Happy New Year! 2014 was a highly collaborative year for the Cho Lab. Let’s take a look back at our lab’s accomplishments in 2014…
The Ashkenazi Genome Consortium (September 2014)
As part of the Ashkenazi Genome Consortium, our lab contributed to the sequencing and analysis of 128 Ashkenazi Jewish genomes. These efforts shed light on the demography and genetic architecture of this population, and established an invaluable resource for future genetic studies, including studies of IBD.
Publication:
Carmi, S. et al. Sequencing an Ashkenazi reference panel supports population-targeted personal genomics and illuminates Jewish and European origins. Nat Comms 5, 4835 (2014).
The microbiome in inflammatory bowel disease (August 2014)
In collaboration with the Flavell lab, we showed that the intestinal microbiota of IBD patients, when grown in anaerobic culture and given to mice, contributes to the development of colitis in previously germ-free mice. This suggests that certain commensal bacteria may be drivers of intestinal inflammation in IBD.
Publication:
Palm. N. et al. Immunoglobulin A coating identifies colitogenic bacteria in inflammatory bowel disease. 158, 1000–1010 (2014).
Functional characterization of CD risk alleles in dendritic cells (May 2014)
In collaboration with the Abraham lab, we showed that immune cells from carriers of the ICOSLG CD risk allele have reduced PRR-induced cytokine responses, and the same risk allele is associated with an ileal Crohn’s disease phenotype. This work elucidates the relationship between ICOSLG and NOD2 and further characterizes Crohn’s disease as a disruption of immune homeostasis.
Publication:
Hedl, M. et al. Pattern recognition receptor signaling in human dendritic cells is enhanced by ICOS ligand and modulated by the Crohn’s disease ICOSLG risk allele. 40, 734–746 (2014).
Leveraging network analysis for inflammatory bowel disease gene prioritization (May 2014)
Genetic studies of IBD have implicated over a hundred loci, but many remain to be discovered, and establishing the most biologically relevant genes is a real challenge. In collaboration with the Zhao lab, we explored the utility of gene expression networks in understanding the pathology of IBD. Studying how these gene networks are rewired in IBD patients compared to healthy controls has the potential to identify genes that, when disrupted, take an entire network with them. This can provide a method for ranking the contribution of known and novel genes to the disease.
Publication:
Hou, L. et al. Guilt by rewiring: gene prioritization through network rewiring in genome wide association studies. 23, 2780–2790 (2014).