membrane attack complex การใช้

• An example of type II hypersensitivity is the membrane attack complexes cause cell lysis and death.
• Complement proteins C6-C9 all contain a MACPF domain and assemble into the membrane attack complex.
• The C5b then recruits and assembles C6, C7, C8 and multiple C9 molecules to assemble the membrane attack complex.
• C5b binds sequentially to C6, C7, C8 and then to multiple molecules of C9 to form membrane attack complex.
• In lieu of the membrane attack complex, complement proteins ( particularly C3b and C4b ) are deposited on red blood cells.
• If the complement response is sufficient, red blood cells are damaged by the membrane attack complex, an effector of the complement cascade.
• If the complement response is insufficient to form membrane attack complexes, then extravascular lysis will be favored over intravascular red blood cell lysis.
• C8 alpha-gamma induces the polymerization of 10-16 molecules of C9 into a pore-forming structure known as the membrane attack complex.
• The complement system is part of the innate immune system and has a variety of functions, from destroying invading microorganisms by opsonization to direct destabilization by the membrane attack complex.
• The immune complex serves as an activator that triggers a response from the C5b-C9 complements, which form a membrane attack complex ( MAC ) on the glomerular epithelial cells.
• The membrane attack complex forms after c3b has bound to the surface of the target pathogen and is able to bind to c4a, which was formed earlier, and an enzyme called c5 convertase.
• An activation peptide, C5a, which is an anaphylatoxin that possesses potent C6 complement component, and this complex is the basis for formation of the membrane attack complex, which includes additional complement components.
• Perforin, a pore-making monomeric granule released from natural killer cells and cytotoxic T lymphocytes, kills target cells by forming polymers and tubular structures not unlike the membrane attack complex of the complement system.
• The subsequent complement cascade catalyzed by C3-convertase results in creating a membrane attack complex, which causes lysis of the pathogen as well as altered-self in the context of apoptotic and necrotic cells.
• Deficiencies of the terminal pathway predispose to both autoimmune disease and infections ( particularly Neisseria meningitidis, due to the role that the membrane attack complex ( " MAC " ) plays in attacking Gram-negative bacteria ).
• In the formation of the membrane attack complex, several complement proteins are inserted into the red blood cell membrane, forming pores that lead to membrane instability and intravascular hemolysis ( destruction of the red blood cell within the blood vessels ).
• This branch of the complement system is activated by IgA immune complexes and bacterial endotoxins, polysaccharides, and cell walls, and results in producing anaphylatoxins, opsonins, chemotactic factors, and the membrane attack complex, all of which help fight pathogens.
• "' CD59 antigen "'( also called 1F-5Ag, H19, HRF20, MACIF, MIRL, P-18 or protectin ) inhibits formation of membrane attack complex ( MAC ), thus protecting cells from complement-mediated lysis.
• The smaller fragment called C3a serves to increase vascular permeability and promote extravasatisation of phagocytes, while the larger C3b fragment can be used as an opsonin or bind to either type of C3 convertase to form the trimolecular C5 convertase to activate C5 for the membrane attack complex.
• The end result of this "'complement activation "'or "'complement fixation "'cascade is stimulation of phagocytes to clear foreign and damaged material, proxy inflammation to attract additional phagocytes, and activation of the cell-killing membrane attack complex.