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Project

Molecular determinants of regulatory T cell lineage identity and fate loss

Regulatory T cells (Tregs) are specialized white blood cells that prevent autoimmune diseases and allergies. While other T cells cause inflammation, Tregs suppress inflammation. Absence or malfunction of Tregs therefore leads to immune action against the body, with detrimental consequences or even death. In order for a T cell to become a Treg it needs to be “re-wired” to express a different set of genes that give the cell this critical suppressive function. The main way in which a Treg expresses this set of new genes is by first expressing the gene Foxp3. Foxp3 then in turn activates the expression of all the other genes needed for suppressive function. Mutations in the Foxp3 gene block this process, causing a lack of Tregs and fatal inflammation. Foxp3 also blocks the expression of other genes, that would make the cell inflammatory. Here, we aim to understand exactly how Foxp3 makes a T cell into a Treg, to find out how Foxp3 blocks the Treg from becoming inflammatory, and what happens when Foxp3 is lost. This knowledge will help us make Tregs even better at suppressing inflammation, in order to turn these cells into a therapeutic strategy.

Date:1 Oct 2019 →  1 Oct 2023
Keywords:Foxp3 gene, regulatory T-cells, autoimmunity, inflammation, cancer
Disciplines:Adaptive immunology, Inflammation, Autoimmunity, Cancer biology, Immunogenetics
Project type:PhD project