自身免疫性甲状腺炎
点头
甲状腺炎
内分泌学
甲状腺球蛋白
甲状腺
II型干扰素
过继性细胞移植
免疫学
内科学
B细胞
MHC II级
T细胞
干扰素γ
医学
细胞因子
抗体
免疫系统
糖尿病
作者
Shiguang Yu,Gordon C. Sharp,Helen Braley‐Mullen
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2002-10-01
卷期号:169 (7): 3999-4007
被引量:54
标识
DOI:10.4049/jimmunol.169.7.3999
摘要
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-gamma(-/-) 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-gamma(-/-) mice produced significantly less anti-MTg IgG1 and IgG2b. Absence of IFN-gamma resulted in abnormal proliferation of thyroid epithelial cells with minimal lymphocyte infiltration. Thyroids of IFN-gamma(-/-) 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-gamma(-/-) 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-gamma plays a dual role in the development of SAT. IFN-gamma is required for development of L-SAT, and it also functions to inhibit thyroid epithelial cell proliferation.
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