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Departments of
*
Internal Medicine,
Molecular Microbiology & Immunology, and
Pathology, University of Missouri-Columbia School of Medicine, Columbia, MO 65212
To study the role of IL-4 in development of granulomatous
experimental autoimmune thyroiditis (EAT), IL-4 gene-disrupted mice
expressing the EAT-susceptible H-2k haplotype were
generated and used for EAT induction. Spleen cells from mouse
thyroglobulin (MTg) and LPS-primed IL-4+/+ and
IL-4-/- donors could induce severe granulomatous EAT when
spleen cells were activated with MTg and anti-IL-2R mAb in the
presence of IL-12. Thyroid lesions had extensive follicular cell
proliferation, large numbers of histiocytes, polymorphonuclear
leukocytes, and multinucleated giant cells, in addition to lymphocytes
and other mononuclear cells. Expression of IFN-
gene mRNA and
production of IFN- by effector spleen cells stimulated with MTg and
IL-12 were similar for both IL-4+/+ and
IL-4-/- mice. Although IL-4 was undetectable in
IL-4-/- mice, expression of mRNA for IL-5, IL-10, and
IL-13 and production of IL-5 by both MTg-activated spleen cells and
anti-CD3-activated CD4+ T cells were comparable for
cells from IL-4+/+ and IL-4-/- mice,
indicating that the absence of IL-4 did not prevent production of other
Th2 cytokines. Production of MTg-specific IgG1 was very low or
undetectable in IL-4-/- mice. IL-4 gene mRNA and
MTg-specific IgG1 could be detected in IL-4+/+ or
IL-4-/- recipients only when they received effector cells
from IL-4+/+ donor mice, indicating that IL-4- and
IgG1-secreting cells are of donor origin. These results demonstrate
that IL-4 is not essential for development of granulomatous EAT.
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