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| {{review}} | | {{review}} |
| ==Introduction== | | ==Introduction== |
− | Complement is so called because it complements the function of antibody. It is a [[Triggered Enzyme Cascade - WikiBlood|triggered enzyme cascade]] and there are more than 20 different proteins in the complement cascades, with most being enzymes or pro-enzymes. It can be activated by both the innate and adaptive immune systems and is one of the main innate protective mechanisms of invertebrates. Due to its destructive potential the complement system is heavily regulated but when activated it works largely by forming pore complexes as well as triggering acute inflammation and by promoting phagocytosis by macrophages and neutrophils. | + | Complement is so called because it complements the function of antibody. It is a [[Triggered Enzyme Cascade - WikiBlood|triggered enzyme cascade]] and there are more than 20 different proteins in the complement cascades, with most being enzymes or pro-enzymes. It can be activated by both the innate and adaptive immune systems and is one of the main innate protective mechanisms of invertebrates. Due to its destructive potential the complement system is heavily regulated but when activated it works largely by forming pore complexes as well as triggering acute inflammation and by promoting [[Phagocytosis|phagocytosis]] by [[Macrophages|macrophages]] and [[Neutrophils|neutrophils]]. |
| ==Complement Fixation Pathways== | | ==Complement Fixation Pathways== |
| [[Image:LH Complement pathway.png|thumb|right|250px|'''Classical and alternative pathways''']] | | [[Image:LH Complement pathway.png|thumb|right|250px|'''Classical and alternative pathways''']] |
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| <p>The main effects of alternative complement activation are therefore: | | <p>The main effects of alternative complement activation are therefore: |
| #To coat bacteria with iC3b | | #To coat bacteria with iC3b |
− | #*A major target for phagocytosis by [[Macrophages|macrophages]] and [[Neutrophils|neutrophils]] via the complement receptors | + | #*A major target for [[Phagocytosis|phagocytosis]] by [[Macrophages|macrophages]] and [[Neutrophils|neutrophils]] via the complement receptors |
| #To induce an acute inflammatory response via C3a and C5a. | | #To induce an acute inflammatory response via C3a and C5a. |
| #*Chemotactic for [[Neutrophils|neutrophils]] | | #*Chemotactic for [[Neutrophils|neutrophils]] |
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| ===Opsonisation=== | | ===Opsonisation=== |
| <p>Once activated the complement system deposits a shell of protein on the bacterial cell surface. C4b, C3b, C5b and C7 molecules contain active binding sites that anchor the complex to the surface and the major protein on the cell surface is iC3b (some of the smaller C3 breakdown products (e.g. C3d) are also present).</p> | | <p>Once activated the complement system deposits a shell of protein on the bacterial cell surface. C4b, C3b, C5b and C7 molecules contain active binding sites that anchor the complex to the surface and the major protein on the cell surface is iC3b (some of the smaller C3 breakdown products (e.g. C3d) are also present).</p> |
− | <p>Complement fragments (C2b, C3a, C4a and especially C5a) released after complement activation are chemotactic for phagocytes and iC3b acts as a target for phagocytosis. Phagocytes have receptors that bind avidly with the complement fragments. Complement-mediated opsonisation of microorganisms is several thousand times more efficient that innate receptors.</p> | + | <p>Complement fragments (C2b, C3a, C4a and especially C5a) released after complement activation are chemotactic for phagocytes and iC3b acts as a target for [[Phagocytosis|phagocytosis]]. Phagocytes have receptors that bind avidly with the complement fragments. Complement-mediated opsonisation of microorganisms is several thousand times more efficient that innate receptors.</p> |
| | | |
| ===Inflammation=== | | ===Inflammation=== |