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Multiple sclerosis (MS) is a chronic immune mediated disorder of the CNS spanning decades, that figures as a leading cause of permanent disability in young adults.1 Converging evidence suggests that its immunopathology is heterogeneous. While its aetiology remains enigmatic, immunomodulating drugs, the beta-interferons and glatiramer acetate, introduced in the 1990s, changed the therapeutic approach and outlook of this crippling disease. All of the first generation disease modifying drugs, in their pivotal trials, produced an approximately one-third reduction in relapse rate. Some also showed a moderate impact on impairment or disability.2
Given the partial efficacy of beta-interferons in the treatment of relapsing–remitting multiple sclerosis (RRMS),2 investigators have intensively searched for treatment response markers. The recent availability of more efficacious therapy (ie, natalizumab, a monoclonal antibody directed against VLA-4 integrin3 which impairs immune cell invasion into the CNS) and accumulating evidence, albeit partly controversial, that humoral immune responses to the injectable interferons (neutralising antibodies (NAb)) diminish or abrogate their therapeutic effects,4–6 enforce timely treatment changes in patients who demonstrate an unfavourable response to interferon β (IFNβ).
The paper by Durelli …