Multiple inducers and novel roles of autoantibodies against the obligatory NMDAR subunit NR1: a translational study from chronic life stress to brain injury.


Journal

Molecular psychiatry
ISSN: 1476-5578
Titre abrégé: Mol Psychiatry
Pays: England
ID NLM: 9607835

Informations de publication

Date de publication:
06 2021
Historique:
received: 05 11 2019
accepted: 23 01 2020
revised: 13 01 2020
pubmed: 25 2 2020
medline: 12 10 2021
entrez: 25 2 2020
Statut: ppublish

Résumé

Circulating autoantibodies (AB) of different immunoglobulin classes (IgM, IgA, and IgG), directed against the obligatory N-methyl-D-aspartate-receptor subunit NR1 (NMDAR1-AB), belong to the mammalian autoimmune repertoire, and appear with age-dependently high seroprevalence across health and disease. Upon access to the brain, they can exert NMDAR-antagonistic/ketamine-like actions. Still unanswered key questions, addressed here, are conditions of NMDAR1-AB formation/boosting, intraindividual persistence/course in serum over time, and (patho)physiological significance of NMDAR1-AB in modulating neuropsychiatric phenotypes. We demonstrate in a translational fashion from mouse to human that (1) serum NMDAR1-AB fluctuate upon long-term observation, independent of blood-brain barrier (BBB) perturbation; (2) a standardized small brain lesion in juvenile mice leads to increased NMDAR1-AB seroprevalence (IgM + IgG), together with enhanced Ig-class diversity; (3) CTLA4 (immune-checkpoint) genotypes, previously found associated with autoimmune disease, predispose to serum NMDAR1-AB in humans; (4) finally, pursuing our prior findings of an early increase in NMDAR1-AB seroprevalence in human migrants, which implicated chronic life stress as inducer, we independently replicate these results with prospectively recruited refugee minors. Most importantly, we here provide the first experimental evidence in mice of chronic life stress promoting serum NMDAR1-AB (IgA). Strikingly, stress-induced depressive-like behavior in mice and depression/anxiety in humans are reduced in NMDAR1-AB carriers with compromised BBB where NMDAR1-AB can readily reach the brain. To conclude, NMDAR1-AB may have a role as endogenous NMDAR antagonists, formed or boosted under various circumstances, ranging from genetic predisposition to, e.g., tumors, infection, brain injury, and stress, altogether increasing over lifetime, and exerting a spectrum of possible effects, also including beneficial functions.

Identifiants

pubmed: 32089545
doi: 10.1038/s41380-020-0672-1
pii: 10.1038/s41380-020-0672-1
pmc: PMC8440197
doi:

Substances chimiques

Autoantibodies 0
Receptors, N-Methyl-D-Aspartate 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2471-2482

Informations de copyright

© 2020. The Author(s).

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Auteurs

Hong Pan (H)

Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Agnes A Steixner-Kumar (AA)

Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Anna Seelbach (A)

Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Nadine Deutsch (N)

Department of Neurology, Hannover Medical School, Hannover, Germany.

Anja Ronnenberg (A)

Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Daniel Tapken (D)

Department of Biochemistry I-Receptor Biochemistry, Ruhr University, Bochum, Germany.

Nico von Ahsen (N)

Institute of Clinical Chemistry, University Medical Center Göttingen, Göttingen, Germany.

Marina Mitjans (M)

Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Hans Worthmann (H)

Department of Neurology, Hannover Medical School, Hannover, Germany.

Ralf Trippe (R)

Department of Biochemistry I-Receptor Biochemistry, Ruhr University, Bochum, Germany.

Christina Klein-Schmidt (C)

Department of Biochemistry I-Receptor Biochemistry, Ruhr University, Bochum, Germany.

Nadine Schopf (N)

Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Kristin Rentzsch (K)

Institute for Experimental Immunology, Euroimmun, Lübeck, Germany.

Martin Begemann (M)

Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Department of Psychiatry & Psychotherapy, University Medical Center Göttingen, Göttingen, Germany.

Jürgen Wienands (J)

Institute for Cellular and Molecular Immunology, Georg August University, Göttingen, Germany.

Winfried Stöcker (W)

Institute for Experimental Immunology, Euroimmun, Lübeck, Germany.

Karin Weissenborn (K)

Department of Neurology, Hannover Medical School, Hannover, Germany.

Michael Hollmann (M)

Department of Biochemistry I-Receptor Biochemistry, Ruhr University, Bochum, Germany.

Klaus-Armin Nave (KA)

Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Fred Lühder (F)

Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, Göttingen, Germany.

Hannelore Ehrenreich (H)

Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany. ehrenreich@em.mpg.de.

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