Km. Chen et al., Characterization of thyroid fibrosis in a murine model of granulomatous experimental autoimmune thyroiditis, J LEUK BIOL, 68(6), 2000, pp. 828-835
This study was initiated to identify and characterize thyroid fibrosis in a
murine model of granulomatous experimental autoimmune thyroiditis (G-EAT)
and determine if TGF-beta1 might be involved in fibrosis. G-EAT was induced
by transfer of mouse thyroglobulin-sensitized spleen cells activated in vi
tro with thyroglobulin, anti-IL-2R, and IL-12, There was almost complete de
struction of thyroid follicles, leading to fibrosis of the gland and reduce
d serum T4 levels. Fibrosis was confirmed by staining for collagen and alph
a smooth-muscle actin, a marker of myofibroblasts. Kinetic studies characte
rized the onset and development of thyroid fibrosis. TGF-beta1 was increase
d at mRNA and protein levels, and expression of TGF-beta1 protein parallele
d G-EAT severity. Comparison of staining patterns showed that TGF-beta1 was
expressed in areas of myofibroblast and collagen accummulation, implying t
hat TGF-beta1 may play a role in fibrosis in G-EAT, Further studies demonst
rated that myofibroblasts, macrophages, and thyrocytes contributed to TGF-b
eta1 production. This provides an excellent model to study the mechanisms o
f fibrosis associated with autoimmune damage.