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Scheme of the complement system. The complement system, also known as complement cascade, is a part of the humoral, innate immune system and enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane. [1]
The classical pathway is distinct from the other complement pathways in its unique activation triggers and cascade sequence. Activation of the complement pathway through the classical, lectin or alternative complement pathway is followed by a cascade of reactions eventually leading to the membrane attack complex.
Structure of mannose in its α-D mannopyranose form. Mannan is a polymer of mannose.. The lectin pathway or MBL pathway is a type of cascade reaction in the complement system, similar in structure to the classical complement pathway, [1] in that, after activation, it proceeds through the action of C4 and C2 to produce activated complement proteins further down the cascade.
The alternative pathway is a type of cascade reaction of the complement system and is a component of the innate immune system, a natural defense against infections. The alternative pathway is one of three complement pathways that opsonize and kill pathogens. The pathway is triggered when the C3b protein directly binds a microbe. It can also be ...
The C1 complex (complement component 1, C1) is a protein complex involved in the complement system. It is the first component of the classical complement pathway and is composed of the subcomponents C1q, C1r and C1s. [1] [2] [3]
Additionally, C3b molecules can attach to the Fc regions of antigen-bound antibodies leading to phagocytosis or movement to the liver, where the C3b-tagged immune complex is then destroyed. In both cases C3b interacts with the C3b receptor, complement receptor 1 on phagocytic cells, such as macrophages and neutrophils , allowing for engulfment ...
Complement 3a and complement 5a are intermediate products of the complement cascade. [citation needed] Their synthesis is joined to the three alternative pathways (classical, lectin-dependent, and alternative) of complement activation by a convertase enzyme.
These antibodies initiate a complement-dependent inflammatory cascade, culminating in tissue damage and destruction. [ 50 ] [ 51 ] Given that AQP4 is primarily expressed on perivascular astrocytic endfeet in the spinal cord and by Müller cells in the retina , NMOSD preferentially affects the spinal cord, and the anterior visual system.