BioLegend Microglia
Microglia are a glial cell type residing in the central nervous system (CNS) and are recognized for their role in CNS development (e.g. synapse remodeling and maturation), maintenance of homeostasis, and involvement in degenerative diseases. This page provides background detail about microglia and mechanisms by which they contribute to disease. BioLegend offers a wide range of products including antibodies, immunoassay solutions, and magnetic cell separation kits to identify and study microglia.
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Microglia are the resident macrophages in the CNS, and are ontogenically distinct from other phagocytic cells in the mononuclear phagocyte system such as dendritic cells, macrophages and monocytes. Microglia originate from primitive macrophages derived from erythro-myeloid precursors in the yolk sac. These cells colonize the brain during development and remain of embryonic origin in the healthy CNS. In the steady-state condition, microglia can be identified using several common markers which they share with macrophages, such as CD11b, CD45, CD68 and CX3CR1. These cells also express specific markers such as P2RY12, which allow for their distinction from other cell types in the brain as well as peripheral immune cells.

Microglia actively survey their surrounding domain and can rapidly respond to environmental changes such as an immune threat. As a consequence, these cells undergo morphological changes to take on an amoeboid shape and become phagocytic to remove the encountered threat. Under inflammatory conditions, microglia upregulate markers such as CD45 and MHC class II. These morphological changes are also accompanied by expression and secretion of inflammatory molecules such as cytokines and chemokines, which help microglia communicate with astrocytes and peripheral immune cells.
 
Microglia markers (steady state)
CD45low
CD11b
CD68low
CX3CR1
Iba-1
MHC class IIlow
MerTK
P2RY12
Siglec-H
TMEM119
 
 
Microglia markers (Inflammation)
CD45int
CD11b+
CD11cint
CD68hi
CX3CR1hi
Iba-1hi
MHC class IIint
P2RY12low
TMEM119
 
 
References:
1. Prinz M, et al. 2017. Nat. Immunol. 18:385. Pubmed
2. Greter M, et al. 2015. Front. Immunol. 6:249. Pubmed
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