Environmental triggers of autoimmune thyroiditis

被引:128
作者
Burek, C. Lynne [1 ]
Talor, Monica V. [1 ]
机构
[1] Johns Hopkins Med Inst, Baltimore, MD 21205 USA
关键词
Autoimmune thyroiditis; Environmental triggers; Iodine; NOD.H2(h4) mice; SPONTANEOUS LYMPHOCYTIC THYROIDITIS; HUMAN THYROGLOBULIN TG; IODINE RESTRICTION; L-THYROXINE; DISEASE; HYPOTHYROIDISM; CELLS; RAT; IMMUNOREACTIVITY; SUSCEPTIBILITY;
D O I
10.1016/j.jaut.2009.09.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Autoimmune thyroiditis is among the most prevalent of all the autoimmunities. Autoimmune thyroiditis is multifactorial with contributions from genetic and environmental factors. Much information has been published about the genetic predisposition to autoimmune thyroiditis both in experimental animals and humans. There is, in contrast, very little data on environmental agents that can serve as the trigger for autoimmunity in a genetically predisposed host. The best-established environmental factor is excess dietary iodine. Increased iodine consumption is strongly implicated as a trigger for thyroiditis, but only in genetically susceptible individuals. However, excess iodine is not the only environmental agent implicated as a trigger leading to autoimmune thyroiditis. There are a wide variety of other synthetic chemicals that affect the thyroid gland or have the ability to promote immune dysfunction in the host. These chemicals are released into the environment by design, such as in pesticides, or as a by-product of industry. Candidate pollutants include polyaromatic hydrocarbons, polybrominated biphenols, and polychlorinated biphenols, among others. Infections are also reputed to trigger autoimmunity and may act alone or in concert with environmental chemicals. We have utilized a unique animal model, the NOD.H2(h4) mouse to explore the influence of iodine and other environmental factors on autoimmune thyroiditis. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:183 / 189
页数:7
相关论文
共 69 条
[1]   HCV E2 protein binds directly to thyroid cells and induces IL-8 production: A new mechanism for HCV induced thyroid autoimmunity [J].
Akeno, Nagako ;
Blackard, Jason T. ;
Tomer, Yaron .
JOURNAL OF AUTOIMMUNITY, 2008, 31 (04) :339-344
[2]   THE EFFECT OF IODINE ON LYMPHOCYTIC THYROIDITIS IN THE THYMECTOMIZED BUFFALO RAT [J].
ALLEN, EM ;
BRAVERMAN, LE .
ENDOCRINOLOGY, 1990, 127 (04) :1613-1616
[3]   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
[4]   INDUCTION OF AUTOIMMUNE-THYROIDITIS IN CHICKENS BY DIETARY IODINE [J].
BAGCHI, N ;
BROWN, TR ;
URDANIVIA, E ;
SUNDICK, RS .
SCIENCE, 1985, 230 (4723) :325-327
[5]   The regulatory T cell gene FOXP3 and genetic susceptibility to thyroid autoimmunity:: An association analysis in Caucasian and Japanese cohorts [J].
Ban, Yoshiyuki ;
Tozaki, Teruaki ;
Tobe, Takashi ;
Ban, Yoshio ;
Jacobson, Eric M. ;
Concepcion, Erlinda S. ;
Tomer, Yaron .
JOURNAL OF AUTOIMMUNITY, 2007, 28 (04) :201-207
[6]  
BEIERWALTES WH, 1969, B ALL INDIA I MED SC, V3, P145
[7]   Autoimmunity: From the mosaic to the kaleidoscope [J].
Blank, Miri ;
Gershwin, M. Eric .
JOURNAL OF AUTOIMMUNITY, 2008, 30 (1-2) :1-4
[8]   Adhesion molecules as susceptibility factors in spontaneous autoimmune thyroiditis in the NOD-H2h4 mouse [J].
Bonita, RE ;
Rose, NR ;
Rasooly, L ;
Caturegli, P ;
Burek, CL .
EXPERIMENTAL AND MOLECULAR PATHOLOGY, 2002, 73 (03) :155-163
[9]  
BONITA RE, 1999, CLIN IMMNOL, V90, P437
[10]   Spontaneous autoimmune thyroiditis in NOD.H-2h4 mice [J].
Braley-Mullen, H ;
Sharp, GC ;
Medling, B ;
Tang, HW .
JOURNAL OF AUTOIMMUNITY, 1999, 12 (03) :157-165