Genomic signatures of immune system aging 

​The functional decline of the immune system with aging, i.e., immunosenescence, has been associated with increased disease susceptibility, infections, and poor response to treatments and vaccination in elderly. However, we have yet to discover which genes, enhancers and regulatory interactions in which immune cells can explain the functional decline of immune functions with aging and whether these changes are similar between sexes and different populations. In collaboration with Banchereau Lab and UCHC Center on Aging we study chromatin signatures of human immune system aging and to quantify the clinical implications of these signatures.

 

Systems biology and immunology

Capturing the dynamics of epigenomic patterns is essential to understand how gene expression patterns are established and maintained in healthy human cells, and how they are disrupted by pathologies. However, discovering these patterns and interpreting their biological meaning is a significant computational challenge. We tackle this challenge by developing computational tools to mine and integrate diverse data sources (ChIA-PET, ATAC-seq, RNA-seq), since intricate regulatory interactions and diverse regulatory elements cannot be inferred from a single data type. We develop machine learning models or network mining algorithms to integrate and interpret genomics data from primary human cells under the light of data accumulated in public repositories. 

 

 

Genomic and genetics of T2D

In collaboration with the Stitzel lab we study genomic and epigenomic profiles in human islets and changes in these profiles associated with Type-2-Diabetes (T2D). For this we profile epigenomes/transcriptomes of human islet samples from healthy and diabetic individuals to uncover genomic signatures of T2D. We also integrate these data with genotypes of individuals via QTL analyses to uncover to what extent islet functions and responses are genetically modulated.