Neuronal ‘On’ and ‘Off’ signals control microglia

Biber, Knut; Neumann, Harald; Inoue, Kazuhide; Boddeke, Hendrikus W.G.M.

doi:10.1016/j.tins.2007.08.007

Cited by 787Neuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology ResearchPain Mechanisms and Treatments

Neuronal ‘On’ and ‘Off’ signals control microglia

Biber, Knut, Neumann, Harald, Inoue, Kazuhide, Boddeke, Hendrikus W.G.M.·2007·Trends in Neurosciences

DOI 10.1016/j.tins.2007.08.007

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Abstract

Recent findings indicate that neurons are not merely passive targets of microglia but rather control microglial activity. The variety of different signals that neurons use to control microglia can be divided into two categories: 'Off' signals constitutively keep microglia in their resting state and antagonize proinflammatory activity. 'On' signals are inducible and include purines, chemokines, glutamate. They instruct microglia activation under pathological conditions towards a beneficial or detrimental phenotype. Various neuronal signaling molecules thus actively control microglia function, thereby contribute to the inflammatory milieu of the central nervous system. Thus, neurons should be envisaged as key immune modulators in the brain.

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Microglia have the capacity to interact with synaptic elements in response to neurotransmitter release and/or sensory experience.
“Previous work has demonstrated that microglia have the capacity to interact with synaptic elements in response to neurotransmitter release and/or sensory experience (Biber et al., 2007; Fontainhas et al., 2011; Nimmerjahn et al., 2005; Ransohoff and Perry, 2009; Tremblay et al., 2010a; Wake et al., 2009).”
From Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner (2012) · cites this paper as Biber et al., 2007
Downregulation of CX3CR1 and CD200R may impair microglia return to homeostasis during AD.
“The ability of microglia to return to homeostasis during AD may be impaired by the downregulation of the microglial receptors CX3CR1 and CD200R, which bind to neuronal ligands and act as immune checkpoints that maintain microglia homeostasis [30]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [30]
Both soluble and surface CNS cues are factors in microglia maturation.
“Overall, these results implicate both soluble and surface CNS cues as factors in microglia maturation (Biber et al., 2007)(Figure 5E,F).”
From iPSC-derived human microglia-like cells to study neurological diseases (2017) · cites this paper as Biber et al., 2007
Microglia are strictly regulated by factors within the CNS microenvironment during homeostasis.
“Microglia are strictly regulated by factors within the CNS microenvironment during homeostasis (Biber et al, 2007).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Biber et al, 2007
Neuronal signals regulating microglial activation have been categorized as Off signals and On signals; Off signals are constitutively expressed signals (such as CX3CL1 and CD200) that maintain homeostatic functions of microglia, whereas On signals are inducible signals (such as ATP and TREM2 ligand) that trigger pro- and anti-inflammatory activation in microglia.
“Neuronal signals regulating microglial activation have been categorized as Off signals and On signals.The former refer to constitutively expressed signals (such as, CX3CL1 and CD200) that maintain the homeostatic functions of microglia, whereas the latter refer to inducible signals (such as, ATP and TREM2 ligand) that trigger pro-and anti-inflammatory activation in microglia (Biber et al, 2007).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Biber et al, 2007

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Authors: Biber, K., Neumann, H., Inoue, K., & Boddeke, H. W. G. M.
Affiliations: University Medical Center Groningen (NL)
University of Bonn (DE)
Kyushu University (JP)
Corresponding author: Biber, Knut
ORCID: Biber, Knut
Neumann, Harald
Inoue, Kazuhide
Boddeke, Hendrikus W.G.M.
Venue: Trends in Neurosciences
Publisher: Elsevier BV
Published: 2007-11
Volume: 30
Issue: 11
Pages: 596-602
ISSN: 0166-2236 (ISSN-L)
DOI: 10.1016/j.tins.2007.08.007
OpenAlex: W2164191009
Cited by: 787
References: 73
Citations by year: 2026: 18 · 2025: 18 · 2024: 40 · 2023: 40 · 2022: 48 · 2021: 82 · 2020: 47 · 2019: 53 · 2018: 46 · 2017: 37 · 2016: 40 · 2015: 39 · 2014: 59 · 2013: 50 · 2012: 40
FWCI: 2.42
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Trends in Neurosciences (publishedVersion)
PubMed (publishedVersion)
University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
Keywords: microglia, microglial activation, resting microglia, pro-inflammatory signaling, purines, chemokines, glutamate, neuroinflammation, central nervous system
MeSH terms: Animals, Cell Communication, Models, Neurological, Neurons, Signal Transduction, Microglia, Chemokines

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