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. 2018 Apr 4;8:5633. doi: 10.1038/s41598-018-24032-8

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Representation of molecular mimicry and bystander activation mechanisms. Molecular mimicry (a) is defined where pathogen and self-antigens are believed to share epitopes, and antigen-cross reaction can occur through T cell receptors (TCR). Bystander activation (b) can also reach CNS autoimmunity. In this process, pathogen or endogenous ligands can activate APCs through Toll-like receptors (TLRs), stimulating APCs production of pro-inflammatory cytokines (i.e. IL1, IL6, IL12), over- differentiation and activation of autoreactive T-cells.