Teams at the Karolinska Institute and The University of Tokyo have separately disclosed new targets for multiple sclerosis. Intervention in their pathways could yield new MS therapeutics if the pathways can be targeted more specifically than the standard therapies of steroids and interferon-b.
MS is an autoimmune disease that causes neurological inflammation and demyelination. Recent studies have shown that dysfunctional T helper type 1 (TH1) and TH17 cells cause autoreactivity, which can prompt the immune system to attack the myelin sheath around neurons.1 Thus, many groups are focused on identifying the pathways that lead to the aberrant T cell activation.
In a paper published in Science Translational Medicine, a Karolinska team reported that increased levels of Vav 1 guanine nucleotide exchange factor (VAV1), a protein involved in T and B cell activation, are associated with MS.2
Meanwhile, The University of Tokyo researchers identified