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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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Related Experiment Video

Updated: Jul 15, 2025

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Selenium regulates T cell differentiation in experimental autoimmune thyroiditis in mice.

Wei Wang1, Qi-Lan Jiang2, Qin Xu3

  • 1Department of General Surgery/Thyroid Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China; Department of Thyroid, Head, Neck and Maxillofacial Surgery, Third Hospital of Mianyang & Sichuan Mental Health Center, Mianyang, Sichuan, China.

International Immunopharmacology
|September 30, 2023
PubMed
Summary

Selenium supplementation may improve outcomes for autoimmune thyroiditis by modulating T-cell responses. This study shows selenium reduces thyroid damage and alters immune cell function in a mouse model, suggesting therapeutic potential.

Keywords:
Experimental autoimmune thyroiditis (EAT)Hashimoto's thyroiditisNOD/ShiLtJ mouseSeleniumT cell differentiation

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Area of Science:

  • Immunology
  • Endocrinology
  • Trace Element Research

Background:

  • Selenium (Se) is vital for thyroid function and may impact autoimmune thyroid diseases like Hashimoto's thyroiditis (HT).
  • The precise mechanisms by which selenium affects immune cells, particularly T cells, in autoimmune thyroiditis (AIT) remain unclear.
  • Existing clinical evidence for long-term selenium benefits in HT is limited, necessitating further research.

Purpose of the Study:

  • To investigate the effects of selenium supplementation on a mouse model of experimental autoimmune thyroiditis (EAT).
  • To elucidate the impact of selenium on T-cell subsets and cytokine production in the context of AIT.
  • To assess selenium's potential to mitigate thyroid damage and immune dysregulation in EAT.

Main Methods:

  • A mouse model of experimental autoimmune thyroiditis (EAT) was established using a high-iodine diet.
  • Mice with EAT were treated with selenium supplementation.
  • Thyroid histology, lymphocyte infiltration, thyroid hormone levels, autoantibodies, and T-cell subset profiles (Th1, Th2, Th17, Treg) were analyzed.

Main Results:

  • Selenium supplementation significantly reduced thyroid follicle destruction and lymphocyte infiltration in EAT mice.
  • Selenium reversed disruptions in peripheral blood thyroxine and thyroid autoantibody levels.
  • Selenium modulated T-cell subsets by decreasing pro-inflammatory cytokines from Th1 cells, inhibiting Th2 and Th17 cells, and enhancing Treg cells.

Conclusions:

  • Selenium supplementation demonstrates potential therapeutic benefits for autoimmune thyroiditis.
  • Selenium exerts broad effects on CD4+ T-cell subsets, influencing their differentiation and cytokine production.
  • Modulation of T-cell responses by selenium may be a key mechanism for improving EAT prognosis.