Microglial nodules provide the environment for pathogenic T cells in human encephalitis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-04

AUTHORS

Anna R. Tröscher, Isabella Wimmer, Lucía Quemada-Garrido, Ulrike Köck, Denise Gessl, Sanne G. S. Verberk, Bethany Martin, Hans Lassmann, Christian G. Bien, Jan Bauer

ABSTRACT

Microglia nodule formation is a common feature in inflammatory brain diseases mediated by T lymphocytes such as viral and paraneoplastic encephalitis, multiple sclerosis, and Rasmussen encephalitis (RE). However, its role has not been fully understood yet. We hypothesized that, in RE, microglial nodules provide an environment for the initiation of the later dominating T-cell cytotoxicity. In RE stage 0, small primary microglia nodules could be identified in the absence of T cells. These primary nodules showed inflammasome activation and endosomal Toll-like receptor upregulation. In stage 1, T cells migrate into the parenchyma and intermingle with microglial cells, thereby forming secondary nodules in which neurons are destroyed. Whole-genome transcriptome analysis at this point showed upregulation of several inflammatory pathways including interferon signaling and major histocompatibility complex-I signaling. Inflammatory profiles, like the ones observed in RE, could be induced upon TLR3 stimulation in neonatal microglial cell cultures. Taken together, our results point towards activation of endosomal TLRs, resulting in increased interferon signaling, inflammasome activation, and chemokine upregulation as early steps in RE pathogenesis. This activity sets the scene for subsequent infiltration of T cells and destruction of neurons. Similar to RE, this microglial microenvironment might be a crucial step in other T-cell-mediated inflammatory brain diseases. More... »

PAGES

619-635

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00401-019-01958-5

DOI

http://dx.doi.org/10.1007/s00401-019-01958-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1111574754

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30663001


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