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IHO Week 2 > Complement - Regal > Flashcards

Complement - Regal Flashcards

1
Q

What order is complement activated in?

A

C142356789

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2
Q

What is the function of the complement system?

A

A group of plasma proteins that acts as an auxiliary system in immunity, both on its own and in conjunction with humoral immunity.

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3
Q

Define the complement system

A

A primitive surveillance system for microbes, independent of T-cells and antibodies.

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4
Q

What are the 6 specific functions of complement?

A
  1. Lysis of microorganisms
  2. Opsonization of antigen
  3. Mediators of inflammatory response
  4. Solubilization and clearance of immune complexes
  5. Clearance of apoptotic cells
  6. Augments stimulation of B-cell
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5
Q

What are the 3 pathways of Complement Activation?

A

Classical Pathway
Lectin Pathway
Alternative Pathway

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6
Q

What are the 5 additional proteins operating in the alternative pathway?

A

Factors B, D, H, I, P = Properdin

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7
Q

What types of interactions occur after C5 is cleaved?

A

C6, C7, C8, and C9 only have protein-protein interactions.

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8
Q

When C1 is cleaved, what remains?

A 
C1q = binds antigen-antibody complex
C1qr2s2 = cleaves C4
C1r2s2 = cleaves C2
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9
Q

When C4 is cleaved by C1 esterase (C1qr2s2), what remains?

A

C4b and C4a (little)

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10
Q

When C2 is cleaved by C1s, what remains?

A

C2a and C2b (little)

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11
Q

What cleaves C3?

A

C4bC2a Enzyme C3 Convertase

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12
Q

When C3 is cleaved by C4bC2a, what remains?

A

C3b and C3a (little)

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13
Q

What cleaves C5?

A

C4bC2aC3b Enzyme C5 Convertase

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14
Q

When C5 is cleaved, what remains

A

C5b and C5a (little)

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15
Q

How is the Classical Pathway activated?

A

Antigen-Antibody Complexes with IgG (dimer) or IgM (pentamer)

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16
Q

How is the Mannose-Binding Lectin Pathway activated?

A

Mannose, sugar, polysaccharides on microbes

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17
Q

How is the Alternative Pathway activated?

A

Recognizes LPS/Endotoxin, foreign surfaces, carbohydrates, nucleophiles, Human IgA, IgG, IgE complexes by complement itself

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18
Q

What enzyme catalyzes the cleavage of complements?

A

Serine Esterases

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19
Q

Define Activating Surface.

A

Deficient in Sialic Acid, free hydroxyl or amino groups, rich in carbohydrates

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20
Q

MBL is similar to C1qr2s2 in what way?

A

C4bC2 is cleaved by MBL interacting with MASP-1 and MASP-2 to C4bC2a similar to the C1q-C1r-C1s interaction

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21
Q

Define Deactivating Surface.

A

Lots of Sialic Acid

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22
Q

What is C3 Tickover?

A

A little bit of C3 all the time in the blood is getting hydrolyzing thioester and picking up water. This causes Factor B to bind to C3 [C3(H20)B]. Then Factor D comes in and enzymatically cleaves Factor B to C3(H20)Bb.

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23
Q

True/False: C3 activates itself via C3(H20)Bb cleaving C3 to C3b.

A

True

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24
Q

How is C3b inactivated on a non-activated bacterial surface?

A

Factor I and Factor H

25
Q

C3 Convertase

A

C4b2a

C3bBb

26
Q

C5 Convertase

A

C4b2aC3b

C3bBbC3b

27
Q

What Complement Deficiencies would cause SLE?

A

C1, C4, C2, C3

28
Q

What Complement Deficiencies are associated with high incidence of immunocompromised disease?

A

C1, C4, C2

Infections of encapsulated bacterial infections or pyogenic infections
Classical Pathway
Immune Complexes

29
Q

MBL pathway Complement Deficiency is common where and increases susceptibility to what?

A

Common in UK

Increased susceptibility to Bacterial Infections

30
Q

What Complement Deficiency is associated with Glomerulonephritis (Immune Complex)?

A

C3

31
Q

What Complement Deficiencies cause Neisseria Meningococcal Infections?

