Both CD4+ T cells and CD8+ T cells are required for iodine accelerated thyroiditis in NOD mice

被引:72
作者
Hutchings, PR [1 ]
Verma, S [1 ]
Phillips, JM [1 ]
Harach, SZ [1 ]
Howlett, S [1 ]
Cooke, A [1 ]
机构
[1] Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England
关键词
NOD mice; thyroiditis; iodine;
D O I
10.1006/cimm.1998.1446
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The nonobese diabetic (NOD) mouse, a spontaneous animal model for insulin-dependent diabetes mellitus, displays a tendency in common with human diabetic populations to develop autoimmune thyroiditis although incidence and severity of thyroid lesions vary widely among different colonies around the world. A congenic strain of NOD mice bearing I-Ak on a NOD background (NOD-H2(h4)) has recently been derived and displays a much greater tendency to develop thyroiditis and autoantibodies to mouse thyroglobulin (MTg) although it is free of diabetes. Both thyroid infiltrates and autoantibody formation are accelerated and enhanced in NOD-H2(h4) mice by increased iodine intake. The effect of increased iodine intake on NOD mice themselves has not been directly investigated although a recent study of these animals given high or low doses of iodine showed no follicular destruction unless the mice were first rendered goitrous by iodine deprivation. We found that dietary iodine increased both the incidence and the severity of thyroid lesions in our NOD mice although autoantibodies to MTg were absent. NOD background genes appear to be essential for the development of these lesions, which were maximal after 4 weeks of iodine administration and showed no significant regression when the iodine was stopped. Furthermore, our studies show for the first time that both CD4(+) and CD8(+) T cells are necessary for the development of this accelerated but essentially spontaneous murine thyroid disease. (C) 1999 Academic Press.
引用
收藏
页码:113 / 121
页数:9
相关论文
共 31 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]   THYROID-CELL INJURY IS AN INITIAL EVENT IN THE INDUCTION OF AUTOIMMUNE-THYROIDITIS BY IODINE IN OBESE STRAIN CHICKENS [J].
BAGCHI, N ;
BROWN, TR ;
SUNDICK, RS .
ENDOCRINOLOGY, 1995, 136 (11) :5054-5060
[3]   INDUCTION OF AUTOIMMUNE-THYROIDITIS IN CHICKENS BY DIETARY IODINE [J].
BAGCHI, N ;
BROWN, TR ;
URDANIVIA, E ;
SUNDICK, RS .
SCIENCE, 1985, 230 (4723) :325-327
[4]   HIGH AND LOW DIABETES INCIDENCE NONOBESE DIABETIC (NOD) MICE - ORIGINS AND CHARACTERIZATION [J].
BAXTER, AG ;
KOULMANDA, M ;
MANDEL, TE .
AUTOIMMUNITY, 1991, 9 (01) :61-67
[5]   HIGH-INCIDENCE OF THYROIDITIS AND ANTITHYROID AUTOANTIBODIES IN NOD MICE [J].
BERNARD, NF ;
ERTUG, F ;
MARGOLESE, H .
DIABETES, 1992, 41 (01) :40-46
[6]   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
[7]  
CHAMPION BR, 1987, J IMMUNOL, V139, P3665
[8]   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
[9]   Analysis of susceptibility of NOD mice to spontaneous and experimentally induced thyroiditis [J].
Damotte, D ;
Colomb, E ;
Cailleau, C ;
Brousse, N ;
Charreire, J ;
Carnaud, C .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1997, 27 (11) :2854-2862
[10]   ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA) QUANTITATIVE ASSAY OF IMMUNOGLOBULIN-G [J].
ENGVALL, E ;
PERLMANN, P .
IMMUNOCHEMISTRY, 1971, 8 (09) :871-&