effector mechanisms of humoral immunity: elimination of extracellular microbes and toxins Flashcards

1
Q

Effector functions of Abs

A
  1. neutralize - microbial toxins
  2. opsonize - tags pathogens for ehancing phagocytosis (IgG)
  3. sensitize - enhances NK cell kiling of target
  4. mediation of phagocytosis (IgG)
  5. activation of complement (IgM and IgD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

effector functions of Abs are mediated via

A

Fc (heavy chain contant region) of Ig molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

neutralization

  1. blocks the binding of microbes and toxins to cellular ____
  2. prevents ____ of microbes from infected to healthy cells
A
  1. receptors
  2. spread
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

virulence factors refer to the properties of bacterial gene ____ that enable a microorganism to cause disease

A

products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

FcgammaRI has a ____ affinity

A

high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

FcgammaRII has a ____ affinity

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

FcgammaRIII has a ____ affinity

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

FcepislonRI has a ____ affinity

A

high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

FcbgammaRIIB:

  1. found on ___ cells
  2. can bind ____ complexes via Fc portion
  3. activates ____ → inhibits signaling in B cell
  4. ____ affinity receptor meaning in works later in immune response
A
  1. B cells
  2. Ag-Ab
  3. phosphatases
  4. low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

isotypes ____ and ____ are the most effiient opsonins for promoting phagocytosis via high-affinity FcgammaRI

A

IgG3 and IgG1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

due to its ____ affinity, FcgammaRI works ____ in immune responses

A

high

early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

due to its ____ affinity, FcgammaRIIB works ____ in immune responses when large amounts of immune complexes are formed

A

low

later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

FcepsilonRI:

  1. found on ____ cells and ____
  2. bind Fc portion of ____
  3. useful in protection against ____
  4. when bound to Fc portion of IgE → release cationic protein ( ____ ____ ____ ) that is toxic to worms
  5. this happens in immediate reactions due to its ___ affinity
A
  1. mast cells and eosinophils
  2. IgE
  3. helminths
  4. major basic protein (MBP)
  5. high
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

antibody dependent cellular cytotoxicity (ADCC):

  1. Ab binds to microbe, then Fc portion bind to ____ on ____
  2. activates NK cells to kill Ab-coated cells via ____ and ____
  3. ____ affinity → works later in immune response
A
  1. FcgammaRIII on NK cells
  2. perforin and granzymes
  3. low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

alternative complement pathway:

  1. C3 spontaneously celave to ____ on cell surface
  2. Factor ____ binds to C3b
  3. Factor ____ binds to and cleaves Factor B
  4. Factor B is cleaved into ____ and Ba
  5. Bb is bound to C3b, forming ____ (C3 alternative convertase)
  6. C3 convertase cleaves C3 into ____ and C3a
  7. C3b combines with C3bBb forming ____ (C5 convertase)
  8. C5 convertase cleaves C5 into ____ and C5a
  9. formation of ____

properdin:

A
  1. C3b
  2. B
  3. D
  4. Bb
  5. C3bBb
  6. C3b
  7. C3b3bBb
  8. C5b
  9. MAC

Properdin: stabilizes the interactions of the alternative pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

classical complement pathway:

  1. ____ or ____ bind to the surface of bacterial pathogen
  2. ____ binds to staple formation of IgM (sometimes IgG) (bind to Fc portin)
  3. C1q activates ____ which activates ____
  4. C1s cleaves ____ (into C2a and C2b) and ____ (into C4a and C4b)
  5. C4b combines with C2a to form ____ (C3 convertase) (which is deposited on surface)
  6. C3 convertase cleaves C3 into ____ and C3a
  7. C3b combines with C4b2a to form ____ (C5 convertase)
  8. C5 convertase cleaves C5 into ____ and C5a
  9. formation of ____
A
  1. IgM or IgG
  2. C1q
  3. C1r C1s
  4. C2. C4
  5. C4b2a
  6. C3b
  7. C4b3b2a
  8. C5b
  9. MAC
17
Q

lectin complement pathway:

