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, But Not for IL-4, in Spontaneous Autoimmune Thyroiditis in NOD.H-2h4 Mice1
,
Departments of
* Internal Medicine,
Pathology, and
Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO 65212; and
Veterans Affairs Research Service, Columbia, MO 65212
Spontaneous autoimmune thyroiditis (SAT) is an organ-specific
autoimmune disease characterized by chronic inflammation of the thyroid
by T and B lymphocytes. To investigate the roles of Th1 and Th2
cytokines in the pathogenesis of SAT, IFN-
-/- and
IL-4-/- NOD.H-2h4 mice were generated.
IL-4-/- mice developed lymphocytic SAT (L-SAT) comparable
to that of wild-type (WT) mice. They produced little anti-mouse
thyroglobulin (MTg) IgG1, but had levels of anti-MTg IgG2b
comparable to WT mice. Compared with WT mice, IFN--/-
mice produced significantly less anti-MTg IgG1 and IgG2b. Absence
of IFN- resulted in abnormal proliferation of thyroid epithelial
cells with minimal lymphocyte infiltration. Thyroids of
IFN--/- mice had markedly reduced B lymphocyte
chemoattractant expression, B cell and plasma cell infiltration, and
decreased MHC class II expression on thyrocytes compared with WT mice.
Adoptive transfer of WT splenocytes to IFN--/- mice
restored the capacity to develop typical L-SAT, enhanced anti-MTg
IgG1 and IgG2b production, up-regulated MHC class II expression on
thyrocytes and decreased thyrocyte proliferation. These results suggest
that IFN- plays a dual role in the development of SAT. IFN- is
required for development of L-SAT, and it also functions to inhibit
thyroid epithelial cell proliferation.
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