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August 27, 2013; 81 (9) Editorial

Premature immune senescence in children with MS

Too young to go steady

Amit Bar-Or, Paolo A. Muraro
First published August 2, 2013, DOI: https://doi.org/10.1212/WNL.0b013e3182a2dd3f
Amit Bar-Or
From the Neuroimmunology Unit (A.B.-O.), Montreal Neurological Institute, McGill University, Montreal, Canada; and the Division of Brain Sciences (P.A.M.), Department of Medicine, Imperial College London, UK.
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Paolo A. Muraro
From the Neuroimmunology Unit (A.B.-O.), Montreal Neurological Institute, McGill University, Montreal, Canada; and the Division of Brain Sciences (P.A.M.), Department of Medicine, Imperial College London, UK.
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Premature immune senescence in children with MS
Too young to go steady
Amit Bar-Or, Paolo A. Muraro
Neurology Aug 2013, 81 (9) 778-779; DOI: 10.1212/WNL.0b013e3182a2dd3f

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The common view in the field of multiple sclerosis (MS) is that immune-mediated attacks of the CNS reflect some imbalance between effector and regulatory limbs of the immune system. Studies in adults with established MS point to exaggerated responses of effector cells (including Th1 and Th17 CD4 T cells, CD8 T cells) as well as defective suppressive capacities of regulatory cells (including Treg and Breg cells). Traditionally, the focus has been on memory (or “antigen-experienced”) cells, given the premise that the offending immune cells have already been activated to recognize CNS targets. However, it remains unclear whether the abnormalities in effector or regulatory cells emerge after immune cells are activated, or reflect the consequences of a primary defect in development of naive immune cells that have not yet encountered their antigen.

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  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial.

  • See page 784

  • Supplemental data at www.neurology.org

  • © 2013 American Academy of Neurology
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