Regulatory T cells (Treg) are immunosuppressive antigen-specific cells, which restrain activity of the immune system. Treg cells traditionally develop in thymus, where their suppressive phenotype is predetermined based on intensity and duration of TCR stimulation, Foxp3 and CD25 (IL-2 receptor α-chain) expression and epigenetic signature. Regulatory T cells (Treg) are immunosuppressive antigen-specific cells, which restrain activity of the immune system. Treg cells traditionally develop in thymus, where their suppressive phenotype is predetermined based on intensity and duration of TCR stimulation, Foxp3 and CD25 (IL-2 receptor α-chain) expression and epigenetic signature. These cells express transcription factor Foxp3 – it promotes their survival and function. After activation via T cell receptor (TCR), Treg cells secrete anti-inflammatory cytokines, such as IL-10 and TGFβ; kill effector cells with cytotoxic molecules; deprive them of activating cytokine IL-2, binding it by CD25; control dendritic cells through CTLA-4. Similar to proinflammatory conventional effector T cells, Treg cells display considerable heterogeneity. Some activated Treg cells express the effector CD4 T cell transcription factors (T-bet, GATA-3, RORγt, STAT3), which have been suggested to provide Treg cells with enhanced suppressive capacity against respective T helper subset.
Nuclear receptors are a superfamily of transcription factors able to activate via binding of ligands like sterols and thyroid hormones. Analyses of transcriptomic data reveal that expression of multiple nuclear receptor genes is up- regulated in regulatory T cells (Treg) in non-lymphoid tissues, suggesting that these proteins might regulate accumulation, differentiation or function of Treg cells. Some of these receptors were already shown to be markers to distinguish between Treg sub-populations. This study aims to investigate a role of a nuclear receptor ROR-alpha in this context.
