New gene targets for immune drugs

British scientists have found dozens of genes linked to autoimmune disorders, it has been announced.

The action of these cells is altered by genetic variants in people with disorders such as inflammatory bowel disease, asthma and arthritis.

Scientists at the Wellcome Sanger Institute, Cambridge, UK, report identifying 91 genes that play an important role in developing and sustaining such diseases.

Dr Dafni Glinos and colleagues explain in *Cell Genomics* that regulatory T cells (Tregs) are a relatively rare immune cell type, previously linked to immune diseases.

The cells are difficult to culture in a lab, but the new research found a way to isolate Tregs from 124 healthy people, to examine how genetic variants regulate their expression.

Findings were compared with gene variants from patients, highlighting the 91 genes, of which 31 were specifically impaired in Tregs but not other immune cells.

Dr Glinos said: "Regulatory T cells (Tregs) act as a break on the immune system to help it fight infection without escalating uncontrollably and harming the tissues of the body.

"If Tregs are not working as they should or are low in number, tissues can become too inflamed and result in immune disorders such as inflammatory bowel disease and arthritis.

"This study is an important step towards understanding how genetic variants influence the function of Tregs and what role this can play in disease.”

In further tests, the researchers found seven genes they describe as known drug targets – for which current medicines could be repurposed – and 63 gene targets that are suitable for novel drug development.

Commenting on the findings, Dr Ian Dunham of the European Bioinformatics Institute said: “We were able to narrow down the genes involved in immune disease from thousands to less than a hundred. This makes the task of identifying viable drug targets far easier.”

Bossini-Castillo, L. et al. Immune disease variants modulate gene expression in regulatory CD4+ T cells. *Cell Genetics* 6 April 2022 doi: 10.1016/j.xgen.2022.100117


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