Fig. 2: Validation of immunization, analysis of main peripheral immune cell distribution, and assessment of BBB functionality in Cnp−/− (KO) and WT mice. | Molecular Psychiatry

Fig. 2: Validation of immunization, analysis of main peripheral immune cell distribution, and assessment of BBB functionality in Cnp−/− (KO) and WT mice.

From: NMDAR1 autoantibodies amplify behavioral phenotypes of genetic white matter inflammation: a mild encephalitis model with neuropsychiatric relevance

Fig. 2

A Experimental outline depicting time points of blood sampling, immunization, and tissue processing. B NR1-antigen ELISA, showing substantial NMDAR1-AB formation at the start of behavioral testing and NMDAR1-AB persistence throughout the experimental period (~3 months); data of 13–14 mice/group; mean ± SEM. C Immunocytochemical co-localization of NR1-immunized mouse plasma (1:100, green) with a commercial rabbit GluN1-AB (red) in a cell-based (HEK293T) clinical standard assay for NMDAR1-AB (Euroimmun); plasma (1:100) of OVA-immunized mice did not show specific staining for NMDAR1; GluN1/NR1, glutamate ionotropic receptor NMDA type subunit 1; OVA, ovalbumin. (D, E) Flow cytometric analysis of peripheral blood immune cells before (D) and 1 month after immunization (E). Note the physiological peripheral immune cell subsets in all groups, despite white matter inflammation in Cnp−/− mice; data of 13–14 mice/group mean ± SEM. F Experimental outline for the assessment of blood–brain barrier (BBB) function in 18-week-old male Cnp−/− and WT mice. G Extravasation of Evans blue and fluorescein into CNS tissue as well as increased brain water content in Cnp−/− mice; data of 4–5 mice/group; two-tailed unpaired Welch’s corrected t-test or Mann–Whitney U tests; mean ± SEM.

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