Interleukin-1beta and anaphylatoxins exert a synergistic effect on NGF expression by astrocytes.

C3a and C5a anaphylatoxins are proinflammatory polypeptides released during complement activation. They exert their biological activities through interaction with two G protein-coupled receptors named C3aR and C5aR, respectively. In the brain, these receptors are expressed on glial cells, and some recent data have suggested that anaphylatoxins could mediate neuroprotection.

Complement component anaphylatoxins upregulate chemokine expression by human astrocytes.

The complement (C) system, a major component of the innate immune system, has been described as a factor implicated in some brain disorders. C activation leads to the release of anaphylatoxins, two proinflammatory polypeptides acting through specific receptors that have been detected on brain cells. Here, we examined the effect of anaphylatoxins on chemokine expression by human astrocytes.