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• W2912510154 abstract "CD4 T cells adapt their immune function to the local tissue environment by differentiating into various functional subsets. At steady state, regulatory CD4 T cells (Treg) and interleukin (IL)-17-producing CD4 T cells (Th17 cells) reside in the intestinal lamina propria whereas CD4 cytotoxic T lymphocytes (CTL) are present in the epithelial layer. The differentiation into these functional subtypes is mutually exclusive and controlled by key transcription factors. Cytokine TGFβ, an important regulator of CD4 T helper subset differentiation, induces the master transcription factor, FOXP3 in Treg or RORγt in Th17 cells. TGFβ is also important for the CD4 CTL differentiation, characterized by T-BET and RUNX3 expression, whereas Foxp3 and Rorc genes are repressed in these cells. A hallmark of CD4 CTL differentiation in the intestine is the reactivation of the Cd8 locus, which coincides with the re-expression of CD8α, controlled by an enhancer (E8I enhancer) located within the intergenic region of the Cd8 locus. Interestingly, CD4 T cells with a deletion of this Cd8 region not only fail to re-express CD8α but they also show impaired coordinated expression and function of T-BET and RUNX3, and lack of Foxp3 and Rorc suppression when differentiated under CTL conditions. The inability of Cd8 intergenic deletion mutant CD4 donor T cells to regulate these key transcription factors led to the accumulation of potent inflammatory donor T cells and severe immune pathology in the large and small intestine of Rag1-/- recipient mice. Increased and accelerated disease coincided with a significant accumulation of inflammatory IL-17A and IL-17A/IFNγ double producing CD4 T cells in the small and large intestine. We isolated and characterized a long noncoding RNA transcribed from this Cd8 locus region in mouse and human, as the critical regulatory of the functional polarization of CD4 T cells in the intestine. Moreover, the findings suggest that defects in the regulation by this LncRNA lead to the aberrant differentiation of pathogenic CD4 effector T cells in vivo and hence may form a significant underlying cause in inflammatory bowel diseases. A thorough understanding of the regulation mechanisms employed by this LncRNAs will lead to the design of alternative therapeutic strategies to manipulate adaptive immune functions in the treatment of inflammatory bowel diseases and cancers." @default.
• W2912510154 created "2019-02-21" @default.
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• W2912510154 date "2019-02-01" @default.
• W2912510154 modified "2023-09-25" @default.
• W2912510154 title "P141 A LONG NONCODING RNA TRANSCRIBED FROM THE CD8 LOCUS CONTROLS FUNCTIONAL DIFFERENTIATION OF CD4 T CELLS IN THE INTESTINE" @default.
• W2912510154 doi "https://doi.org/10.1053/j.gastro.2019.01.220" @default.
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