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  • Title: IL-12 prevents tolerance induction with mouse thyroglobulin by priming pathogenic T cells in experimental autoimmune thyroiditis: role of IFN-gamma and the costimulatory molecules CD40l and CD28.
    Author: Zhang W, Flynn JC, Kong YC.
    Journal: Cell Immunol; 2001 Feb 25; 208(1):52-61. PubMed ID: 11277619.
    Abstract:
    Deaggregated mouse thyroglobulin (dMTg) induces tolerance to experimental autoimmune thyroiditis (EAT), a Th1-cell-mediated disease. To test whether IL-12, a potent activator of Th1 cells, can overcome tolerance induction, different doses of IL-12 were given to CBA/J mice during the critical interval of 2--3 days after dMTg administration. After challenge with MTg/LPS, dMTg/IL-12-pretreated mice showed more extensive thyroiditis than immunized controls, but comparable levels of anti-MTg and T cell proliferation. Without challenge, few MTg antibodies were produced. In contrast, pretreatment with dMTg/poly A:U or dMTg/IL-1, two other T cell activators which also interfere with tolerance induction, induced antibodies before challenge, but not more severe thyroiditis. Mice pretreated with IL-12 without dMTg developed thyroiditis comparable to immunized controls, but less severe thyroiditis than dMTg/IL-12-pretreated mice. Clearly, IL-12 not only blocked tolerance induction, but also primed antigen-specific T cells during the tolerogenic period of dMTg pretreatment, resulting in stronger thyroiditis than immunization only. Neither treatment with anti-IFN-gamma nor the use of IFN-gamma knockout mice altered the capacity of IL-12 to prevent tolerance induction. However, both anti-CD28 and anti-CD40L antibodies diminished the priming effect by dMTg/IL-12. The mechanisms of IL-12 action include priming of MTg-specific T cells and the involvement of T cell costimulatory molecules.
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