Ray Lab


Genetic variation in the human genome controls a compendium of cellular and physiological components that make up human biology. The Ray Lab is interested in better understanding how genetic variation tunes our immune system and how this can put individuals at risk for autoimmune diseases, which is a vital step in developing more effective therapeutics with fewer side effects. 

Because most genetic risk for autoimmune diseases occurs in non-coding regions of the genome, the Ray lab studies how non-coding genetic variants modulate cis-regulatory regions and alter immune cell activities that lead to autoimmune disease susceptibility. We prioritize likely disease-causal variants and cis-regulatory regions, and, in human and mouse systems, identify variant target genes and pathways and define their functional effects on immune cells.

These studies will inform efforts for personalized therapies and disease prevention.

Ray Lab Inline - Group Photo
John Ray
Assistant Member

John Ray, PhD

Assistant Member; Principal Investigator, Ray Lab
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Lab Members

Max Dippel

Maxwell Dippel

Research Technician, Ray Lab
Ingrid Harten

Ingrid Harten, PhD

Staff Scientist, Ray Lab
Alex Ho

Alex Ho, PhD

Postdoctoral Research Associate, Ray Lab
Meghan McQuade

Meghan McQuade

Research Technician, Ray Lab

Research Projects

Ray Lab Research Project Preview - Connecting Risk Variants

Prioritizing autoimmune disease-causal variants in immune cells

Utilizing massively parallel reporter assays and statistical fine-mapping to enrich for functional and disease-causal genetic variation
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Ray Lab Research Project Preview - Mapping cis regulatory regions

Mapping cis-regulatory regions that control immune cell function genome-wide

Identifying enhancers that facilitate T and B cell function throughout the genome using CRISPR screening approaches.
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Ray Lab Research Project Preview - Defining Variants

Defining variants that act collectively to promote disease

Identifying synergistic properties of variants and enhancers on T cell function
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