Defining the Transcriptional Regulation of NR2F6 in T_H17 Cell Responses

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Presentation Time: 11:30 AM - 12:45 PM
Poster Board Number: B723
Abstract ID: 6058

Presenting Author:
Adrianna Wilson , Graduate Student at Scripps Res. Skaggs Grad. Sch. of Chem. and Bio. Sci., Herbert Wertheim University of Florida Scripps Institute for Biomedical Innovation & Technology

Abstract:

NR2F6, an orphan member of the nuclear receptor superfamily of ligand-regulated transcription factors, plays an important role in CD4⁺ T cell differentiation and effector function. NR2F6 has been reported to repress pro-inflammatory cytokines IL-2, IL-17A, IL-21, and IFNγ. While genetic experiments have given us information regarding its global function, the molecular mechanism of NR2F6 mediated transcriptional regulation is unknown. Our data demonstrate that overexpression of NR2F6 in T_H17 cells consistently represses IL-17A expression which can be partially alleviated by introducing a point mutation rendering NR2F6 unable to bind DNA. Given T_H17 cell’s roles in autoimmunity, NR2F6 may play a role in autoimmune regulation and therapy. Here, we are working to elucidate NR2F6’s transcriptional function in T cells through multi-OMIC approaches. Mass spectrometry based proteomics have identified 11 potential transcription factor interactors of NR2F6 in T_H17 cells. This data coupled with RNAseq and CUT&RUN mapping provide insight into NR2F6’s regulatory network. This work will define NR2F6’s molecular niche in T cells, elucidating its’ potential therapeutic applicability for cancer immunotherapy and autoimmunity.