A new study publicized in the latest issue of the journal Nature by a team of analysts has claimed that a genetic variant related to MS causes the anti-Tumour Necrosis Factor (TNF) drugs to fail to treat the same, which are otherwise a promising treatment strategy for many autoimmune diseases.
The group at the Oxford University had conducted a scrutiny in order to find out the reason why the drug treating diseases like inflammatory bowel disease and rheumatoid arthritis fails in case of MS (multiple sclerosis).
It was them found by the researchers that the drug, instead of benefitting a person with advanced MS, was worsening his symptoms.
A gene named TNFRSF1A, which was previously found responsible for triggering the risks of the growth of MS, was tested by the team. It was discovered that the protein in its long version sat on the cell surface.
Following the same, it tended to bind the TNF signalling molecule, which helps conduct many processes in the body. Later, the team found that the variant stopped these signals from triggering by producing a shorter and altered version interacting with TNF.
Thus, Professor Lars Fugger concluded, "Whilst the TNFRSF1A gene variant is linked to a modest risk of developing MS, the drug that mimics the effect of the variant has a considerably greater impact”.