Induction of Autoimmune Thyroiditis in Chickens by Dietary Iodine

Bagchi, Nandalal; Tr, Brown; Urdanivia, Enrique; Sundick, Roy S.

doi:10.1126/science.4048936

Cited by 174 publications

(77 citation statements)

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“…Studies in both humans and animals have demonstrated that iodine administration may enhance autoimmune thyroiditis (4,5,(37)(38)(39)(40)(41)(42)(43)(44)(45)(46). Totally, three mechanisms (47) have been assumed for the development of iodine-induced autoimmune thyroiditis.…”

Section: Discussionmentioning

confidence: 99%

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

Teng¹,

Shan²,

Chen

et al. 2011

European Journal of Endocrinology

152

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Objective: With the introduction of iodized salt worldwide, more and more people are exposed to more than adequate iodine intake levels with median urinary iodine excretion (MUI 200-300 mg/l) or excessive iodine intake levels (MUI O300 mg/l). The objective of this study was to explore the associations between more than adequate iodine intake levels and the development of thyroid diseases (e.g. thyroid dysfunction, thyroid autoimmunity, and thyroid structure) in two Chinese populations. Design: A population-based cross-sectional study was conducted in two areas in which people are exposed to different levels of iodine intake (Rongxing, MUI 261 mg/l; Chengshan, MUI 145 mg/l). A total of 3813 individuals were recruited by random sampling. Thyroid hormones, thyroid autoantibodies in serum, and iodine levels in urine were measured. B-mode ultrasonography of the thyroid was also performed for each participant. Results: The prevalence of subclinical hypothyroidism was significantly higher for subjects who live in Rongxing than those who live in Chengshan (5.03 vs 1.99%, P!0.001). The prevalence of positive anti-thyroid peroxidase antibody (TPOAb) and positive anti-thyroglobulin antibody (TgAb) was significantly higher for subjects in Rongxing than those in Chengshan (TPOAb: 10.64 vs 8.4%, PZ0.02; TgAb: 10.27 vs 7.93%, PZ0.01). The increase in thyroid antibodies was most pronounced in the high concentrations of TPOAb (TPOAb: R500 IU/ml) and low concentrations of TgAb (TgAb: 40-99 IU/ml) in Rongxing. Conclusions: More than adequate iodine intake could be a public health concern in terms of thyroid function and thyroid autoimmunity in the Chinese populations.European Journal of Endocrinology 164 943-950

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Section: Discussionmentioning

confidence: 99%

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

Teng¹,

Shan²,

Chen

et al. 2011

European Journal of Endocrinology

152

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“…ncreased iodine (I) ingestion has been shown to promote induction of autoimmune thyroiditis in humans (1-5) and experimental animals such as chicken (6,7), rats (8 -12), hamsters (13), and mice (14). The mechanisms underlying this association remain poorly understood.…”

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confidence: 99%

Enhanced Iodination of Thyroglobulin Facilitates Processing and Presentation of a Cryptic Pathogenic Peptide

Dai

Rao

Carayanniotis

2002

The Journal of Immunology

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Increased iodine intake has been associated with the development of experimental autoimmune thyroiditis (EAT), but the biological basis for this association remains poorly understood. One hypothesis has been that enhanced incorporation of iodine in thyroglobulin (Tg) promotes the generation of pathogenic T cell determinants. In this study we sought to test this by using the pathogenic nondominant As-binding Tg peptides p2495 and p2694 as model Ags. SJL mice challenged with highly iodinated Tg (I-Tg) developed EAT of higher severity than Tg-primed controls, and lymph node cells (LNC) from I-Tg-primed hosts showed a higher proliferation in response to I-Tg in vitro than Tg-primed LNC reacting to Tg. Interestingly, I-Tg-primed LNC proliferated strongly in vitro against p2495, but not p2694, indicating efficient and selective priming with p2495 following processing of I-Tg in vivo. Tg-primed LNC did not respond to either peptide. Similarly, the p2495-specific, IL-2-secreting T cell hybridoma clone 5E8 was activated when I-Tg-pulsed, but not Tg-pulsed, splenocytes were used as APC, whereas the p2694-specific T cell hybridoma clone 6E10 remained unresponsive to splenic APC pulsed with Tg or I-Tg. The selective in vitro generation of p2495 was observed in macrophages or dendritic cells, but not in B cells, suggesting differential processing of I-Tg among various APC. These data demonstrate that enhanced iodination of Tg facilitates the selective processing and presentation of a cryptic pathogenic peptide in vivo or in vitro and suggest a mechanism that can at least in part account for the association of high iodine intake and the development of EAT.

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“…NOD.H-2h4 mice spontaneously develop SAT (1)(2)(3)(4)(5)(6). Increased dietary iodine accelerates development of SAT in NOD.H-2h4 mice (1-3), humans, obese strain (OS) chickens, and BB/Wor rats (23)(24)(25). Recent work showed that enhanced iodination of thyroglobulin facilitates processing and presentation of a cryptic pathogenic peptide and this might partly account for the association of high iodine intake and autoimmune thyroiditis (26).…”

mentioning

confidence: 99%

Dual Roles for IFN-γ, But Not for IL-4, in Spontaneous Autoimmune Thyroiditis in NOD.H-2h4 Mice

Yu¹,

Sharp²,

Braley‐Mullen

2002

The Journal of Immunology

102

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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-γ−/− 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-γ−/− mice produced significantly less anti-MTg IgG1 and IgG2b. Absence of IFN-γ resulted in abnormal proliferation of thyroid epithelial cells with minimal lymphocyte infiltration. Thyroids of IFN-γ−/− 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-γ−/− 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-γ plays a dual role in the development of SAT. IFN-γ is required for development of L-SAT, and it also functions to inhibit thyroid epithelial cell proliferation.

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Induction of Autoimmune Thyroiditis in Chickens by Dietary Iodine

Cited by 174 publications

References 15 publications

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

Enhanced Iodination of Thyroglobulin Facilitates Processing and Presentation of a Cryptic Pathogenic Peptide

Dual Roles for IFN-γ, But Not for IL-4, in Spontaneous Autoimmune Thyroiditis in NOD.H-2h4 Mice

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