Spontaneous autoimmune thyroiditis in NOD.H-2h4 mice

被引:160
作者
Braley-Mullen, H
Sharp, GC
Medling, B
Tang, HW
机构
[1] Univ Missouri, Sch Med, Dept Internal Med, Columbia, MO 65212 USA
[2] Univ Missouri, Sch Med, Dept Mol Microbiol & Immunol, Columbia, MO 65212 USA
[3] Univ Missouri, Sch Med, Dept Pathol, Columbia, MO 65212 USA
[4] Dept Vet Affairs Med Ctr, Res Serv, Columbia, MO 65212 USA
关键词
autoimmunity; cytokines; T cells; thyroiditis;
D O I
10.1006/jaut.1999.0272
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
NOD.H-2h4 mice, which express I-A(k) on the NOD genetic background, spontaneously develop autoimmune thyroiditis (SAT) and anti-mouse thyroglobulin (MTg) autoantibodies. The incidence of SAT is nearly 100% in mice of both sexes 6-8 weeks after administration of 0.05% NaI in the drinking water. After reaching maximum severity, inflammation is chronic over the next 3-4 months. All mice that develop thyroid lesions also produce MTg-specific IgG1 and IgG2b autoantibodies. Thyroid lesions and anti-MTg autoantibodies did not develop in CBA/J (H-2(k)) or NOD.SWR(H-2(q)) mice after administration of NaI water. Both CD4(+) and CD8(+) T cells are involved in the initial development of SAT. Depletion of CD4(+), but not CD8(+), T cells after thyroid lesions have developed also markedly reduced SAT severity, indicating that CD4(+) T cells are required for both developing and maintaining SAT. Analysis of cytokine gene expression indicated that both Th1 and Th2 cytokines were expressed in thyroids of NOD.H-2h4 mice with SAT. Th1 and proinflammatory cytokines were maximally expressed 4-6 weeks after mice began receiving NaI water, while Th2 cytokine gene expression was greatest at 8-15 weeks, when lesions had reached maximal severity and were in the chronic phase. TGF-beta was highly expressed in NOD.H-2h4 thyroids, irrespective of whether the mice had received NaI water or had thyroid lesions, (C) 1999 Academic Press.
引用
收藏
页码:157 / 165
页数:9
相关论文
共 47 条
[1]   THE EFFECT OF IODIDE INGESTION ON THE DEVELOPMENT OF SPONTANEOUS LYMPHOCYTIC THYROIDITIS IN THE DIABETES-PRONE BB/W RAT [J].
ALLEN, EM ;
APPEL, MC ;
BRAVERMAN, LE .
ENDOCRINOLOGY, 1986, 118 (05) :1977-1981
[2]   INDUCTION OF AUTOIMMUNE-THYROIDITIS IN CHICKENS BY DIETARY IODINE [J].
BAGCHI, N ;
BROWN, TR ;
URDANIVIA, E ;
SUNDICK, RS .
SCIENCE, 1985, 230 (4723) :325-327
[3]   HIGH-INCIDENCE OF THYROIDITIS AND ANTITHYROID AUTOANTIBODIES IN NOD MICE [J].
BERNARD, NF ;
ERTUG, F ;
MARGOLESE, H .
DIABETES, 1992, 41 (01) :40-46
[4]  
Braley-Mullen H, 1998, AM J PATHOL, V152, P1347
[5]   INDUCTION OF SEVERE GRANULOMATOUS EXPERIMENTAL AUTOIMMUNE-THYROIDITIS IN MICE BY EFFECTOR-CELLS ACTIVATED IN THE PRESENCE OF ANTI-INTERLEUKIN-2 RECEPTOR ANTIBODY [J].
BRALEYMULLEN, H ;
SHARP, GC ;
BICKEL, JT ;
KYRIAKOS, M .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 173 (04) :899-912
[6]   INDUCTION OF EXPERIMENTAL AUTOIMMUNE-THYROIDITIS IN MICE WITH INVITRO ACTIVATED SPLENIC T-CELLS [J].
BRALEYMULLEN, H ;
JOHNSON, M ;
SHARP, GC ;
KYRIAKOS, M .
CELLULAR IMMUNOLOGY, 1985, 93 (01) :132-143
[7]   REGULATION OF THE INDUCTION AND RESOLUTION OF GRANULOMATOUS EXPERIMENTAL AUTOIMMUNE-THYROIDITIS IN MICE BY CD8(+) T-CELLS [J].
BRALEYMULLEN, H ;
MCMURRAY, RW ;
SHARP, GC ;
KYRIAKOS, M .
CELLULAR IMMUNOLOGY, 1994, 153 (02) :492-504
[8]   IMMUNE-MECHANISMS IN AUTOIMMUNE-THYROIDITIS [J].
CHARREIRE, J .
ADVANCES IN IMMUNOLOGY, 1989, 46 :263-+
[9]   Inhibition of the development of spontaneous autoimmune thyroiditis in the obese strain (OS) chickens by in vivo treatment with anti-CD4 or anti-CD8 antibodies [J].
Cihak, J ;
Hoffmann-Fezer, G ;
Wasl, M ;
Merkle, H ;
Kaspers, B ;
Vainio, O ;
Plachy, J ;
Hala, K ;
Wick, G ;
Stangassinger, M ;
Losch, U .
JOURNAL OF AUTOIMMUNITY, 1998, 11 (02) :119-126
[10]   THE EFFECT OF T-CELL SUBSET DEPLETION ON AUTOIMMUNE-THYROIDITIS IN THE BUFFALO STRAIN RAT [J].
COHEN, SB ;
DIAMANTSTEIN, T ;
WEETMAN, AP .
IMMUNOLOGY LETTERS, 1990, 23 (04) :263-268