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IHO Week 2 > Regal Complement > Flashcards

Regal Complement Flashcards

1
Q

Order of complement numbers:

A

1 4 2 3 5 6 7 8 9

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2
Q

What are 6 special functions of complement?

A
  1. lysis of pathogens
  2. opsonization of antigen –> uptake by phagocytes
  3. mediates inflammatory response
  4. solubilization and clearance of immune complexes
  5. augments stimulation of B-cells
  6. clearance of apoptotic cells
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3
Q

Complement molecules of the Classical pathway:

A

C1q – C1r2 — C1s2

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4
Q

Most abundant form of complement?

A

C3

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5
Q

C3 convertase is:

A

C4b2a

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6
Q

C5 convertase is:

A

C4b2a3b

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7
Q

Mannose binding pathway is activated by _________ and uses ____, ______, and ______ in place of C1q, C1r, and C1s to get to C4/2 stage.

A

Polysaccharides on microbes

MBL (mannose binding lectin), MASP-1, MASP-2

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8
Q

Alternative pathway is activated by ________ and uses _____, _____, and _____ to get to C3.

A

LPS, carbohydrates, etc.

Factor B
Factor D
Properdin

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9
Q

What is common to all pathways?

A

C3

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10
Q

What are the components unique to the terminal lytic pathway (MAC-major attack complex)?

A

C5, C6, C7, C8, C9

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11
Q

Small fragments are denoted by “a” and float away to act like cytokines, large fragments are denoted by “b” and bind to cell for next activation step. What is the exception to this?

A

C2a is the larger C2 fragment

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12
Q

Antigen binding to 2 _____ or ______ trigger the classical pathway/

A

IgG, IgM

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13
Q

What type of bond do C4b and C3b attach to cell surface via?

A

COVALENT, thioester

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14
Q

C1 esterase (C1qr2s2) does what? And is inhibited by what?

A

cleaves C4 into C4a (small) and C4b (big)

inhibited by C1INH

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15
Q

When C4b covalently binds to activating surface what can it do?

A

interact with CR1 (complement receptor) on white cells

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16
Q

What happens when C4b is bound to active surface and C2 comes along?

A

C1s cleaves it and leaves C2a (remember this is bigger) bound to make C4b2a —-> classical pathway C3 convertase

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17
Q

With C4b2a molecules bound to active surface, what happens when C3 comes along?

A

gets cleaved by C4b2a and C3b stick around to bind covalently and C3a float away.

*now we have C4b2a3b —> C5 convertase

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18
Q

How does the mannose binding lectin pathway get rolling?

A

Binds to cell active surface WITHOUT antibody involvement

  • a C4 float by and gets cleaved leaving C4b
  • then a C2 float by leaving a C2a
  • now at same stage as classic pathway with a C4b2a bound to the cell surface waiting for a C3
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19
Q

Oldest C3 activating pathway and does not require antibody for activation?

A

Alternative patheway

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20
Q

Major activator of Alternative pathway?

A

LPS from Gram - bacteria

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21
Q

What do human cells have that protects them from activation of alternative pathway?

A

sialic acid

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22
Q

In the alternative pathway what comes to bind with C3b first?

A

Factor B

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23
Q

Once Factor B is bound to C3b, what happens next?

A

Factor D comes along and cleaves off Ba (little, just like 3a, 4a, 2b), and leaves Bb bound

Now you have C3bBb—just like C4b2a of classic pathway

24
Q

What is the Alternative pathways equivalent of C3-convertase?

A

C3bBb

25
Q

What stabilizes C3bBb?

A

Properidin

26
Q

What are the two types of C5 convertase and what pathways are they associated with?

A

C4b2aC3b —- classical and Mannose

C3bBbC3b — Alternative

27
Q

Activation of the complement system by antibody coated Strep pneumo leads to formation of a C3 convertase enzyme. The subunit composition of this enzyme is most likely:

A. C3bBbC3b

B. C4bC2a

C. C1qr2s2

D. C3(H2O)Bb

E. C3bBb

A

B. C4bC2a (i think you can also drop the second C and it means the same)

28
Q

Which of the following complement proteins covalently binds to surfaces after enzymatic cleavage and exposure of an internal thioester bond?

