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ATG5 in microglia does not contribute vitally to autoimmune neuroinflammation in mice


Srimat Kandadai, Keertana; Kotur, Monika B; Dokalis, Nikolaos; Amrein, Irmgard; Keller, Christian W; Münz, Christian; Wolfer, David; Prinz, Marco; Lünemann, Jan D (2021). ATG5 in microglia does not contribute vitally to autoimmune neuroinflammation in mice. Autophagy, 17(11):3566-3576.

Abstract

Microglia, resident myeloid immune cells of the central nervous system (CNS), actively shape the circuitry of the brain, maintain CNS homeostasis during the steady state and orchestrate immune responses upon CNS injury. Both canonical and non-canonical functions of the macroautophagy/autophagy-related protein ATG5 regulate myeloid cell survival and immune responses. Here, we report that loss of ATG5 in postnatal microglia does not perturb CNS tissue integrity, microglial cell survival, or immune activation. Learning task performances were unchanged in mutant mice. Furthermore, lack of ATG5 expression in microglia had no impact on the development of experimental autoimmune encephalomyelitis. These data indicate that, basal autophagy, identified to be essential for the survival and function of neuronal cells, is not required to maintain CNS homeostasis if absent in adult microglia and ATG5 expression is dispensable for the development of autoimmune neuroinflammation.

Abstract

Microglia, resident myeloid immune cells of the central nervous system (CNS), actively shape the circuitry of the brain, maintain CNS homeostasis during the steady state and orchestrate immune responses upon CNS injury. Both canonical and non-canonical functions of the macroautophagy/autophagy-related protein ATG5 regulate myeloid cell survival and immune responses. Here, we report that loss of ATG5 in postnatal microglia does not perturb CNS tissue integrity, microglial cell survival, or immune activation. Learning task performances were unchanged in mutant mice. Furthermore, lack of ATG5 expression in microglia had no impact on the development of experimental autoimmune encephalomyelitis. These data indicate that, basal autophagy, identified to be essential for the survival and function of neuronal cells, is not required to maintain CNS homeostasis if absent in adult microglia and ATG5 expression is dispensable for the development of autoimmune neuroinflammation.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Anatomy
04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Life Sciences > Molecular Biology
Life Sciences > Cell Biology
Uncontrolled Keywords:Cell Biology, Molecular Biology
Language:English
Date:2 November 2021
Deposited On:04 Feb 2021 13:55
Last Modified:01 Mar 2022 19:34
Publisher:Taylor & Francis
ISSN:1554-8627
OA Status:Green
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1080/15548627.2021.1883880
PubMed ID:33522362
Project Information:
  • : FunderSNSF
  • : Grant ID310030B_182827
  • : Project TitleExcellence Grant - Role of autophagy proteins in endocytosis and exocytosis
  • : FunderSNSF
  • : Grant IDCRSII5_180323
  • : Project TitleNovel virucidal drugs: From basic to in vivo studies

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