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. 2019 Feb 18;21:62. doi: 10.1186/s13075-019-1836-8

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© The Author(s). 2019

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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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Fig. 1 — Analysis workflow. A list of protein targets was generated based on literature search, previous knowledge, genes known to be upregulated in SLE (microarray data) and on data from global LC-MS-based proteomics analysis on a selection of samples (n = 27). This list was searched through the Human Protein Atlas for available high-quality antibodies towards these proteins. Finally, a selection of antibodies towards 281 proteins was used for affinity proteomic analysis and screening of the Karolinska SLE cohort. The Karolinska SLE cohort comprised 378 SLE patients and 316 age- and gender-matched population-based controls. According to our autoantibody-based definition, the cohort consists of 66 aPL+ SLE and 63 SSA/SSB+ SLE patients