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.
John Ray, PhD
Ingrid Harten, PhD
Alex Ho, PhD
Prioritizing autoimmune disease-causal variants in immune cells
Mapping cis-regulatory regions that control immune cell function genome-wide
Defining variants that act collectively to promote disease
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Finding Genetic Changes That Cause Autoimmunity
To better treat — and even prevent — autoimmune diseases, we need to know exactly what causes them. Scientists have long known that genetics play a role in these diseases but are still working to understand how and why.