On 28th November OxTalks will move to the new Halo platform and will become 'Oxford Events' (full details are available on the Staff Gateway).
There will be an OxTalks freeze beginning on Friday 14th November. This means you will need to publish any of your known events to OxTalks by then as there will be no facility to publish or edit events in that fortnight. During the freeze, all events will be migrated to the new Oxford Events site. It will still be possible to view events on OxTalks during this time.
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Memory B-cells and antibody are key providers of long-lived immunity against
infectious disease. How chronic viral infection disrupts memory B-cells and antibody,
and whether such changes are reversible through therapeutic intervention, remains
unknown. Epigenetic programs establish the identity and function of B-cell subsets.
We therefore set out to determine how antibody responses and memory B-cells are
epigenetically altered by inflammatory signals during chronic viral infection, using
single-cell resolution of the transcriptome and chromatin landscape. Using this
system, our study revealed that type-I interferon (IFN-I) dynamics are a key
determinant in shaping chronic memory B-cell development in vivo. We further
identified the histone modifier BMI-1 as a key target to correct dysregulated antibody
responses during chronic viral infection and autoimmunity. Collectively, our research
identifies key mechanisms to instruct antibody and memory B-cell identity during viral
infection, thus laying the foundation for improving therapeutic interventions in chronic
infectious disease.
