NeuroImmunology

Highlights

 

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MS B cells secrete more IL-6 and less IL-10 than B cells from healthy donors.

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B cell depletion therapy, which ameliorates disease, diminishes IL-6 levels.

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GA therapy temporarily restores immune regulation, as detected by IL-6 levels.

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IL-10 secreted by T regulatory cells and monocytes contribute to immune regulation.

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Agents that enhance IL-10 and immunoregulation are of therapeutic benefit in MS.

Via Krishan Maggon

Dysregulation of the complement system is evident in many CNS diseases but mechanisms regulating complement activation in the CNS remain unclear.

Via Krishan Maggon

Abstract

Multiple sclerosis (MS) is characterized by autoimmune inflammation affecting the central nervous system and subsequent neurodegeneration.

Historically, damage was thought to be mediated exclusively by auto-antigen-activated pro-inflammatory T cells. However, more recently, we are gaining increasing knowledge on the pathogenic role played in MS by B cells, dendritic cells and monocytes.

IFN-β therapy was one the first approved therapy for MS for its ability to reduce relapse rate and MRI lesion activity and to significantly decrease risk of disability progression.

IFN-β-mediated mechanisms of action, even if not completely understood, mainly rely on its multifaceted pleiotropic effects resulting in sustained anti-inflammatory properties directed toward almost every immune cell type.

Here, we will discuss in detail literature data characterizing the pathogenic activity of the different immune cell subsets involved in MS pathogenesis and how IFN-β therapy regulates their function by modulating bystander responses.

We believe that the effectiveness of this drug in MS treatment, even if in use for a long time, can unveil new insights on this disease and still teach a lesson to researchers in the MS field.

Via Krishan Maggon