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Related Concept Videos

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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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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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Related Experiment Video

Updated: Feb 24, 2026

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A20 Restrains Thymic Regulatory T Cell Development.

Julius Clemens Fischer1, Vera Otten1, Maike Kober1

  • 1Klinik und Poliklinik für Innere Medizin III, Klinikum rechts der Isar, Technische Universität, 81675 Munich, Germany.

Journal of Immunology (Baltimore, Md. : 1950)
|August 27, 2017
PubMed
Summary
This summary is machine-generated.

The ubiquitin editing enzyme A20 normally limits regulatory T (Treg) cell numbers. Removing A20 in T cells boosts Treg cell development and function, enhancing immune responses.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Immune tolerance relies on Foxp3-expressing regulatory T (Treg) cells produced in the thymus.
  • NF-κB activation is crucial for Treg cell development, with A20 acting as a negative regulator of this pathway.
  • A20 also plays a role in preventing necroptosis in naive CD4+ T cells.

Purpose of the Study:

  • To investigate the role of the ubiquitin editing enzyme A20 in T regulatory cell development and function.
  • To determine the impact of A20 deficiency in T lineage cells on Treg cell compartments.
  • To elucidate the mechanisms by which A20 influences Treg cell differentiation and activity.

Main Methods:

  • Utilized mice genetically deficient for A20 in T lineage cells.
  • Analyzed thymic and peripheral Treg cell populations using flow cytometry.
  • Assessed Treg cell function in a graft-versus-host disease model.
  • Examined NF-κB pathway activation (RelA and c-Rel) in Treg cells.

Main Results:

  • T cell-specific A20 deficiency led to enlarged thymic and peripheral Treg cell compartments.
  • A20-deficient Treg cells showed reduced IL-2 dependence but normal proliferation and apoptosis rates.
  • Enhanced NF-κB (RelA) activation and decreased c-Rel nuclear translocation were observed in A20-deficient Treg cells.
  • Increased Treg cell numbers were evident early in development, in CD4+ single-positive thymic Treg cell progenitors expressing GITR.
  • A20-deficient Treg cells maintained normal suppressive function in graft-versus-host disease models.

Conclusions:

  • A20 acts as a critical brake on thymic regulatory T cell production.
  • Loss of A20 promotes Treg cell development and enhances their suppressive capacity.
  • A20 integrates Treg cell homeostasis with effector T cell responses for overall immune efficiency.