  1. ____ ____ ____ binds to the surface of mannose on bacterial walls
  2. ____ is bound to the MBL
  3. MASP2 cleaves ____ (into C2a and C2b) and ____ (into C4a and C4b)
  4. C4b combines with C2a to form ____ (C3 convertase)
  5. C3 convertase cleaves ____ into C3b and C3a
  6. C3b combines with C4b2a to form ____ (C5 convertase)
  7. C5 convertase cleaves ____ into C5b and C5a
  8. formation of ____
A
  1. mannose binding lectin
  2. MASP2
  3. C2 C4
  4. C4b2a
  5. C3
  6. C4b3b2a
  7. C5
  8. MAC
18
Q

MAC formation:

  1. after C5 convertase activity, ____ has binding site for C6
  2. when C5b-C6 complex have formed, ____ binds
  3. C5b67 complex is bound to membrane via ____
  4. ____ binds (allowing for complex to be inserted into the membrane
  5. C8 initiates the polymerization of ____
  6. ____ polyemizes to form the pore
A
  1. C5b
  2. C7
  3. C7
  4. C8
  5. C9
  6. C9
19
Q

CR1 functions:

  1. promote ____ of C3b and C4b coated particles
  2. ____ of immune complexes
  3. activates ____ mechanisms of phagocytes
A

phagocytosis

clearance

killing

20
Q

CR 2:

on ____ lymphocytes

____ affinity for cleavage products of C3b

enhances response of B cell to ____ when bound

associated with ____ infections

A

B

high

Ag

EBV

21
Q

CR3:

  1. can bind ____ (necessary for recruitment of leukocytes
  2. binds iC3b to induce ____
A
  1. ICAM-1
  2. phagocytosis
22
Q

C1 INH inhibits ____ activation

23
Q

DAF:

  1. ____ convertase decay
  2. inhibits ____ pathways
A

C2:C4

classical or alternative

24
Q

CR1

C3 convertase decay – inhibits ____ pathways

25
_MCP:_ \_\_\_\_ convertase decay inhibits ____ pathways
C3 all
26
_CD59:_ inhibits ____ formation by blocking the addition of \_\_\_\_
MAC C9
27
_complement function: induction of inflamation:_ inflammation via ____ , ____ , \_\_\_\_ these proteins active:
C5a, C3a, C4a mast cells, NPs, and endothelial cells
28
by binding to Ag-Ab complexes, complement promotes ____ of these complexes and their clearance by phagocytes
solubilization
29
\_\_\_\_ deficiency is the most common human complement dificiency
C2
30
_systemic lupus erythematosus:_ 1. complement deficiency: 2. effect:
1. C1q, C2, C4 2. failure of clearing immune complexes; will be deposited on blood vessels and lead to inflammation
31
_pyogenic bacterial infections:_ 1. complement deficiency: 2. effect:
1. C3 2. can be fatal, inability to produce complement activities
32
deficiencies in ____ and ____ result in increased susceptibility to infection with pygoenic bacteria
properdin and factor D
33
_neisseria bacteria:_ complement deficiency:
C5-C9
34
_pathologies of complement:_ 1. complement system can cause sigificant tissue \_\_\_\_ 2. complement activation is associated with intravascular ____ and can lead to ____ injury to tissues 3. can lead to ____ (MAC mediated)
1. damage 2. thrombosis ischemic 3. neuropathies
35
_evasion of complement of microbes:_ 1. microbes can evade the complement system by recruiting host: 2. many pathogens express ____ acids which can inhibit the alternative pathway of complement by recruiting factor ____ which displaces C3b from Bb 3. example: HIV incorporate host regulatory proteins ____ and ____ when it buds from an infected cell
1. complement regulatory proteins 2. sialic H (which removes C3b from Bb) 3. DAF and CD59
36
_neonatal immunity:_ 1. transport of maternal ____ across the placenta and across the neonatal intetinal epithelium is mediated by \_\_\_\_ 2. maternal ____ in breast milk in ingested by infant 3. Abs in breast milk are transported across the gut epithelium by a process known as \_\_\_\_
1. 1. IgG FcRn 2. IgA 3. transcytosis