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HD Exam 1 > Lecture 14, Compliment > Flashcards

Lecture 14, Compliment Flashcards

1
Q

What are the 3 main effects of compliment activation?

A
  • Recruit inflammatory cells
  • Opsonization
  • Kill via MAC
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2
Q

What are the names of the 3 compliment pathways?

A
  • Lectin pw
  • Classical pw
  • Alternative pw
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3
Q

What molecule recognizes pathogen in the classical complement pw?

A

C1 (macromolecule)

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4
Q

Name the 3 different parts of C1

- Which is the biggest part?

A
  • C1q (6 globular heads that bind AB and extended tails)
  • C1r
  • C1s
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5
Q

How is the C1qrs complex activated?

A

When at least 2 of the heads are bound to AB (on Ag); binding induces conformational change on AB constant region
- Single molecule bound to pentameric IgM can activate C1

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6
Q

What happens to the C1qrs complex upon binding 2+ ABs on Ag?

A
  1. Once C1q bound, C1r undergoes conformational change to become active
  2. C1r cleaves C1s, C1s active now as well
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7
Q

What molecule recognizes pathogen in the lectin complement pw?

A

Mannan Binding Lectin (MBL, a protein)
- Or Ficolins
(trimeric clusters)

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8
Q

While MBL binds mannose, ficolins bind ___________.

A

Oligosaccharides

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9
Q

What 2 serine proteases are MBL associated w/?

What classical pw complement molecules are they similar in function to?

A

MASP 1 and MASP 2

- Similar to C1r and C1s

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10
Q

How are MASP 1/2 activated?

How does this differ from the classical complement pw?

A

Activated upon MBL binding to Ag surface

- Bind directly to pathogen surface, not to AB

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11
Q

Upon initial activation of C1s in the classical complement cascade, what important convertase is first created? (name and function)

A

C4b2a, a C3-convertase

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12
Q

Once C4b2a (C3-convertase) is created in the classical complement pw, what convertase is created next? (name and function)

A

C4b2a3b, a C5-convertase

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13
Q

Upon initial activation of MASP-2 in the lectin complement cascade, what important convertase is first created? (name and function)

A

C4b2a, a C3-convertase

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14
Q

Once C4b2a (C3-convertase) is created in the lectin complement pw, what convertase is created next? (name and function)

A

C4b2a3b, a C5-convertase

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15
Q

What is MAC?
Does it mostly kill gram - or + ? (give e.g.)
How is it created?

A

Membrane Attack Complex: creates a pore in a pathogen to lyse it (many viruses)

  • Gram-negative (Neisseria spp.)
  • Once a C5-convertase is formed, C5 -> C5b. Then C6, C7, C8, and up to 16 C9’s join to form the MAC
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16
Q

How does the alternative complement pw get started?

A
  • Hydrolysis of C3 (slowly occurs spontaneously in plasma)
17
Q

How is the C3-convertase formed in the alternative pw? (name it as well)

A
  • C3b binds factor B (Bb; cleaved by factor D) to form C3bBb, a C3-convertase
18
Q

What products are formed with the hydrolysis of C3?

Which is bound to the pathogen and which is released (soluble)?

A
  • C3a (soluble)

- C3b (bound to pathogen; rapidly degraded if not bound to pathogenic surface)

19
Q

Are C3 and C5 convertases always bound to the pathogen or sometimes soluble?

A

Always bound (I think)

20
Q

In the alternative complement pw, once the C3-convertase C3bBb is formed, how is the C5-convertase formed? (name it as well)

A

Active C3-convertase creates more C3a and C3b. When another molecule of C3b binds the C3bBb, a C5 convertase is formed: C3bBbC3b

21
Q

Review: name the C3- and C5-convertases of each of the pw’s

A

C3-convertase of classical/lectin: C4b2a
C3- convertase of alternative: C3bBb

C5-convertase of classical/lectin: C4b2a3b
C5-convertase of alternative: C3bBbC3b

22
Q

What is opsonization?
What receptors are used?
What do these receptors sense?

A

Basically ingestion of Ag that was coated via complement cascade
- CR1
- C3b
(C4a assists in adherence, C5b in phagocytosis)

23
Q

How are Ag-AB complexes removed from the body?

A

Depends on C3b

  • Bind to CR1 on circulating RBCs
  • Ag-AB’s stripped off by resident macrophages as they pass thru liver, spleen
24
Q

What complement components contribute to chemotaxis and vascular changes during inflammation? (not on the list of things to know)

A
  • C5a is a chemoattractant for different granulocytes

- C3a, C4a, C5a trigger mast cells and basophils to increase vascular permeability

25
Q

What molecule can inhibit the classical pw in its early stages?

A

C1 Inhibitor (C1 INH)

26
Q

What molecule can inhibit the MAC’s formation?

A

CD59

27
Q

What disease would a deficiency in C1 INH lead to?
Sx?
Tx?

A

Hereditary angioneurotic edema

  • Fluid accumulation, epiglottal swelling, abd attacks
  • C1-INH concentrate
28
Q

What disease would a deficiency in CD59 lead to?

A

Paroxysmal Nocturnal Hemoglobinuria

RBC lysis

29
Q

A deficiency in the early components of compliment would result in what dz? (not on list of things to know)

A

Immune complex disease.

- Poor clearance of immune complexes

HD Exam 1 (15 decks)

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