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Dr Luke Jostins joins the Kennedy Institute to lead a new research group that will develop statistical methods to decode the genetics of complex immune diseases.

The Kennedy Institute would like to welcome Dr Luke Jostins to its team of principal investigators. Luke joins the Institute as a Kennedy Trust for Rheumatology Research Career Development Fellow and will lead a new research group focused on developing statistical methods to decipher how genetic variation predisposes to disease.

Numerous studies over the last decade have shown that variation in the DNA sequence of individuals can confer risk for immune-mediated diseases such as inflammatory bowel disease (IBD) and rheumatoid arthritis. Understanding how these genetic differences alter the immune system could provide new insight into the cause of disease.

As a Sir Henry Wellcome Postdoctoral Fellow, Luke worked with Prof Gil McVean at the Wellcome Trust Centre for Human Genetics, Oxford, on statistical approaches to combine analysis of genetic data from different immune diseases, with measurements of the immune system in patients.

He will continue this line of investigation at the Kennedy Institute, where he will collaborate with immunologists, cell biologists and clinicians to unravel how DNA variants that associate with disease risk cause both healthy and pathological changes in the immune response.

Speaking of his new position Luke said, “I am very excited to be moving to the Kennedy Institute, given the important role is has played in understanding and treating inflammatory diseases. The only way we will ever decode the genetics of complex immune diseases is through close collaboration between statistical, computational and experimental biologists.”

Prior to moving to Oxford, Luke gained his PhD in statistical genetics at the Wellcome Trust Sanger Institute and University of Cambridge. During this time he played a key role in the analysis of large published genetic datasets from the two most common forms of IBD: Crohn’s disease and ulcerative colitis. His work identified 71 new IBD variants, most of which associate with both forms of the disease and show some overlap with other immune-mediated disorders.

By providing insight into the specific pathways that confer genetic risk of chronic disease, Luke hopes that long-term his work will contribute to identification of new drug targets and stratified medicine approaches.

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