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Microglia Activation Markers

Microglia are the cellular mediators of inflammation in the central nervous system (CNS). They exist in a quiescent state in healthy CNS tissue, and will become activated following exposure to an insult or infection. Microglia activation is a highly complex and dynamic action. Reactive microglia acquire diverse phenotypes that display different cell surface and intracellular markers, secrete different factors, and exhibit different functions. It is thought that during the inflammatory response, the phenotype of activated microglia exists along this spectrum.

The “classically” activated microglia, which are typically the initial responders to an insult and the cells that instigate a proinflammatory response, are termed M1 microglia. Cytokines, such as IFN-gamma and TNF-alpha, and bacterial and cellular debris will polarize microglia toward the M1 phenotype. M2 microglia are considered to be the anti-inflammatory microglia. However, research has shown that different M2 phenotypic variations, termed M2a, M2b, and M2c, exist. M2a microglia are the “alternatively” activated microglia that facilitate resolution of neuroinflammation and stimulate tissue repair. Microglia polarize to this phenotype upon exposure to IL-4 or IL-13. M2b microglia are considered to be the type II alternatively activated microglia and are associated with increased phagocytic and immunomodulatory activity. Microglia polarize to the M2b phenotype following exposure to immune complexes and toll-like receptor (TLR) agonists. M2c microglia, also referred to as the acquired deactivation phenotype, are associated with anti-inflammatory actions, tissue repair, debris scavenging, and iron sequestration. The M2c phenotype is evoked by IL-10, and to lesser extent, by glucocorticoid hormones. R&D Systems offers a range of research tools needed for investigating the different microglia activation states.