Neurology Central

IL4I1 decreases inflammation and promotes CNS repair in models of multiple sclerosis

Evaluation of: Psachoulia K, Chamberlain KA, Heo D et al. IL4I1 augments CNS remyelination and axonal protection by modulating T-cell driven inflammation. Brain 139(Pt 12), 3121–3136 (2016).
Multiple sclerosis (MS) is a highly complex disease involving inflammation, demyelination and spontaneous demyelination–remyelination episodes which ultimately fail during the course of the disease. The prognosis for patients is often bleak. Molecular evidence has demonstrated that activated inflammatory mediators are important for the differentiation of oligodendrocyte progenitors into functional myelin. In the paper published in Brain under discussion, the researchers categorized the role of alternatively activated macrophages (AAM) versus classically activated macrophages (CAM) as being beneficial for the promotion of remyelination. There is distinct temporal activation of macrophages within lesions of the CNS. During CNS remyelination and tissue repair processes, inflammatory processes are tightly regulated. IL4I1 is highly expressed during CNS remyelination. IL4I1 is expressed by immune cells, is stimulated by IL-4 and has immunomodulatory functions in various tumors and bacterial infections. The authors set out to determine whether IL4I1 affects remyelination or protects axonal damage in a mouse model of MS. 
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