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Related Concept Videos

General Transcription Factors01:30

General Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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...
Lymphoid Cells and Tissues01:18

Lymphoid Cells and Tissues

Lymphoid cells and tissues are integral to the immune system, which is crucial in maintaining our body's defense against harmful pathogens. They form the building blocks of lymphoid organs, which include the spleen, thymus, and lymph nodes.
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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.
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B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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Related Experiment Video

Updated: Jun 21, 2026

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

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Association Between FOXP3 and OX40 Expression in Adult T-Cell Leukemia Cells.

Mariko Mizuguchi1,2, Yoshiaki Takahashi2, Reiko Tanaka3

  • 1Laboratory of Immunology, Department of Medical Technology, School of Life and Environmental Science, Azabu University, Sagamihara 252-5201, Japan.

Viruses
|November 27, 2025
PubMed
Summary
This summary is machine-generated.

Regulatory T (Treg) cells expressing FOXP3 are key in adult T-cell leukemia/lymphoma (ATL). OX40 and OX40L interactions may drive the expansion of these FOXP3+ ATL cells, contributing to immune suppression.

Keywords:
ATLFOXP3HTLV-1OX40OX40L

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Area of Science:

  • Immunology
  • Oncology
  • Cell Biology

Background:

  • Forkhead box P3 (FOXP3) defines regulatory T (Treg) cells, and their expansion is linked to immune suppression in adult T-cell leukemia/lymphoma (ATL).
  • The mechanisms driving FOXP3+ ATL cell expansion remain largely unknown.
  • OX40 signaling promotes Treg cell differentiation and proliferation in mouse models, and OX40 is expressed on ATL cells.

Purpose of the Study:

  • To investigate the role of OX40 and OX40L in the expansion of FOXP3+ ATL cells.
  • To examine the expression patterns of OX40 and OX40L in ATL patients.
  • To elucidate the cellular interactions potentially driving ATL pathogenesis.

Main Methods:

  • Flow cytometry was used to analyze OX40 and OX40L expression on peripheral blood mononuclear cells (PBMCs) from ATL patients.
  • Small interfering RNA (siRNA) was employed to knockdown FOXP3 expression in HTLV-1-infected cell lines.
  • Cellular expression levels of OX40 and OX40L were quantified.

Main Results:

  • OX40 expression was significantly elevated in ATL patients with a high frequency of FOXP3+ ATL cells.
  • FOXP3- cells predominantly expressed OX40L, while FOXP3+ cells expressed OX40.
  • FOXP3 knockdown in HTLV-1-infected cells led to increased OX40L expression.
  • Findings suggest a potential interaction between FOXP3- OX40L+ cells and FOXP3+ OX40+ cells.

Conclusions:

  • Interactions between FOXP3- OX40L+ and FOXP3+ OX40+ cells may drive the proliferation of FOXP3+ ATL cells.
  • This interaction could be a key mechanism contributing to immune suppression in ATL.
  • Targeting the OX40/OX40L pathway warrants further investigation for ATL treatment.