Thursday complement lecture Flashcards
the “Order” of complement numbers in a cascade
c142356789
complement responsible for opsonization (increasing the amount that the adaptive immunity can phagocytize)
C3b
Complements that result in inflammation and t cell reculation
C3a C5a
factor p stands for
properidin
Complement that are “really instrumental in clearing immune complexes”
C1(q,r2,s2)
C4
C2
C3
Immune complexes “really instrumental in clearing Neiserria” via formation of membrane attack complexes
C5b C6 C7 C8 C9
“also the alternitive pathway (C3 + H20, factor B, factor D)
“what is complement good for?”
lysing bacteria
clearing immune complexes
Opsonization (C3b and C4b and their degradation products do this)
solubilization and clearance of immune complexes (C4b and C3b binding to CR1 receptor helps here)
Augmentation of humoral immunity (C4b and C3b binding to CR2 receptor (CD21) helps here)
complement that is most abundant in plasma
C3
it makes up about 5 percent of plasma protein
The classical complement path way
Triggered by antigen binding to IgG or IgM antibodies
C1(q,r,s) (aka c1 esterase) cleaves C4. C2 then binds C4b and the C1 esterase cleaves C2 in order to make the C4b2a complex (this is now the C3 convertase).
Whaaaat no way after that the C3 convertase cleaves C3 and forms a complex as C4b2a3b which cleaves enzyme C5, whose components go on to participate in proteolytic cleavages of complement components in order to lyse the infiltrate? Get outta here!
Whats weird about the nomemclature of complement with regards to “a” and “b” products of clevage
“b” fragments are always the larger, membrane bound ones, except for complement 2a and 2b, where 2a is the larger one.
which complements covalently bind to the bacteria and dont come off? this is on the test probably
C4b and C3b
mind blown
What complements participate in the terminal lytic pathway
c5,6,7,8,9
Mannose binding lectin complement pathway
You don’t need antibody to start this pathway
the polysaccharides on the bacteria are contacted by mannose binding lectin (MBL) as well as MASP-1 and MASP-2, which recruit C4, then its all the same as the classical pathway from there
C1 INDEPENDANT FORM OF THE CLASSICAL COMPLEMENT PATHWAY
alternative complement path
C3 hydrolized by water, factor b binds. factor d cleaves factor b. Form C3(H2O)Bb, which cleaves C3, making C3b, which looks for something to bind to (bacteria).
Once C3b binds a surface, factor b binds again, which makes C3b a substrate for factor d, which makes C3bBb. This cleaves more C3
triggered by recognintion of foreign structures (LPS (endotoxin), dextran sulfate, radiographic contrast media, morphine); NO ANTIBODY NEEDED; C3 activates C3 (self activation)
What is one common thing on the surface of cells that prohibit the binding of the C3b via the alternative pathway?
C3 does not activate: sialic acid (when factor C3b binds something with this, it then gets bound by factor H or I and they inactivate it)
does activate: lack of sialic acid
What does properdin do
stabilizes the alternative pathway C3 convertase (C3bBb)
What is the long ass name from the C5 convertase IN THE ALTERNATIVE PATHWAY
its that high yield C3bBbC3b enzyme
excessive complement activation in immune complex disease would most likely result in depletion of which complement most according to the human who said this things
C4
s protein
binds to C5b-7 and blocks integration into membranes
CD59
wont let C9 bind, stop complement from binding you own cells.
C3bBb
alternative pathway C3 convertase
CD46
doesn’t cause anything to decay, but has “cofactor activity”
………..
factor H
fluid phase inhibitor of alternate pathway C3 convertase (C3bBb)
can be a cofactor for clevage of C3bBb. (allows factor I to inactivate it)
C1 Inhibitor deficiency
Results in uncontrolled complement activation with leads to consumption of C4 and C2, as well and the possibility of immune complex disease
HEREDITARY ANGIOEDEMA
deficiency in DAF (CD55) and CD59
CD55 usually decays convertase
CD59 usually stops C9
If you have neither of those, erythrocytes lyse.
get neisseria
What complements can mimic sx of inflammation and anaphylaxis?
C3a and C5a
CR1
on RBCs
binds C3b, C4b bound infiltrates
transport of immune complexes by the RBCs
promotes immune adherance and opsonization FOR PHAGOCYTOSIS
CR2
mostly on b cells
Ups the immune response NOT NECESSARILY BY PROMOTING PHAGOCYTOSIS, HOWEVER. THAT IS MORE LIKE CR1s JOB
binds epstein barr virus (thats how it gets into the be cell)
CR3
binds iC3b. opsonizes shit for phagocytosis
