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SUMMARY:Immune disease GWAS variants converge on regulation of cd4 T cell 
 activation - Dr Gosia Trynka\; Group Leader - Immune Genomics Group\, Well
 come Sanger Institute 
DTSTART:20190503T120000Z
DTEND:20190503T130000Z
UID:TALK122470@talks.cam.ac.uk
CONTACT:Bobbie Claxton
DESCRIPTION:Thousands of genetic variants are associated with common immun
 e-mediated diseases\, such as type 1 diabetes\, rheumatoid arthritis\, cel
 iac disease and inflammatory bowel disease. However\, the molecular mechan
 isms by which genetic variants predispose an individual to the development
  of an immune disease are largely unknown because most of the disease vari
 ants localise in non-coding parts of the genome - therefore\, making it ch
 allenging to infer their functional consequences. \n\nUsing a broad genomi
 c toolkit\, from profiling chromatin landscape (ATACseq\, ChIP-seq)\, thro
 ugh to measuring gene expression in bulk and at the single cell level\, we
  are dissecting the role of immune disease variants in different aspects o
 f regulation of CD4 T cell functions. Our results point towards the role o
 f immune disease variants in modulating early activation of memory cells. 
 Additionally\, we show that immune disease variants regulate the enhancer 
 activity and gene expression in regulatory T cells (Tregs)\, a rare subset
  of CD4 T cells that is critical in dampening immune response. We show tha
 t these effects result in impaired suppressive function of Tregs.\n\nOur r
 esults suggest that a proportion of immune disease variants can lead to es
 calated immune response by 1) promoting early activation of memory T cells
  and 2) impairing the suppressive capacity of Tregs\, leading to deregulat
 ion of CD4 T cell activation circuitry.
LOCATION:Babraham - The Cambridge Building - The Kings Hedges Room
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