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micr 386 > module 08 section 05 (membrane attack complex) > Flashcards

module 08 section 05 (membrane attack complex) Flashcards

1
Q

what is the purpose of the membrane attack complex (MAC)?

A

form a pore in the target cell membrane leading to its destruction

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2
Q

what is step 1 of the complement cascade after C5 convertase formation?

A
  • cell-associated C5 convertase cleaves C5 into C5a and C5b

- C5b remains bound to C5 convertase

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3
Q

what is step 2 of the complement cascade after C5 convertase formation?

A
  • C6 and C7 sequentially bind to C5b

- C5bC6C7 complex becomes directly inserted into the lipid bilayer of the target cell membrane

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4
Q

what is step 3 of the complement cascade after C5 convertase formation?

A

after insertion of the C5bC6C7 complex into the lipid bilayer, C8 is bound to C7 to stabilize the complex

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5
Q

what is step 4 of the complement cascade after C5 convertase formation?

A

up to 15 C9 molecules polymerize around the C5bC6C7C8 complex to form the membrane attack complex (MAC)

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6
Q

each pore made by the MAC is made of what protein?

A

C9

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7
Q

what does a pore in the membrane result in?

A

spilling of the inracellular components, initiating cell death

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8
Q

can complement activation result in normal cell damage? why or why not?

A
  • yes - constantly occuring at a low level, so can cause damage if not regulated
  • also fragment complement proteins can diffuse to adjacent cells and injure them
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9
Q

what is complement activation inhibited by?

A

regulatory proteins present on normal host cells but not on microbes

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10
Q

what are C1r and C1 complexess inactivated by? how?

A
  • plasma protein called C1 inhibitor (C1 INH)
  • normally C1q binds to antigen-complexed antibodies resulting in activation of the C1 complex, C1 INH prevents C1 complex from becoming proteolytically active
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11
Q

what is the formation of C3 convertase inhibited by (in all pathways)?

A
  • DAF (decay-accelerating factor)
  • MCP (membrane cofactor protein)
  • CR1 (type-1 complement receptor
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12
Q

what is C3b inactivated by? how?

A

MCP and CR1 act as cofactors for Factor I which mediates the proteolytic cleavage of C3b, producing iC3b and a fragment C3f

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13
Q

how is the formation of MAC inhibited?

A

by membrane protein CD59 and plasma protein S

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14
Q

what does the timeline for complement pathway activation depend on?

A

the type of activator component

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15
Q

explain the lectin pathway timeline

A

lectin pathways involved in the first line of defence as its activated by pathogen surfaces

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16
Q

explain the alternative pathway timeline

A

involved in the first line of defense (after lectin tho) as its activated by pathogen surfaces

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17
Q

explain the classical pathway timeline

A

involved later, after antibodies have been produced

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18
Q

what pathway(s) are C5-C9 involved in

A

all three (classical, lectin and alternative)

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19
Q

what pathway(s) is MBL involved in?

A

lectin only

20
Q

what pathway(s) is factor B involved in?

A

alternative only

21
Q

what pathway(s) is C4 involved in?

A

classical and lectin

22
Q

what pathway(s) is C3 involved in?

A

all three (lectin, classical and alterantive)

23
Q

what pathway(s) is C1 involved in?

A

classical only

24
Q

what pathway(s) is MASP-1/2 involved in?

A

lectin only

25
Q

what pathway(s) is factor D involved in?

A

alternative only

26
Q

recall - each of the fragments produced through the complement activation act as:

A

mediators of inflammation and phagocytic recruitment

27
Q

what is an anaphylatoxin?

A

a substance produced by complement activation that causes the release of histamine and other mediators, from basophils and mast cells, producing signs and symptoms of anaphylaxis

28
Q

explain anaphylatoxin in terms of the fragments produced by complement activation

A

each of the fragments has a unique anaphylatoxin potency

29
Q

what is the most anaphylatoxin potnent complement protein?

A

C5a

30
Q

what does anaphylatoxin potency promote?

A

mast cell degranulation and contraction of the vasculature

31
Q

what are the anaphylatoxin complement proteins?

A

C3a, C4a, and C5a (because they can trigger degranulation of mast cells)

32
Q

how does degranulation of mast cells cause anaphylaxis?

A

mast cells secrete mediators which enter the capillaries, cause contraction of the vessel and elict an anaphylaxis reaction

33
Q

what are the systemic anaphylaxis effects on the GI tract?

A

increased fluid secretion and peristalsis

34
Q

what are the systemic anaphylaxis effects on the airways?

A

constriction and increased mucus

35
Q

what are the systemic anaphylaxis effects on the bvs?

A

increased flow and permeability

36
Q

explain how complement pathways result in phagocytosis

A
  • during opsonization, C3b (opsonin) binds to pathogens, and is then recognized by the complement receptor on phagocytic cells
  • this leads to phagocytosis od the pathogen
  • C3b can also bind immune complexes to modify their solubility for removal from circulation
37
Q

explain the role of complememt proteins in MAC

A
  • MAC’s composed of 6 unique glycoprotein macromolecules
  • C3b binds to the pathogen to activate the late components of the complement system, resulting in the formation of MAC
  • MAC results in lysis of pathogens and cells by forming a pore in the target cell membrane
38
Q

have complement deficiencies been discovered for all complement proteins?

A

almost all the ones we covered in three early/late systems yes

39
Q

what can complement deficiencies be caused by?

A
  • partial or complete loss of protein synthesis in pyogenic infections caused by streptococcus pneumoniae
  • or due to the formation of an incomplete or abnormal protein
40
Q

less then 10% of complement disorders are diagnosed, why?

A

redundancy in the immune system

41
Q

list complement diseases and their associated outcomes (4)

A
  • C1, C2, C4 deficiency - immune complex disease
  • MAC deficiency - increased risk of infection
  • C3, factor D, factor I deficiency - pyogenic infections
  • MBL deficiency - susceptibility to recurrent infections and decreased lung function is cystic fibrosis patients
42
Q

are homozygous deficiencies rare or more common?

A

rare

43
Q

are heterozygous deficiencies more easy or harder to detect?

A

not easily detected

44
Q

a genetic deficiency of C1-INH results in an overproduction of C2b and is the cause of:

A

hereditary angioedema

45
Q

recap: the biological functions of the complement system include: (5)

A
  • opsonization
  • activation of inflammatory cells by anaphylaxis
  • cytolysis mediated by MAC formation
  • solubilization and clearance of immune complexes
  • enhancement of humoral immune responses

micr 386 (31 decks)

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