Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Search for Light Pseudoscalar Bosons, Pair-Produced in Higgs Boson Decays in the Four-Electron Final State in Proton-Proton Collisions at sqrt[s]=13  TeV.

Physical review letters·2026
Same author

First Evidence for Mixing-Induced CP Violation in B_{s}^{0}→J/ψϕ(1020) Decays in pp Collisions at sqrt[s]=13  TeV.

Physical review letters·2026
Same author

Observation of Suppressed Charged-Particle Production in Ultrarelativistic Oxygen-Oxygen Collisions.

Physical review letters·2026
Same author

Measurement of D^{0} Meson Photoproduction in Ultraperipheral Heavy Ion Collisions.

Physical review letters·2026
Same author

Observation of tWZ Production at the CMS Experiment.

Physical review letters·2026
Same author

First Exclusive Reconstruction of the B^{*+}, B^{*0}, and B_{s}^{*0} Mesons and Precise Measurement of Their Masses.

Physical review letters·2026

Related Experiment Video

Updated: May 16, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Reduced DNASE1 gene expression in thyroid autoimmunity.

M Dittmar1, K Woletz, G J Kahaly

  • 1Department of Medicine I, Gutenberg University Medical Center, Mainz, Germany.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|December 11, 2012
PubMed
Summary

Patients with autoimmune thyroid disease exhibit significantly reduced DNASE1 gene expression. This DNASE1 downregulation may contribute to the development of thyroid autoimmunity by impairing DNA clearance from dying cells.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Related Experiment Videos

Last Updated: May 16, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Area of Science:

  • Molecular Biology
  • Immunology
  • Endocrinology

Background:

  • DNASE1 enzyme is crucial for DNA hydrolysis and potentially linked to autoimmune conditions.
  • Autoimmune thyroid diseases (AITD) like Hashimoto's thyroiditis and Graves' disease involve immune system dysfunction.
  • Reduced DNASE1 expression could impair the clearance of cellular debris, potentially triggering autoimmune responses.

Purpose of the Study:

  • To investigate the hypothesis that DNASE1 gene expression is reduced in patients with autoimmune thyroid disease.
  • To quantitatively compare DNASE1 mRNA levels between AITD patients and healthy controls.

Main Methods:

  • Quantitative real-time reverse transcription PCR (RT-PCR) was employed to measure DNASE1 mRNA levels.
  • DNASE1 mRNA expression was normalized to the housekeeping gene β2-MICROGLOBULIN.
  • The study included 20 AITD patients (10 Hashimoto's, 10 Graves') and 20 matched healthy controls.

Main Results:

  • DNASE1 mRNA expression was significantly lower in AITD patients (0.52±0.22) compared to healthy controls (0.95±0.22).
  • The mean expression level in patients was 54.7% of that in controls (p<0.001).
  • No correlation was found between lowered DNASE1 expression and patient age or sex.

Conclusions:

  • This study provides the first evidence of DNASE1 mRNA downregulation in patients with autoimmune thyroid disease.
  • Reduced DNASE1 expression may lead to insufficient degradation of DNA from dying cells, promoting thyroid autoimmunity.
  • The findings suggest a potential role for DNASE1 in the pathogenesis of AITD.