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. 2023 Aug 9;10:5. doi: 10.1186/s40348-023-00161-7

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Proposed pathomechanisms of CNS vasculitis in NP-jSLE. Several, likely connected pathways may be involved in the pathogenesis of vasculitis in NP-jSLE. Circulating autoantibodies can recruit to vascular epithelia and/or form immune complexes that contribute to complement activation. Both, antibody binding and the presence of activated complement contribute to endothelial activation that, in turn, mediates the upregulation of adhesion molecules (including intercellular adhesion molecule 1/ICAM1 and vascular cell adhesion molecule 1/VCAM1) and the expression of pro-inflammatory cytokines, including IL-6 and IL-8. As a result, B and T lymphocytes are attracted, adhere to ICAM1/VCAM1 and infiltrate the perivascular region where they produce inflammatory cytokines and B cell survival factors (BAFF/BLys) [49]