These data demonstrate direct classical complement pathway activation on endothelial cells.

Mammalian C-type retroviruses are inactivated by human serum, following triggering of the classical complement cascade.

Several studies have suggested an association between the classical complement pathway and the clearance of apoptotic cells.

Antibody mediated rejection (AMR) activates the classical complement pathway and can be detrimental to graft survival.

This protein also has the capacity to accelerate the decay of human C3 convertase of the classical complement pathway.

By engaging the Fc end of antiviral IgG, the parent strain resisted neutralization mediated by the classical complement pathway.

Experiments were performed to investigate classical complement pathway activation on resting endothelial cells and endothelial cells exposed to shear stress.

The induced immune response includes activation of the classical complement pathway and enhancement of the phagocytosis of the recognized target.

This contrast with reports of other parasite CRT that inhibited activation of the classical complement pathway through sequestration of C1q.

The classical complement cascade, a key component of innate immune pathogen defence, mediates synaptic pruning by microglia during early postnatal development.

These results suggest that retroviruses are not inactivated by utilizing the same pathway leading to cell lysis by the classical complement system.

Biotinylated aptamer binding successfully initiated the classical complement pathway leading to complement fixation on the target cells via a streptavidin-C1q conjugate as previously reported.

Although activation of the classical complement pathway may occur in some anti-lymphocyte monoclonal antibody infusions, this does not appear to explain immediate-type anaphylactoid reactions.

Soluble complement receptor type 1 (sCR1, BRL 55730) is a potent inhibitor of the alternative and classical complement pathways.

While in later stages classical complement pathway activation by C1q exacerbates disease progression, C1q also plays a beneficial role in early disease.

C4 activation failed to occur in C1q depleted serum, but was not affected by Factor B depleted serum, confirming classical complement pathway activation.