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Related Concept Videos

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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.
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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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.
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Epigenetic Regulation01:37

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
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Related Experiment Video

Updated: Feb 26, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

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Epigenetics and Autoimmune Thyroid Diseases.

Fabio Coppedè1

  • 1Department of Translational Research and New Technologies in Medicine and Surgery, Section of Medical Genetics, University of Pisa, Pisa, Italy.

Frontiers in Endocrinology
|July 15, 2017
PubMed
Summary
This summary is machine-generated.

Epigenetic changes like DNA methylation are involved in autoimmune thyroid diseases (AITD). Further research is needed to understand these epigenetic marks for potential diagnostic and therapeutic applications in Graves

Keywords:
DNA methylationGraves’ diseaseHashimoto’s thyroiditisautoimmune thyroid diseasesepigeneticshistone tail modificationsmicroRNAnon-coding RNAs

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Area of Science:

  • Immunology
  • Genetics
  • Endocrinology

Background:

  • Epigenetic modifications (DNA methylation, histone tails, non-coding RNA) are implicated in autoimmune disorders.
  • Autoimmune thyroid diseases (AITD), including Graves' disease (GD) and Hashimoto's thyroiditis (HT), show altered epigenetic marks.
  • Current data are limited for clinical translation, with few genome-wide studies in GD and descriptive microRNA data in AITD.

Purpose of the Study:

  • To review the role of epigenetic modifications in the pathogenesis of AITD.
  • To highlight the current limitations and future research directions for epigenetic studies in AITD.

Main Methods:

  • Review of existing literature on epigenetic modifications in AITD.
  • Analysis of studies focusing on DNA methylation, histone modifications, and non-coding RNAs in GD and HT patients.
  • Assessment of the clinical relevance and translational potential of current findings.

Main Results:

  • Evidence indicates altered epigenetic marks in AITD, affecting gene expression.
  • Genome-wide screenings and microRNA studies in AITD are limited and largely descriptive.
  • The diagnostic and prognostic utility of observed epigenetic changes remains unclear.

Conclusions:

  • Epigenetic impairment is evident in AITD, suggesting a role in pathogenesis.
  • Further research is required to elucidate epigenetic networks and their interplay with environmental factors.
  • Understanding these mechanisms could lead to novel diagnostic, prognostic, and therapeutic strategies for AITD.