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microglial cell

Tuesday 14 April 2009

Microglial cells can be activated by binding of various ligands to various cell-surface innate immune receptors: CD14 binds lipopolysaccharide (LPS) and components of Protollin; Toll-like receptor 2 (TLR2) and TLR4 bind Protollin components; MHC class II molecules interact with T-cell receptors; CD40 binds CD40 ligand expressed by T cells and astrocytes; complement receptors bind complement components such as C1q; and Fc receptors (FcRs) bind amyloid—specific antibodies.

Activated microglial cells express various scavenger receptors (SRs) that mediate phagocytosis of amyloid-beta, such as integrin-alpha/beta, CD36, CD47, SR-A and SR-BI, the triggering of which leads to phagocytosis of amyloid- fibrils and oligomers.

Ligation of cell-surface heparan sulphate proteoglycans (HSPGs), insulin receptors and proteinase inhibitor (serpin)–enzyme complex receptor (SEC-R) on activated microglial cells leads to phagocytosis of soluble amyloid-beta.

Microglial cells can also degrade amyloid- by releasing amyloid—degrading enzymes, such as metalloproteases, insulin-degrading enzyme and gelatinase A.

Protollin, a proteosome-based adjuvant composed of purified outer membrane proteins of Neisseria meningitidis and lipopolysaccharide.