A study led by researchers at the Babraham Institute, in collaboration with scientists at the Wellcome Sanger Institute, has uncovered how variations in a non-protein-coding “dark matter” region of the genome could make patients susceptible to complex autoimmune and allergic diseases such as inflammatory bowel disease. The study in mice and human cells reveals a key genetic switch that helps immune responses remain in check. Published on May 13, 2020 in Nature, the research, involving collaborations with research institutions in the UK and worldwide, identifies a new potential therapeutic target for the treatment of inflammatory diseases. The Nature article is titled “A Distal Enhancer At Risk Locus 11q13.5 Promotes Suppression of Colitis By Treg Cells.” Over the last twenty years, the genetic basis of susceptibility to complex autoimmune and allergic diseases, such as Crohn's disease, ulcerative colitis, type 1 diabetes, and asthma, has been narrowed down to a particular region of chromosome 11. This work has involved large-scale genome-wide association studies (GWAS), a genome-wide “spot-the-difference” comparison between the genomes of individuals with or without a disease, to highlight regions of variation in the DNA code. This can identify potential genetic causes, and reveal possible drug targets. However, most of the genetic variations responsible for the susceptibility to complex immune and allergic diseases are concentrated within regions of the genome that don't encode proteins - the genome's so-called “dark matter.” This means there is not always a clear gene target for further investigation and the development of treatments.
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