Analyzing several studies, researchers found that the risk linked with HLA-DRB1 variants is due to a specific DNA modification called methylation. Methylation is a process by which methyl groups are added to the DNA molecule; it can change the activity of DNA, but not its sequence.
DNA methylation in some HLA-DRB1 variants may predispose or protect against the disease.
The discovery may help develop new therapeutic approaches to treat multiple sclerosis by tackling this molecular mechanism.
The findings were published in the study “DNA methylation as a mediator of HLA-DRB1*15:01 and a protective variant in multiple sclerosis” in the journal Nature Communications.
Variations in genes belonging to the human leukocyte antigen (HLA) complex have been known for more than 40 years to influence people’s susceptibility for multiple sclerosis. A variation in one such gene — HLA-DRB1*15:01 — is the strongest genetic risk factor known for the disease.
Together with other HLA genes, HLA-DRB1 codes information essential for the immune system to be able to distinguish the body’s own molecules from foreign molecules produced, for instance, by viruses and bacteria.
Although the function of HLA-DRB1 is known, researchers did not understand until now why genetic variations of the gene would increase the chances of a person developing multiple sclerosis.
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