Quiz 2 Flashcards

1
Q

What are the goals of the complement system?

A

anaphlaltoxins
MAC
opsonization

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2
Q

What is complement fixation?

A

attachment of protein fragments to the surface of pathogens marking them for phagocytosis and avoiding host cells

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3
Q

What is the membrane attack complex (MAC)?

A

5 subunit complex that forms pores in pathogens

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4
Q

What is an anaphylatoxin?

A

complement protein fragments that induce inflammation

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5
Q

What is the first complement pathway to activate and why?

A

alternative pathway; its proteins circulate the blood

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6
Q

What 2 complement pathways require inflammation to activate?

A

lectin and classical

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7
Q

What is the C3 convertase for the alternative pathway?

A

C3Bb

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8
Q

What is the C3 convertase of the lectin pathway?

A

C4b2b

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8
Q

What is the C3 convertase of the classical pathway?

A

C4b2a

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9
Q

What do all 5 of the MAC subunit do?

A

C5b, C6, C7 bind together exposing C7’s hydrophobic site so it can insert into the pathogen
C8 binds to the rest of complex as a docking site for C9

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10
Q

What are the 2 MAC regulation proteins?

A

plasma proteins
cell-surface proteins

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11
Q

How do PLASMA MAC regulation proteins prevent host cell damage?

A

prevent soluble C6 and C7 from binding to host cells

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12
Q

How do CELL-SURFACE MAC regulation protein prevent host cell damage?

A

prevents C9 recruitment

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13
Q

What are 3 examples of plasma MAC regulation protein?

A
  1. S protein
  2. clusterin
  3. factor J
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14
Q

What are 2 examples of cell-surface MAC regulation protein?

A
  1. CD59 (protectin)
  2. HRF
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15
Q

What are 2 examples of anaphaltoxins in the alternative complement pathway?

A

C3a and C5a

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16
Q

What 3 places do alternative anaphalatoxins bind and why?

A
  1. endothelial cells (increase blood flow)
  2. granulocytes (induce degranulation)
  3. phagocytes (attract phagocytes)
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17
Q

What do protease inhibitors do and an example?

A

inhibit bacterial proteases
alpha 1-macroglobulin: traps microbes like a venus fly trap

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18
Q

What do defensins do?

A

poke holes in pathogen membrane

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19
Q

What kinds of cells express alpha-defensins?

A

neutrophils and paneth cells

20
Q

What kinds of cells express beta-defensins?

A

epithelial cells

21
Q

What cell is involved in the most common immunodeficiencies?

A

B cells

22
Q

What is the difference between primary and secondary immunodeficiencies?

A

primary - inherited
secondary - aquired

23
Q

Primary immunodeficiencies are ______ which tend to be rare

A

monogenic

24
Q

What are the 5 categories of immunodeficiencies?

A
  1. physical/microbial
  2. complement
  3. pattern recognition receptors
  4. phagocytic
  5. NK cells
25
Q

What are 2 examples of microbial immunodeficiencies?

A
  1. cystic fibrosis
  2. crohns
26
Q

What are 3 examples of complement immunodeficiencies?

A
  1. Factor H/I
  2. MAC deficiency
  3. C1, 2, 3, 4 deficiency
27
Q

What is an example of a PRR immunodeficiencies?

A

recurrent HSE (herpes)

28
Q

What are 3 examples of phagocytic immunodeficiencies?

A
  1. leukocyte adhesion deficency
  2. Chediak-Higashi syndrome
  3. chronic granulomatous disease
29
Q

What are 2 examples of NK cell immunodeficiencies?

A
  1. classical NK cell deficiency
  2. Functional NK cell deficiency
30
Q

How is cystic fibrosus an immunodeficiency?

A

mucous formed is too thick causing biofilms ; CFTR protein is faulty

31
Q

How is crohns disease an immunodeficiency?

A

paneth epitheial cells lack expression of a-definsins causing increased microflora

32
Q

How is Factor H and I deficiency an immunodeficiency?

A

Factor H and I cleave C3b to make iCb3 which stops complement
without complement is over activated and C3 is depleted from serum

33
Q

How is improper formation of MAC an immunodeficiency?

A

if any of the 5 subunits are messed up MAC wont form

34
Q

How is Hereditary Angioneurotic Edema (HANE) an immunodeficiency?

A

improper activation of classical C3 convertase causing non-specific cleavage of C2 and C4 causing inflammation that doesn’t respond to medication and protein depletion in plasma

35
Q

What is pyogenic bacteria?

A

induces acute neutrophilic inflammation and pus

36
Q

How is recurrent HSE an immunodeficiency?

A

PRR signaling is impaired causing a NK cells to not do their job and viral replication to be uncontrolled (INF not working)

37
Q

How is leukocyte adhesion deficiency (LAD) an immunodeficiency?

A

cell is not able to bind to microbe
tight binding for neutrophils impaired because b2-integrin doesn’t work

38
Q

How is Chediak-Higagi syndrome an immunodeficiency and what does it cause on the cellular level of other immune cells?

A

phagosome cannot bind to to lysosome to create phagolysosome
causing giant granules and deficient NK cells

39
Q

How is Chronic Degranulomatous syndrome an immunodeficiency?

A

NADPH oxidase doesn’t work and cell degradation doesn’t happen
causing neutrophil build up

40
Q

How is classical NK cell deficiency an immunodeficiency?

A

absence of very low number of NK cells

41
Q

How is functional NK cell deficiency an immunodeficiency?

A

defective NK cells where Fc receptor cannot interact with microbe

42
Q

_______ binds to all C3 convertases to create C5 convertases which is cleaved into C5a and C5b to create MAC

A

C3b

43
Q

Is C5a or C5b the beginning of the MAC?

A

C5b

44
Q

What is the job of Properdin (Factor P)?

A

protects alternative C3 convertase on pathogen’s surface

45
Q

What is the job of Factor H and I?

A

cleaves bound C3b making it inactive (stopping complement)

46
Q

What are the two PLASMA C3b regulating proteins?

A
  1. Properdin (Factor P)
  2. Factor H and I
47
Q

What are the two MEMBRANE C3b regulating proteins?

A
  1. Decay-accelerating factor (DAF)
  2. Membrane cofactor protein (MCP)
48
Q

What is the job of Decay-accelerating factor (DAF) and Membrane cofactor protein (MCP)?

A

protects host cells (disassembling of alternative C3 convertase)