Apoptosis-induced Decrease of Intrathyroidal CD4+CD25+Regulatory T Cells in Autoimmune Thyroid Diseases

Nakano, Aiko; Watanabe, Mikio; Iida, Takao; Kuroda, Seika; Matsuzuka, Fumio; Miyauchi, Akira; Iwatani, Yoshinori

doi:10.1089/thy.2006.0231

Cited by 66 publications

(63 citation statements)

References 39 publications

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“…Deficiency and impaired function of these cells may be the cause of autoimmune thyroid disease. Nakano et al found that the percentage of regulatory T cells within the thyroid lymphocyte cells was lower in patients with autoimmune thyroid disease [19,20].…”

Section: Szkolenie Podyplomowementioning

confidence: 99%

Rola układu immunologicznego oraz udział cytokin w patomechanizmie autoimmunologicznej choroby tarczycy (AITD)

Mikos¹,

Mikoś²,

Obara-Moszynska³

et al. 2014

Endokrynologia Polska

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Autoimmune thyroid disease (AITD) is the most common organ-specific autoimmune disorder. AITD development occurs due to loss of immune tolerance and reactivity to thyroid autoantigens: thyroid peroxidase (TPO), thyroglobulin (TG) and thyroid stimulating hormone receptor (TSHR). This leads to infiltration of the gland by T cells and B cells that produce antibodies specific for clinical manifestations of hyperthyroidism in Graves' disease (GD) and chronic autoimmune thyroiditis (cAIT). In addition, T cells in Hashimoto's thyroiditis induce apoptosis in thyroid follicular cells, leading ultimately to the destruction of the gland. Cytokines are involved in the pathogenesis of thyroid diseases working in both the immune system and directly targeting the thyroid follicular cells. They are involved in the induction and effector phase of the immune response and inflammation, playing a key role in the pathogenesis of autoimmune thyroid disease. The presence of multiple cytokines has been demonstrated: IL-1a, IL-1b, IL-2, IL-4 , IL-6, IL-8, IL-10, IL-12, IL-13, IL-14, TNF-a and IFN-g within the inflammatory cells and thyroid follicular cells. Finally, cytokines derived from T cells can directly damage thyroid cells, leading to functional disorders and may also stimulate the production of nitric oxide (NO) and prostaglandin (PG), thus increasing the inflammatory response in AITD. Immunological mechanisms involved in the pathogenesis of AITD are strongly related to each other, but differences in the image of cAIT and GD phenotype are possibly due to a different type of immune response observed in these two counteracting clinical thyroid diseases. This article describes the potential role of cytokines and immune mechanisms in the pathogenesis of AITD. (Endokrynol Pol 2014; 65 (2): 150-155)

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Section: Szkolenie Podyplomowementioning

confidence: 99%

Rola układu immunologicznego oraz udział cytokin w patomechanizmie autoimmunologicznej choroby tarczycy (AITD)

Mikos¹,

Mikoś²,

Obara-Moszynska³

et al. 2014

Endokrynologia Polska

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“…Moreover, ICOS + Treg have stronger suppressive activity and superior survival than ICOS -Treg [24]. We previously reported that intrathyroidal Treg cells in autoimmune thyroid diseases were decreased by apoptosis [38]. Therefore, the AA genotype of ICOSL SNP2 may be weak to Treg expansion and may show Th17 cell predominance more easily.…”

Section: Discussionmentioning

confidence: 98%

Association of polymorphisms in the ICOS and ICOSL genes with the pathogenesis of autoimmune thyroid diseases

et al. 2016

Self Cite

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“…It was shown that CD4+ CD25 + cells may experimentally prevent development of autoimmune thyroiditis (Gangi, Vasu et al, 2005;Vergini, Li et al, 2005). As the proportion and function of Tregs seems altered in the ATD when analyzing peripheral and cells of the thyroid ambient itself without the ability to downmodulate the autoimmune 98 response in the thyroid environment (Marazuela, Garcia-Lopez et al, 2006), or even suffer increased apoptosis in the thyroid environment (Nakano, Watanabe et al, 2007) a significant event considering that regulatory action of Treg cells modulates and inhibits inflammatory immune response Th1, Th2 and Th17.…”

Section: Loss Of Tolerance and Natural Regulatory T Cellsmentioning

confidence: 99%

Immune Profile and Signal Transduction of T-Cell Receptor in Autoimmune Thyroid Diseases

Cury¹

2012

Thyroid and Parathyroid Diseases - New Insights Into Some Old and Some New Issues

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Apoptosis-induced Decrease of Intrathyroidal CD4⁺CD25⁺Regulatory T Cells in Autoimmune Thyroid Diseases

Abstract: These results indicate that intrathyroidal Treg cells are decreased in response to apoptosis in patients with AITD. This decrease in Treg cells may contribute to the incomplete regulation of autoreactive T cells in AITD.

Cited by 66 publications

References 39 publications

Rola układu immunologicznego oraz udział cytokin w patomechanizmie autoimmunologicznej choroby tarczycy (AITD)

Rola układu immunologicznego oraz udział cytokin w patomechanizmie autoimmunologicznej choroby tarczycy (AITD)

Association of polymorphisms in the <i>ICOS</i> and <i>ICOSL</i> genes with the pathogenesis of autoimmune thyroid diseases

Immune Profile and Signal Transduction of T-Cell Receptor in Autoimmune Thyroid Diseases

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