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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
Published on: December 30, 2016
From Treg, FOXP3 to RBPJ: Linking basic science and clinical medicine
Lung-Fang Chen1, Chung-Jen Chen2
1Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Regulatory T cells (Treg) and the FOXP3 gene are crucial for immune tolerance. Treg-based therapies show promise for autoimmune diseases, pregnancy loss, and graft-versus-host disease.
Area of Science:
- Immunology
- Cell Biology
- Genetics
Background:
- Regulatory T cells (Treg) and the FOXP3 gene are key to peripheral tolerance.
- Treg dysfunction is implicated in autoimmune diseases like SLE, UC, and GVHD.
- Abnormal Treg function is linked to pregnancy complications such as recurrent pregnancy loss and preterm birth.
Purpose of the Study:
- To review the discovery and clinical significance of Tregs and FOXP3.
- To explore the role of Tregs in various diseases and pregnancy outcomes.
- To discuss potential Treg-based therapies and novel regulatory mechanisms.
Main Methods:
- Literature review of Treg and FOXP3 research.
- Analysis of clinical studies on Treg involvement in diseases.
- Discussion of Epigallocatechin gallate (EGCG) and RBPJ gene regulation of FOXP3.
Main Results:
- Treg and FOXP3 discoveries have advanced understanding of immune tolerance.
- Treg abnormalities are associated with autoimmune diseases, GVHD, and pregnancy complications.
- Epigallocatechin gallate (EGCG) may influence Treg function.
- RBPJ gene regulates FOXP3 in induced Tregs (iTregs).
Conclusions:
- Treg-based therapy offers significant potential for treating autoimmune diseases, GVHD, and pregnancy loss.
- Further research into Treg regulation and function is warranted.
- Targeting Tregs could revolutionize treatments for immune-related disorders.
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