Dr. Shigeki Nakagome

Shigeki Nakagome is Ussher Assistant Professor in Genomic Medicine at School of Medicine. Dr. Nakagome received his Ph.D. at The University of Tokyo in 2010 with the focus on the evolutionary model in which high risk variants associated with Crohn's disease at the NOD2 locus may have exclusively spread into European populations by natural selection. As a postdoctoral researcher, Dr. Nakagome first joined The Institute of Statistical Mathematics from 2011 to 2014 where he was awarded a competitive Research Fellowship of the Japan Society for the Promotion of Science (JSPS) for Young Scientists and developed a new statistical method that incorporates kernel methods into Approximate Bayesian Computation (kernel ABC). Dr. Nakagome obtained further postdoctoral training on experimental aspects of functional genomics at The University of Chicago from 2013 to 2016 as JSPS Overseas Research Fellow. During this training, Dr. Nakagome has acquired expertise in population and functional genomics to develop statistical approaches for understanding selective pressures on immunity genes and to connect genetic polymorphisms to their functional consequences in the immune system.

  BAYESIAN COMPUTATION   Bioinformatics   Evolution   Evolutionary Biology   Evolutionary genetics   GENE POLYMORPHISMS   GENE REGULATION   GENE-EXPRESSION   Genomes, Genomics   Genomic structure and function, molecular approaches to gene function   Genomics   Host-pathogen interaction   Human Evolution   Human Population Genetics   INFLAMMATORY BOWEL DISEASE   microbiome   MOLECULAR EVOLUTION   POPULATION GENETICS

Symbiosis between human host and gut microbiota is essential for our health, a disruption of which leads to autoimmune conditions, as is the case in inflammatory bowel disease (IBD). A critical challenge for the host under the intestinal environment is to mount an efficient and appropriate immune response to pathogens while maintaining tolerance to symbiotic bacteria. However, we still do not know the underlying molecular mechanisms whereby humans acquire tolerance to host trillions of microorganisms in their intestine. Our research team aims to understand the nature and function of host immune repertoires that provide the ability to discriminate pathogenic from symbiotic bacteria. Outcomes from our research will not only yield deeper insights into the host-microbiota crosstalk in IBD, but also pioneer personalized and targeted interventions to control this interaction for prevention and treatment of IBD. Taking advantage of our expertise in quantitative genetics and its application to high-throughput sequencing, we develop statistical and computational approaches to immunogenomics profiling on patients affected by IBD. Our research aims to describe (i) the patterns of inter-individual variation in the host immunity and bacterial activity, (ii) the processes of immune development that ends up with the breakdown of host tolerance to gut bacteria, and (iii) the impacts of past selective pressures during human evolution on an individual's ability to adapt to its own intestinal environments.