Fig. 1 | Signal Transduction and Targeted Therapy

Fig. 1

From: Induced regulatory T cells for therapy: targeting RBPJ to enhance stability and function

Fig. 1

Model of how RBPJ knock-out can aid in the generation of stable iTreg cells. a Situation in wild-type iTreg cells. The RBPJ protein forms a repressive complex with other proteins, including NCOR1, NCOR2, and HDAC3. The enhancer region CNS2 in the first intron of the FOXP3 gene is methylated, and FOXP3 is not stably expressed or expression is lost during expansion. b Situation in iTreg cells upon RBPJ knock-out. Chromatin accessibility and histone acetylation around the FOXP3 promoter are increased. CNS2 is demethylated. FOXP3 is continuously transcribed, leading to a stable Treg cell identity. Treg cell effector genes are more strongly expressed, leading to enhanced Treg cell function. CNS conserved non-coding sequence, CTLA4 cytotoxic T-lymphocyte associated protein 4, FOXP3 forkhead-box P3, HDAC3 histone deacetylase 3, KO knock-out, NCOR nuclear co-receptor co-repressor, RBPJ recombination signal binding protein for immunoglobulin kappa J region, TIGIT T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif ___domain, WT wild-type. The figure was generated using BioRender.com

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