Inducing neuronal mitochondrial activity during central nervous system inflammation counteracts inflammation-induced neuronal electron transport chain deficiency and calcium toxicity, thereby protecting against neuronal loss in a multiple sclerosis mouse model.

Oligodendroglia express major histocompatibility complex (MHC) pathways in response to inflammation and MHC reporter mice allow for the investigation of MHC molecule expressing cells in vivo.

Imaging mass cytometry simultaneously lights up distinct immune cells in the brain.

Imprecision in decoding information and swap error, that is, mistakenly reporting a non-target feature, contributes to working memory deficit in the multiple sclerosis population.

Spontaneous remyelination is a common phenomenon in the marmoset experimental autoimmune encephalomyelitis model, reliably detected using in vivo magnetic resonance imaging, rendering this an indispensable model to further investigate the pathobiology of remyelination in multiple sclerosis.

Together, our multi-tissue single-cell data shows that CD56^bright NK cells accumulate in the periventricular brain regions of multiple sclerosis (MS) patients, bringing NK cells back to the spotlight of MS pathology.

Pain sensation induces relapse in a mouse model of multiple sclerosis via a sensory-sympathetic signaling pathway.

SARS-CoV-2 experienced ocrelizumab-treated MS patients benefit from SARS-CoV-2 mRNA vaccination by inducing broadprotective CD8+ T-cells, whereas methotrexate-treated RA patients induce delayed but strong antibody responses, which support vaccine strategies for these patient groups.

Regeneration of oligodendrocytes in the cerebral cortex results in reorganization of the pattern of myelination, potentially impacting information processing within cortical networks in diseases such as multiple sclerosis.

Antigen-specific control of CD4+ T cell trans-migration by brain endothelial cells via presentation of CNS-derived antigens in MHC-II molecules.