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- W4313359025 abstract "Abstract CD39 is an ectonucleotidase that hydrolyzes extracellular ATP/ADP to generate immunosuppressive adenosine. CD39 is expressed by Tregs, where it contributes to immunosuppression; and by a subset of effector Th17 cells where it limits pathogenicity. CD39 is regulated at the genetic level via single nucleotide polymorphisms in non-coding regions of the gene. These are associated with decreased CD39 expression and with predisposition to Crohn’s disease. CD39 is also regulated at transcriptional level through the activation of pathways involving the aryl-hydrocarbon-receptor and O2. We have noted the presence of antisense RNA at the 3’ end of the human CD39/ENTPD1 gene. Hence, another form of regulation might be operational at post-transcriptional level and could relate to the presence of endogenous antisense RNAs. CD39-specific antisense levels were increased in Treg and Th17 cells obtained from the peripheral blood of Crohn’s patients over controls. CD39 antisense is largely localized in the cell nucleus. CD39 expression was at low levels in both cell types in Crohn’s. When testing lamina propria-derived cells, we noted higher CD39 expression and lower antisense levels in Th17 cells isolated from non-inflamed bioptic areas over inflamed areas. Functional analysis revealed that antisense silencing by FANA oligos (AumBiotec) resulted in consequent CD39 upregulation. In conclusion, our data indicate that regulation of CD39 antisense RNA impacts Treg suppression and Th17 cell modulation of pathogenic potential in Crohn’s disease. Inhibition/blockade of antisense should be considered as a novel therapeutic strategy to restore CD39 along with immune homeostasis in Crohn’s disease and other inflammatory conditions." @default.
- W4313359025 created "2023-01-06" @default.
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- W4313359025 date "2019-05-01" @default.
- W4313359025 modified "2023-09-27" @default.
- W4313359025 title "Endogenous antisense RNA and dysregulation of CD39 expression in inflammatory bowel disease" @default.
- W4313359025 doi "https://doi.org/10.4049/jimmunol.202.supp.182.10" @default.
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