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BAGCHI, SUNDICK
Thyroid cell injury is an initial event in the induction of autoimmune thyroiditis by iodine in obese strain chickens.Bagchi N, Brown TR, Sundick RS. Endocrinology. 1995 Nov;136(11):5054-60.
"The present study examines the role of thyroid cell injury in the initiation of autoimmune thyroiditis by iodine in Obese strain (OS) chickens, a strain genetically susceptible to spontaneous autoimmune thyroiditis. OS and normal strain chickens were placed on an iodine depletion regimen started in ovo. This regimen is known to prevent thyroiditis in OS chickens. The chickens were injected with NaI every 24 h for up to 7 days starting at 3 weeks of age. Both strains showed evidence of mild thyrocyte injury 12 h after NaI. However, significant and sustained infiltration, beginning 24 h after NaI, was seen only in the OS. The infiltrating cells were primarily mononuclear. Polymorphonuclear cells were not observed. Immunohistological analysis showed the infiltrate to be composed of CD8 T cells, CD4 T cells, B cells, and macrophages in the ratio 40:20:22:17. The infiltration was sustained and progressive for at least 7 days. Thyroid infiltration after NaI repletion was significantly reduced in OS chickens tolerized to thyroglobulin at hatching. Prior treatment with the antioxidant drug ethoxyquin completely prevented both the thyrocyte injury and the infiltration induced by iodine. Treatment with antioxidant drugs had no effect on the uptake and incorporation of iodine by the thyroid. In summary, 1) iodine caused thyrocyte injury in both OS and normal chickens. 2) The injury was followed by cellular infiltration in the OS but not in normal chickens. 3) The infiltration appeared to be immune mediated in being primarily lymphocytic and at least partially thyroglobulin sensitive. 4) Prevention of thyroid injury by antioxidant drug treatment also prevented infiltration. We conclude that thyroid cell injury may be an initial event in the induction of autoimmune thyroiditis by iodine."
The role of iodine in thyroid autoimmunity: from chickens to humans: a review.Sundick RS, Bagchi N, Brown TR. Autoimmunity. 1992;13(1):61-8. Review. [abstract only]
"Evidence has been presented to support the idea that iodine plays an important role in autoimmune thyroiditis. Excessive amounts induce thyroiditis in genetically susceptible animal strains, while intrathyroidal depletion of iodine prevents disease in strains susceptible to severe thyroiditis. While the mechanisms by which iodine promotes thyroiditis is unknown, several hypotheses have been proposed. (1) T and/or B cells may react specifically to iodinated portions of thyroglobulin (Tg) so that severe iodine depletion renders Tg non-immunogenic. (2) A defect in the iodine processing machinery in thyroid epithelial cells of a susceptible person or animal may, in the presence of iodine, result in elevated levels of oxygen or iodine radicals, which could damage membrane lipids or proteins. (3) Defective iodine processing may result in the iodination of lipid or proteins (other than Tg) which could act either as immunogens or polyclonal activators."
Iodine in autoimmune thyroiditis.Sundick RS. Immunol Ser. 1990;52:213-28. Review. [abstract only]
"The aim of this chapter was to present a theory or concept of autoimmune disease that, in a sense, deemphasized the importance of immunoregulatory defects but rather concentrated on defects and/or changes in a target organ that might stimulate immune responses. Defects in immune regulation were not discussed because there is little evidence that generalized defects in immunoregulation occur in patients with autoimmune thyroid disease. There is some evidence of decreased numbers of thyroid-antigen-specific T-suppressor cells in patients with autoimmune thyroid disease; however, this has been detected only after the appearance of frank disease. Thus a reduction of T-suppressor cells specific for the thyroid microsomal antigen at a time when the immune system is responding vigorously to that antigen is to be expected and cannot a priori be assumed to be the reason for the immune response. One other reason for questioning the role of defective antigen-specific T-suppressor cells as an initiating event is that individual patients with autoimmune thyroid disease produce antibodies to a variety of unrelated thyroid antigens (Tg, microsomal antigen, which is now known to be thyroid peroxidase, TSH receptor, and others). One would have to assume that the majority of thyroid patients spontaneously lose several unrelated clones of specific suppressor T cells. An alternative scenario of events in the pathogenesis of autoimmune disease is as follows: An environmental agent, whether it be iodide, alone, or in combination with high TSH, or a virus causes damage to the thyroid gland. The iodide-induced damage, perhaps mediated by hydroxyl radicals, is more severe and/or prolonged if the gland has a defect in iodide organification or perhaps, as seen in some susceptible chicken strains, partially autonomous thyroid function. As a result of the damage, leukocytes migrate into the gland. Once leukocytes arrive, a number of interesting phenomena occur. First, monocytes may secrete IL-1, which is directly cytotoxic for endocrine cells and provides an accessory signal to T-helper cells. Second, T and B cells migrate into the damaged gland and into the follicles, where at least two of the important thyroid antigens are located, thyroglobulin and thyroid peroxidase. These two proteins are highly immunogenic: the thyroglobulin due to its increased iodine content and the thyroid peroxidase because it is a membrane-bound antigen sequestered in thyroid follicles. Third, the T cells, once activated, provide help to B cells and secrete gamma interferon, which induces the expression of class II MHC antigens on the thyroid epithelial cells."
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