A new study highlights the significant potential of drugs targeting a specific immune molecule implicated in multiple sclerosis. The findings could lead to more effective treatments for people living with MS.

Studies in a mouse model of MS, called experimental autoimmune encephalomyelitis, have shown that immune 'T cells', which secrete an immune molecule called 'IL-17', cause damage to the myelin sheath that surrounds nerves in the central nervous system. Early clinical trials with antibody-based drugs that block IL-17 are showing promise in the treatment of relapsing-remitting MS.

The research group at Trinity College in Dublin, Ireland, outlines an entirely new role for IL-17 in EAE and, potentially, in MS. The researchers found that IL-17 plays a critical 'priming' role in kick-starting the disease-causing immune response that mediates the damage in EAE and MS. The new research shows that, instead of playing a direct part in CNS pathology, a key role of IL-17 is to mobilise and activate an army of disease-causing immune cells in the lymph nodes that then migrate to the CNS to cause the nerve damage.

Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. However, the researchers said the findings suggest drugs that block IL-17 may not need to get across the blood-brain-barrier to be effective in treating MS. 

The study was published in the journal Immunity.