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. 2021 Feb 25;60(12):5620–5629. doi: 10.1093/rheumatology/keab160

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© The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 1 — Lupus psychosis sample showing GABA_BR positivity on fixed cell-based assay

Immunostaining of commercial cell-based assay (a–f) showing HEK cells expressing: (a) GABA_BR (R1/R2), (b) DPPX, (c) LGI1, (d) AMPAR1/2, (e) CASPR2, (f) NMDAR. Sera were diluted 1:10 and antibody binding visualised with goat anti-human IgG. Note the surface binding of the GABA_BR (a) and the nuclear staining of the NMDAR cells, which are strongly permeabilised (f), and seen in all ANA-positive SLE patients (g, h). Higher magnifications of GABA_BR and NMDAR expressing cells, taken from a, f. AMPA: alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; CASPR2: contactin associated protein 2; DPPX: dipeptidyl aminopeptidase-like protein 6; GABA: gamma-Aminobutyric acid; HEK: human epithelial kidney; LGI1: leucine-rich glioma inactivated 1; NMDA: N-methyl-D-aspartate; SLE: systemic lupus erythematosus.