Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
Celiac disease (CeD) is a complex T cell–mediated enteropathy induced by gluten. Although genome-wide association studies have identified numerous genomic regions associated with CeD, it is difficult to accurately pinpoint which genes in these loci are most likely to cause CeD. We used four different in silico approaches to integrate information gathered from a large transcriptomics dataset. This identified 118 prioritized genes across 50 CeD-associated regions. Co-expression and pathway analysis of these genes indicated an association with adaptive and innate cytokine signalling and T cell activation pathways. 51 of these genes are targets of known drug compounds, suggesting that our methods can be used to pinpoint potential therapeutic targets. In addition, we detected 129 gene-combinations that were affected by our CeD-prioritized genes in trans. Notably, 40 of these trans-mediated genes appear to be under control of one master regulator, TRAFD1, and were found to be involved in IFN signalling and MHC I antigen processing/presentation. We then performed in vitro experiments that validated the role of TRAFD1 as an immune regulator acting in trans. Our strategy has confirmed the role of adaptive immunity in CeD and revealed a genetic link between CeD and the IFNsignalling and MHC I antigen processing pathways, both major players of immune activation and CeD pathogenesis. Our next steps will be to test the role of TRAFD1 in a novel, human model system of the intestinal barrier, the gut-on-chip.
