Genetic susceptibility determines the severity of experimental autoimmune thyroiditis (EAT) in mice and may be related to the balance of Th1 or Th2 responses. rmIL12 treatment concurrent with immunizations of mouse thyroglobulin in complete Freund's adjuvant enhanced thyroid lesion prevalence and severity in genetically nonsusceptible Balb/c mice while genetically susceptible CBA/J mice showed only slightly enhanced disease but an accelerated infiltration of the thyroid by lymphocytes. IL12 treatment after immunization resulted in an increase in lesion prevalence and severity in Balb/c mice similar to the concurrent treatment group, but resulted in a decrease in lesion severity in CBA/J mice. In both strains, concurrent treatment produced a significant decrease in anti-mTg IgG1 production (a surrogate for a Th2 response), but Balb/c mice failed to demonstrate the significant increase in anti-mTg IgG2a (a Th1 response) seen in the CBA/J mice. Treatment after disease was established produced an increase in the ratio of anti-mTg IgG2a:IgG1 in Balb/c mice which correlated with the presence of lesions. In both strains and treatments, an increase in IgG2a:IgG2b correlated with lesion presence. These results demonstrate that IL12 can convert genetically nonsusceptible Balb/c mice to a susceptible phenotype.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology