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27 Cards in this Set
- Front
- Back
What are the six functions of complement cells? (the upside)
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opsonization to enhance phagocytosis
phagocyte attraction and activation lysis of bacteria and infected cells regulation of antibody responses clearance of immune complexes clearance of apoptotic cells |
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What are the down sides to complement action?
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Inflammation and anaphylaxis.
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Most C3, C6, C8 and B complement are made where?
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In the liver
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Which complement components do macrophages make?
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C2, 3, 4, 5, B, D, P, and I
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What complement compounds do neutrophils make?
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large quantities of C6 and C7.
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What does it mean when complement proteins are mentioned and there is a line over them?
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That they are activated.
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When complement proteins are cleaved, which moiety binds to the activation complex (or membrane) and which is released?
In which complement protein is this rule reversed? |
"b" is big, and adds to the membrane-binding peptide, usually.
"a" is small and helps in the chemotactic reactions. In C2, the roles are reversed. |
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What is C-activation?
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The complement compound is altered to interact with the next component
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What is C-fixation?
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Complement being recognized by Ag-Ab complexes
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What is a hemolytic unit?
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A dilution of plasma such that if added to blood, 50% of AB coated RBC in a suspension would be lysed.
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What are the three pathways of complement activation? Which are antibody dependent? At what point in their pathway are they in common?
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Classical, lectin, and alternative pathway.
Only classical is antibody dependent. They all lead to activation of C3 and the generation of C3 convertase. |
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What stimulus leads to activation of the alternative pathway of complement activation?
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Microbial cell wall stimulation
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What stimulus leads to the lectin pathway of complement activation?
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Mannose-rich carbohydrates
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What stimulus leads to the classical pathway of complement activation?
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Antigen-antibody complexes
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Can C3b in the complement activation pathway differentiate between self membranes and foreign membranes to bind to?
What happens? |
Factor H is necessary to recognize self. The red dots are sialic acid, which our own cells have and facilitate factor H binding and then factor I binds. Factors H and I cleave C3b from our own cells.
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What is the spontaneous breakdown pathway of the alternative complement pathway?
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In the alternative complement pathway, B calls in D, which calls in P and this feeds back to the C3 convertase pathway.
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What are the pathways by the classical complement and alternative complement pathways that allows C6 and C7 to bind to the microbial surface?
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read that - do we even need to go to this level?
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How do complement pathways actually poke the hole in the cell membrane?
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Here is the making of the hole
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In the complement activation pathway, what do the smaller fragments function as?
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know smaller fragments from complement cleavage and how they work in chemotaxis for neutrophils
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What complement derived chemotactic factor targets eosinophils?
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C3a
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What complement derived chemotactic factor targets neutrophils, eosinophils and macrophages?
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C5a
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How do viruses use the CD59 complex to confound the complement activation pathway?
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CD59 – this is the terminal complex, 5,6,7,8,9. Most viruses (HIV, herpes) incorporates this virus and that inhibits the complement virus.
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What is the substrate modulation of the regulation of complement system?
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For example: Convertase can act on C5 only after binding to C3b.
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How many molecules of IgG and IgM are needed to initiate the classical complement pathway?
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Two of IgG and one of IgM
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What are the three complement receptors? A deficiency in which one leads to severe recurrent infections?
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CR1, CR2, and CR3
Genetic deficiency in CR3 leads to leukocyte adherence deficiency and severe recurrent infections. Never mind the picture, that's another deficiency - one of C3 not CR3. |
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In CR3 deficiency in Brittany Spaniels, how does the expression of the deficiency effect the individual?
What specifically is the deficiency? |
The heterozygous individuals are normal, though they have less than half the C3 as normal. The homozygous individuals die.
The deficiency is a truncation of C3. (Reminder: C3 is the complement receptor that the endothelial cells put out to bind to macrophages, neutrophils, and NK cells that let them migrate from the blood to the tissues.) |
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What do deficits in factor H look like histologically?
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They deposit between the membranes of a the glomeruli.
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