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HDAC10 deletion promotes Foxp3+ T-regulatory cell function
Satinder Dahiya1, Ulf H Beier2, Liqing Wang1
1Division of Transplant Immunology, Department of Pathology and Laboratory Medicine, and Biesecker Center for Pediatric Liver Disease, Children's Hospital of Philadelphia and University of Pennsylvania, Philadelphia, PA, 19104, USA.
Scientific Reports
|January 18, 2020
Summary
Targeting histone deacetylase 10 (HDAC10) enhances regulatory T-cell (Treg) function, offering potential for treating inflammatory diseases like colitis and improving transplant tolerance.
Area of Science:
- Immunology
- Molecular Biology
- Transplantation Science
Background:
- Foxp3+ T-regulatory (Treg) cells are crucial for immune suppression.
- Lysine acetylation regulates Foxp3 stability and activity, making histone/protein deacetylases (HDACs) important targets for immunotherapy.
- Understanding the specific roles of individual HDACs in Treg function is essential.
Purpose of the Study:
- To investigate the role of HDAC10 in murine Treg function.
- To assess the therapeutic potential of HDAC10 deletion in Treg-based immunotherapy.
Main Methods:
- Generated and analyzed HDAC10 knockout (HDAC10-/-) mice and their Tregs.
- Assessed Treg suppressive function in vitro and in vivo using models of colitis and cardiac transplantation.
Main Results:
- HDAC10 deletion did not affect overall health or other T-cell populations.
- HDAC10-/- Tregs demonstrated enhanced suppressive capacity in vitro and in vivo.
- Adoptive transfer of HDAC10-/- Tregs protected against colitis development.
- HDAC10-/- Tregs promoted long-term survival of MHC-mismatched cardiac allografts.
Conclusions:
- HDAC10 plays a critical role in regulating Treg suppressive function.
- Targeting HDAC10 represents a promising therapeutic strategy for inflammatory conditions and transplantation.
