The approval of immune-active medications for relapsing-remitting multiple sclerosis (RRMS) is often cited as a major advance in our understanding of this disorder. This is only partly true. We have learned that sequestering inflammatory cells out of the brain and spinal cord or depleting leukocytes in the periphery reduces the number of disease relapses and lesions on neuroimaging. Recently, we have also learned that, in addition to T lymphocytes, CD20+ B cells play a significant pathogenic role in MS. While these are meaningful achievements, many questions remain unanswered: Is it the initial inflammatory event that leads to central nervous system tissue damage or an intrinsic central nervous system tissue problem that leads to a secondary immune response directed against central nervous system myelin? If both scenarios exist, what are the biomarkers that can distinguish them and predict responses to therapeutic interventions? Can immunotherapy truly slow disease progression? Can we design immunosuppression that minimally affects adaptive immune responses required for host defense? There are 2 strategies that have been underused in identifying biomarkers that define MS that may hold the key to better therapeutic strategies.
Stüve O, Racke MK. Will Biomarkers Determine What Is Next in Multiple Sclerosis?Biomarkers in Multiple Sclerosis. JAMA Neurol. 2016;73(5):496-497. doi:10.1001/jamaneurol.2015.4841