Leah C. Dorman

TL;DR: It is found that IL-33 signals primarily to microglia under physiologic conditions, that it promotes microglial synapse engulfment, and that it can drive microglian-dependent synapse depletion in vivo, which reveals a cytokine-mediated mechanism required to maintain synapse homeostasis during CNS development.

TL;DR: It is found that neuronal IL-33 instructs microglial engulfment of the extracellular matrix (ECM) and that its loss leads to impaired ECM engulfment and a concomitant accumulation of ECM proteins in contact with synapses, which define a cellular mechanism through which microglia regulate experience-dependent synapse remodeling and promote memory consolidation.

TL;DR: In this paper, the authors identify a molecularly distinct microglial subset in the synapse rich regions of the zebrafish brain and find that ramified microglia increased in synaptic regions of midbrain and hindbrain between 7 and 28 days post fertilization.

TL;DR: The microglial transcriptome at single cell resolution is characterized, highlighting their diversity during development, aging, and pathology.

TL;DR: Using epigenomics, transcriptomics, and functional studies, the authors define mechanisms through which interleukin-33 (IL-33) promotes microglial synapse engulfment during brain development and restricts seizure susceptibility, in part via the induction of pattern recognition receptors including the scavenger receptor MARCO.