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Disease-modifying treatments modulate myeloid cells in multiple sclerosis patients

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Abstract

The role of myeloid cells in the pathogenesis of MS is determined by the polarization they acquire after activation, and mediated by release of extracellular vesicles (MVs). We assessed the effects of treatments for MS on activation and polarization of myeloid cells. MVs levels and markers of polarization of myeloid cells have been assessed at baseline and up to 6 months after the start of a MS treatment. Patients had higher levels of MVs than controls, and these increased significantly over 6 months under natalizumab. Interferon β-1a significantly decreased M1 pro-inflammatory marker IL1β and upregulated Trem2, a receptor important for debris clearance; both interferon β-1a and fingolimod decreased pro-inflammatory marker IL6. Current treatments for MS significantly modulate myeloid cells activity.

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Correspondence to Roberto Furlan.

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Conflict of interest

G. Dalla Costa, A. Finardi, L. Garzetti, T. Carandini and R. Furlan report no discosures. G. Comi has received compensation for consulting services and/or speaking activities from Bayer Schering Pharma AG, Serono Symposia International Foundation, Merck Serono International, Teva, Sanofi-Aventis and Biogen. V. Martinelli has received personal compensation for activities with Biogen, Merck Serono, Bayer Schering, TEVA and Sanofi Aventis as a speaker.

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Highlights:

• MS patients have higher extracellular myeloid vesicles than controls;

• Serum MVs increase under natalizumab and may be a biomarker for monitoring the efficacy of the drug;

• Interferon β-1a and fingolimod decrease IL6 levels, a marker of pro-inflammatory polarization of myeloid cells;

• Interferon β-1a upregulates Trem2 in myeloid cells, a receptor important for debris clearance and recovery from the attacks;

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Dalla Costa, G., Finardi, A., Garzetti, L. et al. Disease-modifying treatments modulate myeloid cells in multiple sclerosis patients. Neurol Sci 39, 373–376 (2018). https://doi.org/10.1007/s10072-017-3176-2

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  • DOI: https://doi.org/10.1007/s10072-017-3176-2

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