A. C1qr2s2

B. C4b

C. C2a

D. Factor B

E. Factor D

A

B. C4b

29
Q

Excessive complement activation in immune complex disease would most likely lead to the depletion of which of the following components?

A. C4

B. MBL

C. Factor B

D. Factor D

A

A. C4

30
Q

What activates the terminal lytic pathway?

A

Cleavage of C5 into C5a and C5b by C5 convertase (either classical or alternative)

– C5b meets up with C6 then C7, C8, C9

– this creates a hole in the membrane and causes lysis and cell death

31
Q

What are the components of the membrane attack complex?

A

C5b, C6, C7, C8, C9

32
Q

What can prevent completion of the MAC?

A

When C5b-7 bind to S protein

33
Q

Can lysis via MAC occur without C9?

A

yes, but it is slower

34
Q

Two proteins that can interact with CR’s on white cells?

A

C3b, C4b —> CR’s 1-4

35
Q

Two major limiting factors of complement activation?

A
  1. short enzymatic half life

2. properties of non-activator surfaces (sialic acid)

36
Q

Control protein that binds to C1s/r in plasma so C4 not cleaved?

A

C1-INH

37
Q

Control protein binds to soluble C5b-7 in the plasma?

A

S protein

38
Q

Control protein that inhibits binding of C9 on human cell membranes?

A

CD59 aka Protectin

39
Q

Control protein that can accelerate the decay of C3bBb so it can’t cleave C3?

A

Factor H

40
Q

Factor H can bind to a membrane if ______ is present?

A

sialic acid

41
Q

Protein that can degrade C3b with Factor H as a co factor?

A

Factor I

42
Q

C1 Inh deficiency leads to:

A

HAE (hereditary angioedema)

*uncontrolled complement activation leads to consumption of C4 and C2

43
Q

Treatment for C1 Inh deficiency:

A

Anabolic steroids to increase synth of C1 Inh

purified C1 inh

Kallikrein inhibitors and B2 receptor inhibitors

44
Q

Control protein with wide distribution on “self” membranes that accelerates the decay of C3 convertase?

A

CD55 aka DAF (decay accelerating factor)

45
Q

Cofactor on self membranes that has activity against C3b and C4b?

A

CD46 aka MCP (membrane cofactor protein)

46
Q

Deficiency in DAF (CD55) and Protectin (CD59)?

A

increased RBC lysis by MACs

intravascular hemolysis in paroxysmal nocturnal hemoglobinuria (PNH)

**also tx with Ig to C5 (eculizamab) reduces hemolysis and increases susceptibility to Neisseria

47
Q

C3a and C5a function after they float away?

A

Inflammatory mediators

48
Q

What’s an anaphylatoxin?

A

C3a and C5a can bind to C3a and C5a receptors and trigger an inflammatory response that can mimic anaphylaxis

** chemotaxis, smooth muscle contraction, increased vascular permiability, degranulation of mast cells

49
Q

Opsonins of this system are?

A

C3b and C4b

50
Q

Solubilization and clearance of immune complexes occur via _______ receptors.

A

CR1 (CD35)

51
Q

Augmentation of humoral immunity occurs via ________ receptors.

A

CR2 (CD21)

52
Q

Whats an important cell that transports immune complexes via CR1?

A

RBCs

53
Q

Major cell (and two others) with CR2s?

A

B-cells

also activated T-cells and epithelial cells

54
Q

CR2 has a high affinity for which virus?

A

EBV

55
Q

Numerous C3b molecules are deposited on the surface of bacteria X. The C3b favors the phagocytosis of the bacteria by neutrophils by binding to which of the following?

A. anaphylatoxin receptor

B. CR1

C. CR2

D. Decay accelerating factor

A

B. CR1

56
Q

Where do immune complexes attached to RBC CR1s go from there?

A

transferred to CR1s on macrophages in the reticuloendothelial system (ie. spleen, liver)

IHO Week 2 (12 decks)

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