The Expression of Dual Oxidase, Thyroid Peroxidase, and Caveolin-1 Differs According to the Type of Immune Response (TH1/TH2) Involved in Thyroid Autoimmune Disorders

Marique, Lancelot; Regemorter, Victoria Van; Gérard, A; Craps, Julie; Sènou, Maximin; Marbaix, Étienne; Rahier, Jacques; Daumerie, Chantal; Mourad, Michel; Lengelé, Benoît; Colin, Ides M.; Many, Marie‐Christine

doi:10.1210/jc.2013-3469

Cited by 40 publications

(39 citation statements)

References 36 publications

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“…30 Moreover, increased expression of Th1-related cytokines has been associated with elevated titres of anti-TPO antibodies, the destruction of thyroxisomes and the induction of apoptosis in thyroid follicular cells. [31][32][33] However, the importance of the role of Th2 cells in the pathogenesis of HT is still debatable.…”

Section: Discussionmentioning

confidence: 99%

Imbalances in T Cell-Related Transcription Factors Among Patients with Hashimoto’s Thyroiditis

Safdari¹,

Alijani²,

Nemati³

et al. 2017

SQUMJ

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abstract:Objectives: Imbalances in effector T cell functioning have been associated with a number of autoimmune diseases, including Hashimoto's thyroiditis (HT). Differentiation of effector T helper (Th) 1, Th2, Th17 and regulatory T cell (Treg) lymphocytes is regulated by transcription factors, including Th1-specific T box (T-bet), GATA binding protein-3 (GATA 3 ), retinoid-related orphan receptor (ROR)-α and forkhead box P3 (FOXP3). This study aimed to investigate Th1/Th2, Th1/Treg, Th2/Treg and Th17/Treg balances at the level of these transcription factors. Methods: This study took place between October 2015 and August 2016. Peripheral blood mononuclear cells were collected from a control group of 40 healthy women recruited from the Zahedan University of Medical Sciences, Zahedan, Iran, and a patient group of 40 women with HT referred to the Hazrat Ali Asghar Hospital, Zahedan. Total ribonucleic acid extraction was performed and the gene expression of transcription factors was quantitated using a real-time polymerase chain reaction technique. Results: Expression of T-bet and GATA 3 was significantly elevated, while FOXP3 expression was significantly diminished among HT patients in comparison with the controls (P = 0.03, 0.01 and 0.05, respectively). Expression of RORα was higher among HT patients, although this difference was not significant (P = 0.15). Expression of T-bet/FOXP3, GATA 3 /FOXP3 and RORα/FOXP3 ratios were increased among HT patients in comparison with the controls (P <0.02, <0.01 and <0.01, respectively). Conclusion: These results indicate that HT patients have imbalances in Th1/Treg, Th2/Treg and Th17/Treg lymphocytes at the level of the transcription factors, deviating towards Th1, Th2 and Th17 cells. Correction of these imbalances may therefore be therapeutic. Keywords

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Section: Discussionmentioning

confidence: 99%

Imbalances in T Cell-Related Transcription Factors Among Patients with Hashimoto’s Thyroiditis

Safdari¹,

Alijani²,

Nemati³

et al. 2017

SQUMJ

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“…It is notable that genetic factors play a prominent role in the occurrence and persistence of AITDs. Given that autoimmune diseases may share a common genetic predisposition, and that immune dysregulation plays a vital role in AITDs [16,17], we hypothesized that variants within the TNFSF4 gene, which is a crucial immune regulator, could also elicit abnormal OX40L expression and dysfunction, thus affecting T-cell activation and leading to unbalanced immune regulation and its resultant occurrence of AITDs.…”

Section: Discussionmentioning

confidence: 99%

TNFSF4 Gene Variations Are Related to Early-Onset Autoimmune Thyroid Diseases and Hypothyroidism of Hashimoto’s Thyroiditis

