Researchers find a protein called lymphotoxin-alpha may play role in Multiple Sclerosis (MS). Image Researchers at the University of Edinburgh, working as part of a large multi-national collaborative consortium, have found genetic factors which influence the levels of inflammatory proteins in the blood of cohort volunteers. They have linked these results from the populations studied, which include Viking Genes (ORCADES), to the risk of developing autoimmune diseases. The project looked at plasma samples from over 15,000 people and found 180 sites in the genome that affect the levels of 91 proteins in the blood. They then combined this information with genetic studies of autoimmune diseases, to reveal proteins that play a causal role in the development of these diseases. Studies of proteins are particularly informative because proteins are the molecules that carry out most biological processes. Furthermore, proteins are the targets of most current drugs.The researchers found that a protein called lymphotoxin-alpha may play a role in Multiple Sclerosis (MS). This could become a new target for drugs in the future, as the development of therapies targeting specific inflammatory proteins has transformed the clinical management of other immune-mediated diseases. The team also found that some proteins have opposite effects on different autoimmune diseases. For example, the protein CD40 increases risk of rheumatoid arthritis, but appears protective against MS and inflammatory bowel disease. Dr James Peters, from Imperial College London, said:This vast dataset builds our understanding of the predisposing molecular factors that lead to the development of various autoimmune diseases. Although it can take years from identifying a drug target to a drug actually entering clinical practice, we hope that this data will ultimately provide the basis for new treatments. The research is published in Nature Immunology.Genetics of circulating inflammatory proteins identifies drivers of immune-mediated disease risk and therapeutic targets This article was published on 2024-01-25