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. Author manuscript; available in PMC: 2020 May 1.
Published in final edited form as: Cell Immunol. 2018 Oct 21;339:10–23. doi: 10.1016/j.cellimm.2018.10.006

Figure 1. B cells mediate MS pathology through antibody-dependent and antibody-independent mechanisms.

Figure 1.

(a) Myelin-reactive antibodies secreted by autoreactive plasmablasts and plasma cells mediate destruction of the myelin sheath by binding C1q and activating the classical complement pathway or initiating FcγRIIIa-mediated antibody-dependent cell-mediated cytotoxicity by NK cells. b) B cells expressing a myelin-reactive BCR are capable of processing myelin protein and presenting myelin peptide to autoreactive CD4+ T cells, resulting in their activation and proliferation. (c, d) B cells are able to foster an environment conducive to autoimmunity by (c) secreting higher amounts of pro-inflammatory cytokines such as IL-6 and GM-CSF compared with regulatory cytokines such as IL-10 and TGF-b and (d) by secreting cytokines/chemokines including CXCL13 and BAFF which promote the differentiation of FDCs and establishment of TLOs, which facilitate the activation and expansion of autoreactive B and T cells. N= Neuron, PB= Plasmablast, PC= Plasma cell, FDC= Follicular dendritic cell, TLO= Tertiary lymphoid organ.