Profiling of microglia nodules in multiple sclerosis reveals propensity for lesion formation

Aletta M. R. Bosch (), Marlijn Poel, Nina L. Fransen, Maria C. J. Vincenten, Anneleen M. Bobeldijk, Aldo Jongejan, Hendrik J. Engelenburg, Perry D. Moerland, Joost Smolders, Inge Huitinga () and Jörg Hamann ()
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Aletta M. R. Bosch: Netherlands Institute for Neuroscience
Marlijn Poel: Netherlands Institute for Neuroscience
Nina L. Fransen: Netherlands Institute for Neuroscience
Maria C. J. Vincenten: Netherlands Institute for Neuroscience
Anneleen M. Bobeldijk: Netherlands Institute for Neuroscience
Aldo Jongejan: Amsterdam University Medical Center
Hendrik J. Engelenburg: Netherlands Institute for Neuroscience
Perry D. Moerland: Amsterdam University Medical Center
Joost Smolders: Netherlands Institute for Neuroscience
Inge Huitinga: Netherlands Institute for Neuroscience
Jörg Hamann: Netherlands Institute for Neuroscience

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Microglia nodules (HLA-DR+ cell clusters) are associated with brain pathology. In this post-mortem study, we investigated whether they represent the first stage of multiple sclerosis (MS) lesion formation. We show that microglia nodules are associated with more severe MS pathology. Compared to microglia nodules in stroke, those in MS show enhanced expression of genes previously found upregulated in MS lesions. Furthermore, genes associated with lipid metabolism, presence of T and B cells, production of immunoglobulins and cytokines, activation of the complement cascade, and metabolic stress are upregulated in microglia nodules in MS. Compared to stroke, they more frequently phagocytose oxidized phospholipids and possess a more tubular mitochondrial network. Strikingly, in MS, some microglia nodules encapsulate partially demyelinated axons. Taken together, we propose that activation of microglia nodules in MS by cytokines and immunoglobulins, together with phagocytosis of oxidized phospholipids, may lead to a microglia phenotype prone to MS lesion formation.

Date: 2024
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DOI: 10.1038/s41467-024-46068-3

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