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Autoimmune Disorders01:29

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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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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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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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CD4+ cells in autoimmune thyroid disease.

Szymon Janyga1, Bogdan Marek2, Dariusz Kajdaniuk3,2

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Summary

Autoimmune thyroid diseases involve CD4+ helper T cells, including Th17, Th22, Th9, and regulatory T cells (Tregs). Imbalances in these CD4+ cell populations contribute to disease pathogenesis and offer potential therapeutic targets.

Keywords:
CD4+ T cellTh lymphocytesTreg lymphocytesautoimmune thyroid disease

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Area of Science:

  • Immunology
  • Endocrinology

Background:

  • Autoimmunity arises from cellular damage triggering immune responses.
  • Autoimmune thyroid diseases (AITD), like Hashimoto's and Graves', are common autoimmune disorders.
  • CD4+ helper T lymphocytes play a crucial role in the pathogenesis of AITD.

Purpose of the Study:

  • To elucidate the role of various CD4+ T cell subtypes in AITD pathogenesis.
  • To investigate the balance and plasticity of CD4+ cell populations in AITD.
  • To identify potential therapeutic targets within CD4+ cell pathways.

Main Methods:

  • Analysis of CD4+ T cell subtypes, including Th1, Th2, Th17, Th22, Th9, and Tregs.
  • Assessment of the differentiation and function of CD4+ T cell subsets.
  • Evaluation of the phenotypic variability and plasticity of CD4+ cells.

Main Results:

  • Th17, Th22, and Th9 lymphocytes, alongside Tregs, are implicated in AITD development.
  • Patients with AITD exhibit an increased proportion of Th17, Th22, and Th9 cells.
  • A defective function of Tregs and an imbalance between effector and regulatory T cells are observed in AITD patients.

Conclusions:

  • CD4+ T cell plasticity is critical for maintaining immune homeostasis in AITD.
  • Dysregulation of CD4+ T cell subsets, particularly Th17/Tregs, contributes significantly to AITD pathogenesis.
  • Targeting specific CD4+ T cell populations offers a promising strategy for AITD treatment.