A

Membrane Attack Complex
C5, C6, C7, C8, C9
Alternative pathway and terminal lytic pathway

32
Q

What is complement good for?

A

Lysing Bacteria and Clearing Immune Complexes

33
Q

Where is complement?

A

In the plasma protein system, but also in secretions (bronchoalveolar lavage fluid)

34
Q

What starts the Classical Complement Pathway?

A

Antigen Antibody Complexes

35
Q

What starts the Mannose-Binding Lectin Pathway?

A

Mannose-Binding Lectin

Mannose-Associated Serine Protease 1 or 2

36
Q

What components of the complement system covalently bind to the surface of the bacteria?

A

C4b and C3b via thioester bonds

37
Q

C1 Inhibitor Deficiency

A

HAE (Hereditary Angioedema)
Recurrent episodes of localized edema in skin, GI, or larynx
C1 Inhibitor inhibits C1 esterase
Uncontrolled activation leads to consumption of C4 and C2

38
Q

What is the treatment for Hereditary Angioedema?

A

Anabolic steroids to increase synthesis of C1 Inhibitor or give purified C1 Inhibitor
Kallikrein inhibitors and B2 receptor inhibitors => less edema

39
Q

Decay Accelerating Factor (CD55) & CD59 Deficiency

A

Increased susceptibility of erythrocytes to MAC-mediated lysis
Complement-mediated intravascular hemolysis in Paroxysmal Nocturnal Hemoglobinuria (PNH)

40
Q

Treatment of DAF Deficiency

A

Antibody to C5 to reduce hemolysis = Eculizumab

41
Q

Where is complement synthesized?

A

Liver hepatocytes and tissue macrophages

Epithelial cells, fibroblasts, monocytes

42
Q

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

A

C4bC2a

Classical Antibody-Antigen Complex Pathway

43
Q

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

A

C4b or C3b

44
Q

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

A

C4

45
Q

Terminal Lytic Pathway

A

Formation of the Membrane Attack Complex (MAC)

46
Q

Describe the steps of the Terminal Lytic Pathway

A

C5 Convertases cleave C5 into C5a and C5b. C5b attaches via protein-protein interactions to C6, C7, C8, C9s leading to a hole in the membrane.

47
Q

True/False: Lysis cannot occur in the absence of C9.

A

False - it’s just slower

48
Q

Limitations to Complement Activation

A

Short half-life
Non-activator surfaces
Fluid phase inhibitors - so active fragments don’t stray
Membrane bound inhibitors - so C3b and C4b can’t attach and lyse our own cells

49
Q

C5b-7 can bind to what in order to prevent membrane insertion and MAC formation?

A

S protein in the fluid phase

50
Q

How does CD59 (Protectin) offer protection for your own cells?

A

Inhibits binding of C9 and its polymerization on self- membranes

51
Q

Factor H is a fluid phase inhibitor of what?

A

C3 Convertase Can also be a cofactor for cleavage of C3b by Factor I

52
Q

What if you have deficiencies of the complement control system?

A

Uncontrolled lysis and consumption of complement components leading to secondary complement deficiency.

53
Q

Anaphylatoxin Receptors

A

Complement peptides that bind to G-Protein coupled receptors to trigger inflammatory and anaphylactic response

54
Q

C3 fragment interaction with CR2 complement receptor on lymphocytes does what?

A

Augments humoral immunity

55
Q

What does CR1 (CD35) do?

A

Ligands: C3b, C4b
Transports immune complexes by RBC and blocks formation of C3 convertase
Cells: RBC, PMN, Macrophages

56
Q

What does CR2 (CD21) do?

A

Ligands: C3d, C3dg, C3bi
Augments stimulation of the B-cells
Affinity for envelope protein of EBV (allowing for viral entry into B-Cells)
Cells: B-Cells

57
Q

What does CR3 (CD11b/CD18) and CR4 (CD11c/CD18) do?

A

Ligand: C3bi
Phagocytosis and cell adhesion
Cells: Monocytes, macrophages, neutrophils, NK cells

58
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

CR1

IHO Week 2 (13 decks)

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