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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
OX40 costimulation turns off Foxp3+ Tregs.
Minh Diem Vu1, Xiang Xiao, Wenda Gao
1Harvard Medical School, Transplant Research Center, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
Blood
|June 19, 2007
Summary
Stimulating OX40 on regulatory T cells (Tregs) impairs their function and inhibits the generation of new Tregs. OX40 acts as a negative regulator of Tregs, impacting transplantation and autoimmunity.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- OX40 is a T-cell costimulatory molecule in the TNF/TNFR superfamily.
- OX40 is expressed on T effector cells and regulatory T cells (Tregs).
- Its role in Treg function and generation is largely unknown.
Purpose of the Study:
- To investigate the role of OX40 in regulating Foxp3(+) Treg suppressor functions.
- To determine OX40's effect on the de novo generation of inducible Tregs.
- To identify OX40 as a potential therapeutic target in immune-related diseases.
Main Methods:
- Utilized a novel foxp3gfp knockin mouse model.
- Stimulated OX40 on naturally arising and T effector cells.
- Assessed Treg suppressive function, proliferation, survival, and gene expression.
- Evaluated allograft rejection models.
Main Results:
- OX40 stimulation abrogated Treg-mediated suppression of T effector cell proliferation and IFN-gamma production.
- OX40 stimulation inhibited T effector cell-mediated allograft rejection.
- OX40 costimulation inhibited Foxp3 gene expression in Tregs.
- OX40 stimulation prevented the induction of new Tregs from T effector cells.
Conclusions:
- OX40 is a key negative regulator of Foxp3(+) Tregs.
- OX40 signaling diminishes Treg suppressive capacity and impedes Treg generation.
- Targeting OX40 may offer therapeutic benefits in transplantation and autoimmunity.
