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. 2018 Sep 14;33(9):1376–1389. doi: 10.1002/mds.27446

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© 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Model of B cell activation in neuronal surface autoantibody‐associated movement disorders. Triggers of immunological activation in CNS autoimmunity may lead to exposure of antigen (red star) and its presentation in the germinal centres of the cervical lymph nodes. Interaction between naïve B cells and CD4⁺ T helper cells in germinal centres causes maturation of B cells into antigen‐specific cells that can switch their immunoglobulin chain to express IgG. These cells can subsequently differentiate into antibody‐secreting plasmablasts and become tissue‐resident plasma cells. Circulating memory B cells and plasmablasts can reach the CNS through the internal carotid artery, re‐encounter the antigen, and produce antibodies (intrathecal synthesis). Modified with permissions from Wilson et al.83 IgG (immunoglobulin G), IL‐2 (interleukin 2), IL‐21 (interleukin 21), IgD (Immunoglobulin D), TNF alpha. CD = cluster of differentiation.