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-Deficient Mice Develop Severe Granulomatous Experimental Autoimmune Thyroiditis with Eosinophil Infiltration in Thyroids1
Departments of
*
Internal Medicine,
Molecular Microbiology and Immunology, and
Pathology, University of Missouri-Columbia School of Medicine, Columbia, MO 65212
To study the role of IFN-
in the development of granulomatous
experimental autoimmune thyroiditis (EAT), DBA1 mice with a disrupted
IFN- gene were used for adoptive EAT induction. Effector cells from
either IFN-+/+ or IFN--/- donor
mice activated with mouse thyroglobulin and anti-IL-2R mAb induced
severe granulomatous EAT. A predominant infiltration of the thyroid by
eosinophils was observed in recipients of IFN--/-
effector cells but not in recipients of IFN-+/+ cells.
Compared with wild-type mice, thyroids of recipients of
IFN--/- effector cells had decreased expression of
mRNA for Th1 cytokines and inducible nitric oxide synthetase.
Expression of Th2 cytokine mRNA was comparable to that of
IFN-+/+ mice, and expression of eotaxin was increased in
the thyroids of recipients of IFN--/- effector cells.
Activation of cells from either IFN-+/+ or
IFN--/- donors in the presence of IL-12 also induced
severe granulomatous EAT. Eosinophil infiltration in recipients of
IFN--/- cells was unaffected when effector cells were
activated with IL-12, and thyroids expressed predominantly Th2
cytokines. The extent of fibrosis of recipient thyroids was generally
greater when donor IFN-+/+ and IFN--/-
cells were activated with IL-12. Compared with IFN-+/+
mice, IFN--/- mice produced lower levels of mouse
thyroglobulin-specific autoantibodies after immunization with MTg and
LPS. These results indicate that cells from both IFN-+/+
and IFN--/- donors can induce severe granulomatous
EAT. However, damage of thyroid follicles by IFN--/-
and that by IFN-+/+ cells appear to involve different
mediators of inflammation.
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