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Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
T Cell Types and Functions01:24

T Cell Types and Functions

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...
T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...

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Related Experiment Video

Updated: Jul 4, 2026

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Na&#239;ve CD4+ T Cells Using a TGF-&#946;-containing Protocol
08:20

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol

Published on: December 30, 2016

Iron Regulates CD4 T Cell Quiescence by Controlling TGF-β Production.

Amber L Siglin, Zelong Han, Afia Nkansah

    Biorxiv : the Preprint Server for Biology
    |July 3, 2026
    PubMed
    Summary

    Transforming growth factor-β (TGF-β) regulates CD4 T cell iron homeostasis, impacting survival and proliferation. This study reveals TGF-β

    Area of Science:

    • Immunology
    • Cell Biology
    • Metabolism

    Background:

    • Transforming growth factor-β (TGF-β) is crucial for T cell function, but its influence on iron metabolism remains unclear.
    • Iron homeostasis is vital for cellular processes, including immune cell activation and differentiation.
    • Dysregulated iron metabolism is implicated in various immune disorders.

    Purpose of the Study:

    • To investigate the role of TGF-β in regulating CD4 T cell iron homeostasis.
    • To determine how iron overload affects TGF-β responsiveness in T cells.
    • To elucidate the molecular mechanisms linking TGF-β signaling and iron metabolism in T cells.

    Main Methods:

    • Utilized genetic manipulation (TGFβR1 deletion, FLVCR1 deficiency) in CD4 T cells.
    • Assessed T cell proliferation, survival, CD71 expression, and intracellular iron levels.

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    Related Experiment Videos

    Last Updated: Jul 4, 2026

    In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Na&#239;ve CD4+ T Cells Using a TGF-&#946;-containing Protocol
    08:20

    In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol

    Published on: December 30, 2016

    Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation
    15:33

    Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation

    Published on: August 13, 2013

  • Measured mitochondrial iron accumulation and reactive oxygen species (ROS) production.
  • Investigated the effects of pharmacologic TGFβR1 inhibition and iron overload (FeSO4).
  • Examined regulatory T cell differentiation and iron acquisition in vitro.

    • Main Results:

    • TGF-β signaling, via TGFβR1, reduces T cell proliferation and cytosolic iron availability while increasing mitochondrial iron during activation.
    • FLVCR1-deficient T cells exhibit hypersensitivity to TGF-β, increased TGF-β secretion, and sustained TGFβR1 expression.
    • Pharmacologic TGFβR1 inhibition rescues proliferation and iron levels in FLVCR1-deficient cells.
    • TGF-β induces ROS in FLVCR1-deficient cells, but ROS is not the sole driver of TGF-β hypersensitivity.
    • TGF-β impairs iron acquisition in regulatory T cells, and excess iron hinders FoxP3 induction.

    Conclusions:

    • TGF-β acts as a context-dependent regulator of CD4 T cell iron homeostasis through TGFβR1 signaling.
    • FLVCR1 deficiency exacerbates TGF-β effects, highlighting the interplay between iron export and TGF-β responsiveness.
    • These findings offer insights into T cell dysfunction in iron overload conditions and potential therapeutic targets.