Microglia Activation During Neuroinflammation: Overview
Click on one of the stages of microglia activation to see the molecules involved in that process.
Get Print CopyMaintenance of
"Resting" Microglia
Maintenance of
"Resting" Microglia
Microglia
Steady-State
Markers
Microglia
Steady-State
Markers
Laminin alpha 3/Laminin-5
Laminin alpha 4
Laminin gamma 1
Laminin S
Laminin-1
Fibronectin
Collagen IV
Collagen IV alpha 1
Hyaluronan
Glypican 1
Glypican 2
Glypican 3
Glypican 5
Glypican 6
Syndecan-1/CD138
Syndecan-2/CD362
Syndecan-3
Syndecan-4
PTP beta/zeta/PTPRZ
Neurocan
Versican
Brevican
Aggrecan
Tenascin C
Tenascin R
Endorepellin/Perlecan
Agrin
(ECM)
(ECM)
Laminin alpha 3/Laminin-5
Laminin alpha 4
Laminin gamma 1
Laminin S
Laminin-1
Fibronectin
Collagen IV
Collagen IV alpha 1
Hyaluronan
Glypican 1
Glypican 2
Glypican 3
Glypican 5
Glypican 6
Syndecan-1/CD138
Syndecan-2/CD362
Syndecan-3
Syndecan-4
PTP beta/zeta/PTPRZ
Neurocan
Versican
Brevican
Aggrecan
Tenascin C
Tenascin R
Endorepellin/Perlecan
Agrin
Injury-Derived
DAMPs
Injury-Derived
DAMPs
DAMPs
DAMPs
Laminin alpha 3/Laminin-5
Laminin alpha 4
Laminin gamma 1
Laminin S
Laminin-1
Fibronectin
Collagen IV
Collagen IV alpha 1
Hyaluronan
Glypican 1
Glypican 2
Glypican 3
Glypican 5
Glypican 6
Syndecan-1/CD138
Syndecan-2/CD362
Syndecan-3
Syndecan-4
PTP beta/zeta/PTPRZ
Neurocan
Versican
Brevican
Aggrecan
Tenascin C
Tenascin R
Endorepellin/Perlecan
Agrin
Microglia
Activation
Microglia
Activation
Disease-Related
DAMPs
Disease-Related
DAMPs
Microglia
Polarization
Microglia
Polarization
IFN-gamma
GM-CSF
IL-1 beta/IL-1F2
IL-6
IFN-gamma
GM-CSF
IL-1 beta/IL-1F2
IL-6
IL-13
IL-13
Neuroinflammation, defined as inflammation of nervous tissue, is initiated in response to a variety of endogenous and exogenous sources including invading pathogens, neuronal injury, and toxic compounds. It is characterized by glial cell activation, the release of inflammatory molecules, increased blood-brain barrier permeability, and recruitment of peripheral immune cells into the brain. Neuroinflammation is initiated by microglia, which are the resident immune cells of the central nervous system. Under steady-state conditions, microglia are maintained in a “resting” state through interactions with cell surface and soluble factors from surrounding cells. Microglia become activated following exposure to pathogen-associated molecular patterns (PAMPs) and/or endogenous damage-associated molecular patterns (DAMPs), and removal of the immune-suppressive signals. Activated microglia can acquire different phenotypes depending on cues in its surrounding environment. M1 microglia are initially present following an insult as they promote a proinflammatory response. Over time, the response is shifted to be anti-inflammatory, which is mediated by M2 microglia. In truth, current research has suggested that microglia activation is more complex than originally believed. It has been suggested that there is a range of microglia activation states that span from the M1 to M2 phenotypes, with each phenotype displaying different markers, secreting different compounds, and exhibiting different functions.
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