complement cascade

It participates in the complement cascade ending with cell death.

Newly created fragments C3a and C3b are important in next steps of complement cascade development.

Inhibition of the complement cascade can decrease this damage.

Bb and C4b.2a, which are bimolecular complexes formed early on in the complement cascade.

In neonates, opsonic activity and the ability to activate the complement cascade is very limited.

Starts the complement cascade to identify bacteria, activate cells and clear out dead cells.

These antibodies bind to antigens, making them easier targets for phagocytes, and trigger the complement cascade.

Complement 3a (C3a) and complement 5a (C5a) are intermediate products of complement cascade.

If the complement response is sufficient, red blood cells are damaged by the membrane attack complex, an effector of the complement cascade.

The subsequent complement cascade catalyzed by C3-convertase results in creating a membrane attack complex, which causes lysis of the pathogen.

Serum sickness is primarily caused by the antibodies clumping during infusion and triggering the complement cascade.

Elements of the complement cascade can be found in many nonmammalian species including plants, birds, fish and some species of invertebrates.

Complement component 6 (C6 protein) in the complement cascade system of immune proteins (native immunity)

The anaphylatoxins C3a, C4a, and C5a are cationic fragments generated during the complement cascade that participate in host defense.

Activation of the complement cascade attracts phagocytes that leak peroxide and other reagents, which may increase the damage for the surviving heart cells.

Eculizumab specifically binds to the terminal Complement component 5, or C5, which acts at a late stage in the complement cascade.

LTA bound to targets can interact with circulating antibodies and activate the complement cascade to induce a passive immune kill phenomenon.

Lending credibility to this has been the discovery of disease-associated genetic polymorphisms in other elements of the complement cascade including complement component 3 (C3).

Eculizumab is a recombinant humanized monoclonal IgG2/4 antibody that selectively targets and inhibits the terminal portion of the complement cascade.

-Expression of human complement regulators (CD55, CD46, and CD59) to inhibit the complement cascade.

MAC is the cytolytic endproduct of the complement cascade; it forms a transmembrane channel, which causes osmotic lysis of the target cell.

Shiga-toxin directly activates the alternative complement pathway and also interferes with complement regulation by binding to complement factor H, an inhibitor of the complement cascade.

Zinc in drusen have been suggested to play a role in drusen formation by precipitating and inhibiting the elements of the complement cascade, especially complement factor H.

Furthermore, genes in the MHC class III region are involved in the regulation of the humoral immune response, including aspects of the complement cascade.

The activation of the complement cascade can cause damage to cells, therefore the inhibition of the complement cascade can work as a medicine in certain conditions.