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| *#* Immune complexes trigger complement activation by binding C1. | | *#* Immune complexes trigger complement activation by binding C1. |
| *#** C1 cross-links two antibody molecules. | | *#** C1 cross-links two antibody molecules. |
− | *#** C1 molecule is a complex of: | + | *#** C1 is a complex of: |
| *#*** C1q | | *#*** C1q |
− | *#**** looks like a bunch of 6 tulips – with each ‘flower’ consisting of a globular protein head and a collagen ‘stem’. At least two C1q globular heads must bind to antibody before the complement cascade is triggered. | + | *#**** Looks like a bunch of 6 tulips. |
| + | *#***** Each "flower" consista of a globular protein head and a collagen "stem". |
| + | *#**** At least two C1q globular heads must bind to antibody before the complement cascade is triggered. |
| *#*** C1r | | *#*** C1r |
− | *#*** C1s. A C1q molecule If this happens the inactive C1r and C1s molecules become activated to form an enzyme called C1 esterase. The first substrate of this enzyme is C4, which it digestes to form C4a and C4b. C4b binds to the antigen (e.g. a bacterial cell). C4b will then bind C2 – this is then, in turn, digested by C1 esterase to form C2a and C2b. All the Ca fragments (C2a, C3a, C4a, C5a) are chemotactic for neutrophils and are potent inducers of acute inflammation (they are termed the anaphylotoxins). The C4b2b complex is an enzyme (C ) that is capable of efficient digestion of C3 into C3a and C3b. The production of C3b can now be amplified by the same mechanism as the alternative pathway. The binding of one C1q molecule produces one C1 esterase molecule that then cause the binding of many hundreds of C molecules. The C3b molecule that is produced by the action of this enzyme can also bind to it, forming the complex enzyme C , which is the second enzyme capable of activating C5 and initiating the MAC. Like the alternative pathway, the major effects of classical pathway activation are to produce iC3b and hence it promotes phagocytosis and initiates inflammation. | + | *#*** C1s. |
| + | *#** C1r and C1s become activated when at least 2 C1q heads are antibopdy-bound. |
| + | *#*** Form the enzyme C1 esterase. |
| + | *#* C1 esterace first digests C4 to C4a and C4b. |
| + | *#** C4b binds to the antigen. |
| + | *#* C4b then binds C2. |
| + | *#** C2 is digested by C1 esterase to form C2a and C2bThe C4b2b complex is an enzyme (C ) that is capable of efficient digestion of C3 into C3a and C3b. The production of C3b can now be amplified by the same mechanism as the alternative pathway. The binding of one C1q molecule produces one C1 esterase molecule that then cause the binding of many hundreds of C molecules. The C3b molecule that is produced by the action of this enzyme can also bind to it, forming the complex enzyme C , which is the second enzyme capable of activating C5 and initiating the MAC. Like the alternative pathway, the major effects of classical pathway activation are to produce iC3b and hence it promotes phagocytosis and initiates inflammation. |
| + | . All the Ca fragments (C2a, C3a, C4a, C5a) are chemotactic for neutrophils and are potent inducers of acute inflammation (they are termed the anaphylotoxins). |
| *# '''The binding of soluble lectins to pathogens'''. | | *# '''The binding of soluble lectins to pathogens'''. |
| *#* E.g. collectins. | | *#* E.g. collectins. |