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27 Cards in this Set

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  • Back
What are the six functions of complement cells? (the upside)
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
What are the down sides to complement action?
Inflammation and anaphylaxis.
Most C3, C6, C8 and B complement are made where?
In the liver
Which complement components do macrophages make?
C2, 3, 4, 5, B, D, P, and I
What complement compounds do neutrophils make?
large quantities of C6 and C7.
What does it mean when complement proteins are mentioned and there is a line over them?
That they are activated.
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.
What is C-activation?
The complement compound is altered to interact with the next component
What is C-fixation?
Complement being recognized by Ag-Ab complexes
What is a hemolytic unit?
A dilution of plasma such that if added to blood, 50% of AB coated RBC in a suspension would be lysed.
What are the three pathways of complement activation? Which are antibody dependent? At what point in their pathway are they in common?
Classical, lectin, and alternative pathway.

Only classical is antibody dependent.

They all lead to activation of C3 and the generation of C3 convertase.
What stimulus leads to activation of the alternative pathway of complement activation?
Microbial cell wall stimulation
What stimulus leads to the lectin pathway of complement activation?
Mannose-rich carbohydrates
What stimulus leads to the classical pathway of complement activation?
Antigen-antibody complexes
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.
What is the spontaneous breakdown pathway of the alternative complement pathway?
In the alternative complement pathway, B calls in D, which calls in P and this feeds back to the C3 convertase pathway.
What are the pathways by the classical complement and alternative complement pathways that allows C6 and C7 to bind to the microbial surface?
read that - do we even need to go to this level?
How do complement pathways actually poke the hole in the cell membrane?
Here is the making of the hole
In the complement activation pathway, what do the smaller fragments function as?
know smaller fragments from complement cleavage and how they work in chemotaxis for neutrophils
What complement derived chemotactic factor targets eosinophils?
C3a
What complement derived chemotactic factor targets neutrophils, eosinophils and macrophages?
C5a
How do viruses use the CD59 complex to confound the complement activation pathway?
CD59 – this is the terminal complex, 5,6,7,8,9. Most viruses (HIV, herpes) incorporates this virus and that inhibits the complement virus.
What is the substrate modulation of the regulation of complement system?
For example: Convertase can act on C5 only after binding to C3b.
How many molecules of IgG and IgM are needed to initiate the classical complement pathway?
Two of IgG and one of IgM
What are the three complement receptors? A deficiency in which one leads to severe recurrent infections?
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.
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.)
What do deficits in factor H look like histologically?
They deposit between the membranes of a the glomeruli.