Song

Wang

Yao

et al. 2016

IJMS

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The aim of the current study was to examine whether the polymorphism loci of the tumor necrosis factor superfamily member 4 (TNFSF4) gene increase the risk of susceptibility to autoimmune thyroid diseases (AITDs) in the Han Chinese population, and a case-control study was performed in a set of 1,048 AITDs patients and 909 normal healthy controls in the study. A total of four tagging single nucleotide polymorphisms (SNPs) in the TNFSF4 region, including rs7514229, rs1234313, rs16845607 and rs3850641, were genotyped using the method of ligase detection reaction. An association between GG genotype of rs3850641 in TNFSF4 gene and AITDs was found (p = 0.046). Additionally, the clinical sub-phenotype analysis revealed a significant association between GG genotype in rs7514229 and AITDs patients who were ≤18 years of age. Furthermore, rs3850641 variant allele G was in strong association with hypothyroidism in Hashimoto’s thyroiditis (HT) (p = 0.018). The polymorphisms of the TNFSF4 gene may contribute to the susceptibility to AITDs pathogenesis.

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“…These two aspects were not present in our cohort and explain the absence of significant vascular changes. The presence of nodularity with ischemic-vascular changes and significant inflammatory infiltrate with local antigen modulation (germinal centers) are responsible for signs of oxidative stress [26, 27]. These are not essential and constant elements of GD.…”

Section: Discussionmentioning

confidence: 99%

Noninflammatory Diffuse Follicular Hypertrophy/Hyperplasia of Graves Disease: Morphometric Evaluation in an Experimental Mouse Model

Schlüter¹,

Eckstein²,

Brenzel³

et al. 2018

Eur Thyroid J

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Objectives: Experimental models of Graves hyperthyroid disease accompanied by Graves orbitopathy (GO) can be efficiently induced in susceptible inbred strains of mice by immunization by electroporation of heterologous human TSH receptor (TSHR) A-subunit plasmid. The interrelated pathological findings in the thyroid glands of Graves disease (GD) that explain the core changes classically include diffuse follicular hyperplasia and multifocal mild lymphocytic infiltrate. However, the relative contributions of different thyroid tissue components (colloid, follicular cells, and stroma) have not been previously evaluated. In this study, we characterize the thyroid gland of an experimental mouse model of autoimmune GD. Our objective was to define the relative contribution of the different thyroid tissue components to the pathology of glands in the experimental model. Methods: Mice were immunized with human TSHR A-subunit plasmid. Antibodies induced to human TSHR were pathogenic in vivo due to their cross-reactivity to mouse TSHR. Results: Autoimmune thyroid disease in the model was characterized by histopathology of hyperplastic glands with large follicular cells. Further examination of thyroid glands of immunized animals revealed a significantly increased follicular area and follicle/stroma ratio, morphometrically correlated with a noninflammatory follicular hyperplasia/hypertrophy. The increased follicle/stroma ratio was the most relevant morphometrically variable summarizing the pathological changes for screening purposes. Conclusion: GD thyroid glands are enlarged and characterized by a noninflammatory diffuse follicular cell hyperplasia/hypertrophy and a significant increase in the follicles with an increased follicle/stroma ratio. Overall, this mouse model is a faithful model of an early hyperthyroid status of GD (diffuse glandular involvement and follicular expansion).

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The Expression of Dual Oxidase, Thyroid Peroxidase, and Caveolin-1 Differs According to the Type of Immune Response (TH1/TH2) Involved in Thyroid Autoimmune Disorders

Cited by 40 publications

References 36 publications

Imbalances in T Cell-Related Transcription Factors Among Patients with Hashimoto’s Thyroiditis

Imbalances in T Cell-Related Transcription Factors Among Patients with Hashimoto’s Thyroiditis

TNFSF4 Gene Variations Are Related to Early-Onset Autoimmune Thyroid Diseases and Hypothyroidism of Hashimoto’s Thyroiditis

Noninflammatory Diffuse Follicular Hypertrophy/Hyperplasia of Graves Disease: Morphometric Evaluation in an Experimental Mouse Model

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