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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
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Human FOXP3 and tumour microenvironment.

Jia Wang1,2, Ruining Gong1, Chenyang Zhao1

  • 1Center of Tumor Immunology and Cytotherapy, Medical Research Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.

Immunology
|June 11, 2022
PubMed
Summary
This summary is machine-generated.

Regulatory T cells (Tregs) expressing the transcription factor forkhead box protein 3 (FOXP3) impact tumor immunity. This review explores FOXP3

Keywords:
FOXP3Treg-FOXP3tumour microenvironmenttumour-FOXP3

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • The tumor microenvironment (TME) comprises cancer, stromal, and immune cells.
  • Regulatory T cells (Tregs) within the TME suppress anti-tumor immune responses.
  • Forkhead box protein 3 (FOXP3) is the primary marker and functional regulator of Tregs.

Purpose of the Study:

  • To review recent advancements in understanding Treg-FOXP3 and tumor-FOXP3 within the TME.
  • To discuss FOXP3's communication mechanisms with effector T cells in the TME.
  • To examine the link between FOXP3 expression, clinical prognosis, and potential therapeutic strategies.

Main Methods:

  • Literature review of recent studies on FOXP3 in the TME.
  • Analysis of FOXP3's role in immune suppression and tumor progression.
  • Exploration of FOXP3-targeted therapies.

Main Results:

  • FOXP3, initially considered Treg-specific, is also found in various tumors with diverse functions.
  • FOXP3+ cells modulate effector T cell activity within the TME.
  • FOXP3 expression correlates with clinical outcomes and presents therapeutic targets.

Conclusions:

  • FOXP3 plays a multifaceted role in the TME beyond its function in Tregs.
  • Understanding FOXP3's interactions is crucial for developing effective cancer immunotherapies.
  • Targeting FOXP3 offers a promising avenue for novel cancer treatments.