• Liver-derived insulin-like growth factor I (IGF-I) is the principal source of IGF-I in blood but is not required for postnatal body growth in mice