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. 2015 Mar 4;13:43. doi: 10.1186/s12916-015-0269-8

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© Kivity et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Proposed pathogenesis of neuropsychiatric lupus. Auto-antibodies enter the brain causing neuronal damage, including impaired neuroplasticity and synaptic transition. In order to reach the brain, the blood–brain barrier must be transiently breached by external (for example, infection) or internal (for example, metabolic derangement, cytokines) triggers. Vascular injury can be antibody mediated by aPL antibodies or via accelerated classical atherosclerosis. aPL, Anti-phospholipid antibodies; BBB, Blood brain barrier; RiboP, Ribosomal-P; NMDAR, NMDA receptor. The authors are responsible for designing the figure above.