A previous immunology tutorial said this:
Adaptive “antibody proteins” float in
the blood and specifically attack “only
one type of antigen.”
Innate “complement proteins” also float
in the blood, but attack a “variety of different
pathogens.”
Complement attacks using a variety of methods,
but let's focus on the “Membrane Attack”
Complex
The “Membrane Attack” Complex is a sensible
name:
“Complex” means that the MAC isn't just
“one simple protein”,
it's a “bunch of proteins” that activate
in sequence, ultimately combining
to “Membrane Attack” or punch a hole in
a bad cell's membrane.
C6,7,8,and 9 combine to punch the hole.
C5 “does the work” joining C6,7,8, and
9
And C3 is the “key protein” - more “C3
activation” means more “complement activation.”
Now for the frequently tested factoid: C3
and C5 are split into “A” and “B”
parts.
The “A parts” signals Allergy-like responses.
The B-parts Binds.
C3B binds to C5.
When C3B binds, it “cuts C5” into “C5a”
and “C5b”
C5B binds to C6,7,8, and 9, becoming part
of the “Membrane Attack” complex.
This sequence of protein activation is the
“constant end-game” that always happens
regardless of how the complement cascade starts.
Now that we know the constant end-game, let's
look at the 3 different ways to start complement,
or 3 ways to split C3, the key protein.
Classically, an antibody binds to an antigen,
and the antibody also binds to C1.
“C1 to antibody to antigen” splits C2
and C4,
C2a and C4b combine to form “C3 convertase,”
and “C3 convertase” is what cuts C3 into
C3a and C3b, starting the “constant end
game.”
There is also the “alternative pathway”
for the “first time” your body meets a
pathogen,
and you have not yet learned how to make antibodies.
If you don't have antibodies to activate C1
classically,
Luckily, C3 randomly splits into C3a and C3b
- just on its own, without other proteins
telling it to.
This “random splitting” also makes a C5
convertase, which continues into the “constant
end game.”
The final pathway is the “lectin pathway.”
Some pathogens have unique sugars on their
cell surface, which our cells lack.
When your body finds these “unique sugars”,
it know that this cell is a pathogen which
must be “Membrane Attacked.”
“Mannose-binding lectin” is what recognizes
these unique sugars,
and MBL eventually activates the constant
end-game.
Review:
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