Journal
FRONTIERS IN IMMUNOLOGY
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.911151
Keywords
Treg; regulatory T cell; T cell; autoimmunity; type 1 diabetes; genetic; FOXP3
Categories
Funding
- National Institutes of Health [R01 AI125301]
Ask authors/readers for more resources
This review highlights the alterations in gene expression and function of regulatory T cells (Tregs) in autoimmune diseases. It discusses the potential impact of genetic, epigenetic, and environmental factors on Treg development and function. The review also explores the influence of the tissue microenvironment on Treg function, stability, and plasticity. Additionally, it provides insights into the current efficacy and future directions of Treg-based therapies for Type 1 Diabetes and other autoimmune diseases.
The importance of regulatory T cells (Tregs) in preventing autoimmunity has been well established; however, the precise alterations in Treg function in autoimmune individuals and how underlying genetic associations impact the development and function of Tregs is still not well understood. Polygenetic susceptibly is a key driving factor in the development of autoimmunity, and many of the pathways implicated in genetic association studies point to a potential alteration or defect in regulatory T cell function. In this review transcriptomic control of Treg development and function is highlighted with a focus on how these pathways are altered during autoimmunity. In combination, observations from autoimmune mouse models and human patients now provide insights into epigenetic control of Treg function and stability. How tissue microenvironment influences Treg function, lineage stability, and functional plasticity is also explored. In conclusion, the current efficacy and future direction of Treg-based therapies for Type 1 Diabetes and other autoimmune diseases is discussed. In total, this review examines Treg function with focuses on genetic, epigenetic, and environmental mechanisms and how Treg functions are altered within the context of autoimmunity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available