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Immuno Unit 1 > A 5 > Flashcards

A 5 Flashcards

1
Q

C3 convertase functions to do what? What are its 2 constituents?

A
  • Cleaves C3 into C3a (phlogistic fever/inflame) and C3b (activates C5 convertase)
  • C4bC2a and C3bBb
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2
Q
  • What activates the classical pathway? (and thus is the first step)
  • What is the rest of the sequence of the classical complement pathway?
A
  • Antigen + Antibody (IgM or C1q for pattern recognition a.k.a. innate, alternatively IgM or IgG for specific recognition a.k.a. adaptive!!)
  • C1q->C1r->C1s (same molecule)
  • C4 (convergence pt. w/ Lectin pathway)
  • C2
  • C3 convertases (C4bC2a)
  • C3 (all paths converge here)
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3
Q

What is the sequence of the lectin (mannose-binding) complement pathway?

A
  • MBP or ficolin ( binds MASP1, MASP2)
  • C4 (Convergence pt. w/ Classical pathway)
  • C2
  • C3 convertases (recall C4bC2a)
  • C3
  • C3b
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4
Q

What is the sequence of the alternative complement pathway?

A
  • C3->C3 h2o (Starts here if it auto-activates)
  • C3b (starts here if activated by other pathway)
  • B (binds C3b, cleaved by D)
  • C3 convertase
  • C3
  • C3b
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5
Q

What is the sequence of complement once all 3 paths converge?

A
  • C3b
  • C5 convertases
  • C5, C6, C7, C8, C9 (form MAC, or Membrane Attack Complex)
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6
Q

-What is the “natural” structural motif in recognition/activation molecules (IgM)?

A

-5 globs hooked to a rod

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7
Q

What molecules recognize the bacterial Phospho-choline pattern? What bacteria do we know carries this pattern?

A
  • CRP, C1q, natural IgM

- S. pneumonia (host cells can also express it when undergoing apoptosis)

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8
Q

Which antibody needs few antibodies but lots of antigen to activate?

A

IgM (alternatively just need 5 close together, not necessarily numerous it is just more likely to find 5 close together that way)

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9
Q

Which antibody needs lots of antibodies but few antigens?

A

IgG (strictly only need 2 IgG’s close together, all 4 sites must be bound. Thus it is more “advanced” than IgM because it can detect lower antigen levels)

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10
Q

Do C3 and C4 attach ionically or covalently to bacteria? What substance makes this attachment possible?

A

-Covalently (permanent)
-C3 thio-ester (used by both C3 and C4) (has both fluid and solid phase)
From review session, also know:
-C3 anchors alternative convertase (C3bBb)
-C4 anchors classical convertase (C4b2a)

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11
Q

Which complement pathway autoactivates?

A

-Alternative

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12
Q

What allows autoactivation of a complement pathway to continue?

A

-Amplification and stabilization of convertase (by Properdin). Alternative pathway is very regulated in ways like this because it is the amplification loop.

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13
Q

What 4 things negatively regulate the complement system?

A
  • C1 inhibition
  • C3 convertase decay
  • C5 convertase decay
  • Inhibition of MAC assembly/insertion
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14
Q

C3 and C4 make ester linkages with what molecules?

A

-OH and -NH

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15
Q

What does C1 INH do?

A

Binds C1r and C1s and breaks them off of C1q, so that they can no longer stick to the bacteria to cleave C4 and C2

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16
Q

What molecules accelerate convertase decay?

A
  • Factor H, C4BP (plasma)

- DAF, CR1

17
Q

What molecules serve as cofactors for Factor I inactivation of C3 or C4?

A
  • Factor H, C4BP (plasma)

- MCP, CR1 (often on splenic macrophages and RBC’s where it helps clear Immune Complexes!!)

18
Q

What happens when C3b is inactivated?

A

-Amplification stops, bacteria killing by complement stops, phagocytosis is unaffected. This is important.

19
Q

What inhibits MAC?

A

CD 59, found on HOST cell membranes. Deficiency: Paroxysmal Nocturnal Hemolysis

20
Q

What do anaphylatoxins & phlogistics do?

A

Promote inflammation (phlogistics also do fever)

21
Q

C1qR , CR1, and CR3 are found where, and do what?

A
  • Professional phagocytes

- opsonization

22
Q

C3dg does what?

A
  • It is an adjuvant that engages CR2 (Complement Receptor 2) on B cells to up IgG production (Up adaptive immunity!)
  • Binds HEL antigen to: lower amt antigen needed, hasten antibody production, AND increase amt antibody made
23
Q

What happens to Immune Complexes that aren’t cleared by circulation?

A

They activate Complement (C3b deposits onto the complex) and get deposited in tissues because solubility drops. Uses up C3 and C4. Vessel deposits create inflammatory response in vessels.(recall Type 3 Hypersensitivity Rxns)

24
Q

What can low C4 and C3 indicate?

A

Possibility of Immune Complex disease

25
Q

How does the liver remove Immune Complexes? How does the spleen do it?
How do RBC’s do it?

A
  • By attaching to Fc portion of antibody
  • Using C3b (C2 deficiency prevents this)
  • Since there are a LOT of RBC’s, their C3b receptors (CR1) add up and really help clearance.
26
Q

What could spherocytosis of RBC’s indicate?

A

-Getting chewed on by spleen (to remove immune complexes)

27
Q

What is phosphocholine?

A

The bacterial structure that is the target of C1q, CRP, and natural IgM that these molecules recognize as foreign.

28
Q

What causes paroxysmal nocturnal hemolysis?

A

A defect in CD59

29
Q

Which molecules trigger for opsonization?

A

C1q, C3b, and iC3b

30
Q

What binds C1q?

A

All phagocytes with C1q receptor (C1qR)

31
Q

What binds C3b and C4b?

A

All phagocytes, presenting cells, and RBC’s through the CR1 receptor.

32
Q

What binds C3dg?

A

CR2 receptor found on the B-lymphocyte. It makes the antigen more obvious ( requiring less antigen) and activates B cell

33
Q

If you have a large buildup of C3b on your RBC’s, where will this “tag” be removed? What about a buildup of antibodies?

A

C3b is removed by the spleen

Antibodies (Fc portion) by the liver

34
Q

What causes Herediatry Angio-edema?

A

Deficiency of C1 INH. (Which normally inhibits C1)

Immuno Unit 1 (6 decks)

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