| Literature DB >> 30850344 |
Emily G O'Koren1, Chen Yu1, Mikael Klingeborn1, Alicia Y W Wong2, Cameron L Prigge3, Rose Mathew1, Joan Kalnitsky1, Rasha A Msallam2, Aymeric Silvin2, Jeremy N Kay4, Catherine Bowes Rickman5, Vadim Y Arshavsky6, Florent Ginhoux2, Miriam Merad7, Daniel R Saban8.
Abstract
Microglia from different nervous system regions are molecularly and anatomically distinct, but whether they also have different functions is unknown. We combined lineage tracing, single-cell transcriptomics, and electrophysiology of the mouse retina and showed that adult retinal microglia shared a common developmental lineage and were long-lived but resided in two distinct niches. Microglia in these niches differed in their interleukin-34 dependency and functional contribution to visual-information processing. During certain retinal-degeneration models, microglia from both pools relocated to the subretinal space, an inducible disease-associated niche that was poorly accessible to monocyte-derived cells. This microglial transition involved transcriptional reprogramming of microglia, characterized by reduced expression of homeostatic checkpoint genes and upregulation of injury-responsive genes. This transition was associated with protection of the retinal pigmented epithelium from damage caused by disease. Together, our data demonstrate that microglial function varies by retinal niche, thereby shedding light on the significance of microglia heterogeneity.Entities:
Keywords: IL-34; macrophages; microglia; microglial heterogeneity; phagocytes; retinal degeneration; retinitis pigmentosa
Mesh:
Year: 2019 PMID: 30850344 PMCID: PMC6592635 DOI: 10.1016/j.immuni.2019.02.007
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 43.474