Induction of hyperthyroxinemia in balb/c but not in several other strains of mice

Neelam M. Wagle, John S. Dallas, Gattadahalli S. Seetharamaiah, Ji Lao Fan, Rajesh K. Desai, Omeed Memar, Srinivasan Rajaraman, Bellur S. Prabhakar

Research output: Contribution to journalArticle

43 Scopus citations


We recently expressed the extracellular domain of the human TSHR (ETSHR) protein using a baculovirus expression system and purified it to homogeneity. The ETSHR specifically binds both TSH and antibodies to TSHR. In the present study, C57BL/6J, SJL/J, BALB/cJ and BlOBR.SgSnJ mice were immunized with the recombinant ETSHR or an equivalent amount of control antigen. All strains of mice produced high titers of antibody against the TSHR protein which were capable of blocking the binding of TSH to native TSHR. However, only BALB/cJ mice showed significantly elevated levels of thyroxine in their sera compared to the control mice. Similarly, BALB/cJ mice primed with ETSHR and then challenged with thyroid membranes showed significantly elevated levels of thyroxine. In addition, histopathological examination of thyroid glands from affected mice showed morphological changes characterized by hydropic and subnuclear vacuolar changes and focal scalloping, with no apparent inflammation or glandular destruction. Moreover, mice with elevated thyroxine levels showed increased in vivo thyroidal uptake of l31 Iodine. Together, these data suggest that BALB/cJ mice are susceptible to the induction of hyperthyroxinemia.

Original languageEnglish (US)
Pages (from-to)103-112
Number of pages10
Issue number2
StatePublished - Jan 1 1994
Externally publishedYes


  • Graves' disease
  • Hyperthyroxinemia
  • Thyrotropin receptor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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