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pubmed:abstractText |
Thyroid peroxidase purified from porcine thyroid (pTPO) was found to induce an experimental murine thyroiditis with genetic restriction which was very different from that induced by mouse thyroglobulin (mTg). C57BL/6 and C57BL/10 (both H-2b) were good responders for thyroiditis, whereas A/J (H-2a), BALB/c (H-2d), DBA/2 (H-2d), CBA (H-2k), C3H/He (H-2k), and SJL/J (H-2s) were poor responders. Genetic analyses using congenic or recombinant strains revealed the following results: The H-2-linked gene (probably the I-A subregion) had a weak association with the induction of thyroiditis, and at least one non-H-2-linked gene controlled the development of thyroid lesions; antibody production to pTPO, porcine thyroglobulin (pTg) and mTg did not correlate with the incidence of thyroiditis in any strain. None of the murine thyroid microsome-specific antibodies tested by the indirect immunofluorescent technique was detected. The T cell line specific for pTPO was successfully transferred to produce thyroid lesions in C57BL/6 mice. Thyroiditis appeared 3 days after the transfer of T cell blasts, and a low concentration of anti-pTPO antibodies was detected concurrently. Thyroid lesions remained up to 48 days with almost the same extent of thyroiditis, but anti-pTPO antibodies gradually increased. In the vaccination experiments using either 0.645 C/kg (2500 rad)-irradiated or 0.3% glutaraldehyde-fixed T cell blasts, the induction of thyroid lesions by transfer was strongly suppressed. Glutaraldehyde fixation was more effective than X-irradiation in preventing thyroiditis after the transfer of T cell blasts. Vaccination also suppressed significantly the development of thyroid lesions after pTPO administration.
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