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. 2022 Jun 13;144(2):381–383. doi: 10.1007/s00401-022-02448-x

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© The Author(s) 2022

Open AccessThis 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. 1 — a Activated complement proteins in CSF and sera of NSAbs⁺ (n = 19) and GAD65-Ab⁺ (n = 19) encephalitis patients compared to RMS patients (n = 25) and HD (n = 25). Right panels depict levels in individual clinical entities of NSAbs-AE. *p ≤ 0.05, **p ≤ 0.001. b Microarray analysis of control (n = 7, CON) and GAD-Ab⁺ limbic encephalitis (n = 5, GAD) hippocampal tissue shows that mRNA expression for complement factors C3, C4A and C4B are strongly upregulated in GAD-Ab⁺ encephalitis. Shown are means of z-scores. (c1) Staining for T cells (CD3), Microglia (Iba-1) and neurons (NeuN) shows infiltration of T cells in the hippocampal parenchyma of a GAD-AE patient. DAPI is used as a nuclear counterstain. (c2) Immunohistochemistry for C3d shows hippocampal neurons. (c3) C3d reactivity also is seen in axonal spheroids in white matter tracts. (c4) Confocal fluorescence staining here shows NeuN⁺ neurons of the DG. The yellow arrowhead points toward a neuron with a condensed nucleus as enlarged in the inset. C3d staining is a representative image of one of the five patients that showed C3d reactivity