Back to Pathways

Interactive Pathways & Processes

Show Categories

Microglia Activation During Neuroinflammation: Steady-State Microglia

Click on one of the other stages of microglia activation to see the molecules involved in that process. Click on Overview to see the generalized process of microglia activation during neuroinflammation.

Get Print Copy

Microglia Steady-State Markers

F4/80/
EMR1

Siglec-H

CD11b/
Integrin alpha M

Fc gamma RI/
CD64

M-CSF R/CD115

Mer

CX3CR1

FCRL4/FcRH4

TMEM119

BDNF
IGF-I

P2Y12/
P2RY12

Microglia

Maintenance of "Resting" Microglia

Neuron

BDNF
beta-NGF
NT-3

p75^NTR
TrkA
TrkB
TrkC

Siglec-2/CD22

CD45

CD200

CD200 R1

Dopamine
GABA
Noradrenaline
VIP

DRD1
DRD2
GABA B Receptor
Adrenergic beta-2 R
VIP R1
VIP R2

HSP60

TREM-2

DAP12

CX3CL1/
Fractalkine

CX3CR1

TGF-beta

TGF-beta RII

TGF-beta RI

CD47

SIRP alpha/
CD172a

IL-10

IL-10 R

sICAM-5

Integrin alpha L
beta 2

Microglia

Microglia, the immune cells of the nervous system, are typically in a quiescent, or immune-suppressed, state during normal conditions in the brain. During this time, they assume a ramified morphology, which is characterized by a very small cell body with elongated, ramified processes. These ramified microglia contribute to brain homeostasis by supporting myelin turnover, eliminating or remodeling synapses, monitoring neural firing, and actively scavenging the local environment for pathogens or tissue damage. Microglial are maintained in the ramified state through interactions with soluble and membrane-bound factors from neighboring cells. For example, Fractalkine and CD200, found on the cell surface of healthy neurons, interact with their respective receptors on microglia. These microglia receptors contain ITIM (immunoreceptor tyrosine-based inhibitory) motifs in their intracellular domain that, when phosphorylated, suppress downstream immune signaling. Additional ligand-receptor interactions that regulate microglia activation includes CD22, HSP60, and CD47 on neurons binding to CD45, TREM-2, and SIRP alpha, respectively, on microglia. Neurons also release neurotrophic factors, such as BDNF and beta-NGF, that contribute to the immune-suppressed state of microglia by inhibiting the expression of MHC class II and co-stimulatory molecules. In addition, various neurotransmitters and neuropeptides, such as GABA and dopamine, will bind to their respective receptors on microglia and suppress the production of proinflammatory cytokines. Activation of microglia is initiated, in part, following the loss of these inhibitory signals.

To learn more about our products for neuroinflammation, please visit our Neuroinflammation Research Area.

Get Print Copy of this Pathway

First Name *

Last Name *

Email Address *

Institution *

Job Title

Department

Address 1 *

Address 2

City *

State

Postal Code *

Country

Pathway

May we contact you?

By checking this box, I agree to receive relevant marketing communications regarding products, industry news, literature, and events from Bio-Techne and its brands: R&D Systems, Novus Biologicals, Tocris Bioscience, ProteinSimple and Advanced Cell Diagnostics. I understand that I can change my preferences at any time. I further understand that any data provided to Bio-Techne and its brands will be stored, used, and deleted consistent with Bio-Techne’s Privacy Notice.

Leave this field blank

View Microglia Activation During Neuroinflammation: Steady-State Microglia Image

Microglia Activation During Neuroinflammation: Steady-State Microglia background image 1