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Immunology > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

do antibodies in different locations function the same or differently

A

differently

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2
Q

antibodies in the blood, lymph, and extracellular fluids function how

A

by binding microbes -> aggregation, neutralization, and complement activation

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3
Q

antibodies in mucusal surface function how

A

by trapping microbes in the mucus layer

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4
Q

b cell activation generating high affinity receptors would include what

A

somatic hypermutation and affinity maturation

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5
Q

what cells do somatic hypermutation

A

TFH cells

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6
Q

what cells do affinity maturation

A

FDCs

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7
Q

b cell activation becoming antibody factories (plasma cells) include

A

class switching

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8
Q

what cells are involved in class switching

A

TFH cells

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9
Q

where does cross-linking BCR inducing signaling occur

A

secondary lympoid organs

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10
Q

BCR binds multiple what on the surface of microbes

A

epitopes

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11
Q

what does the binding of epitopes result in

A

cross-linking BCRs

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12
Q

after the BCR binds multiple epitopes on the surface of microbes creating cross linking what happens

A

kinase of ITAMS on Ig alpha/beta

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13
Q

after the BCR binds multiple epitopes on the surface of microbes creating cross linking what happens and kinase of ITAMs on Ig alpha/ beta what happens

A

activation signals are sent to the nucleus and create in gene expression

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14
Q

what does CR2 do

A

bind to Ag via C3d

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15
Q

what is CD19

A

signaling domain

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16
Q

what is CD81

A

membrane localization of complex

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17
Q

CR1 (b cell) binds what and on what

A

C3b on pathogen

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18
Q

once CR1 binds Csb on pathogen what is recruited

A

factor I

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19
Q

what does factor I do

A

cleaves C3b-> iCsb -> C3d

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20
Q

what does C3d bind

A

CR2

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21
Q

B cell signaling for whole microbe

A
  1. BCR bind to antigen
  2. coreceptor bind C3d
  3. signaling from BCR and coreceptor converge
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22
Q

b cell signaling for part of microbe

A
  1. BCR bind a component of microbe
  2. C3d binds to same component and CR2
  3. converge on signaling
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23
Q

2 ways to activate B cellls is

A

thymus independent and dependent

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24
Q

thymus independent includes what b cells

A

B1 and B2

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25
Q

thymus dependent includes what b cells

A

only b2 cells

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26
Q

thymus (t cell) independent has no

A

TFH cell help: only make low affinity IgM Ab

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27
Q

thymus (t cell) depenedent has

A

TFH cell help:
high affinity receptors (somatic hypermutation and affinity maturation)
class switch

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28
Q

steps for B cell activatioin by a thymus independent antigen

A
  1. BCR cross-linking
  2. co-receptor and BCR signaling
  3. become IgM plasma cell-> low affinity
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29
Q

what stores antigens

A

FDCs

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30
Q

FDC- not derived from

A

hematopoiesis

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31
Q

where are FDCs derived from

A

stromal cells and bone marrow

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32
Q

what do fdcs so

A

capture antigen and store on surface

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33
Q

dendrites have what receptors

A

complement: CR1 and CR2

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34
Q

is CR1 or CR2 dominant

A

CR2

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35
Q

FDCs lack

A

phagocytic activity

36
Q

antigens are captured by

A

macrophages or FDC

37
Q

three steps to how antigens are captured by macrophages or FDC

A
  1. free Ag enter via afferent lymph vessels
  2. in subcapsular sinus they can be trapped by macrophage or
  3. move into B cell zone and be trapped by FDCs
38
Q
A
38
Q

primary focus b cells secrete IgM where

A

medullary chords

39
Q

proliferation of primary focus B cells (2) options

A

plasmablast that secrete IgM
or
plasmablast tha continue differentiation and move to primary follicle

40
Q

what antibody effectors bind IgG

A

FcRn
Fc gamma RI
Fc gamma RIIA
Fc gamma RIIIB
Fc gamma RIII

41
Q

what antibody effector binds IgE

A

Fc epsilon RI

42
Q

what antibody effector binds IgA

A

Fc alpha RI

43
Q

what does transcytosis across endothelial cells mean

A

moving IgG from blood

44
Q

ITAMS are

A

activating

45
Q

ITIMs are

A

inhibitory

46
Q

4 steps for transcytosis across endothelial cells

A
  1. IgG binds FcRn on luminal side of endothelial cell
  2. IgG and FcRn endocytosed
  3. the vesicle is transported to tissue side of the cell
  4. release content outside of the cell
47
Q

polygR binds and what does it interact with

A

J chain and interacts IgA and IgM

48
Q

transcytosis through epithelial cells means

A

crossing epithelial cell tissues->mucus

49
Q

steps for how poly-Ig uses transcytosis through epithelial cells

A
  1. polygR bind to J chain
  2. endocytosis
  3. vesicle transported from bottom to top of cell
  4. vesicle fuses with plasma membrane of apical side to release Ab into mucus
50
Q

IgE protects from

A

parasites

51
Q

what WBC help fight parasites

A

eosinophil
basophil
mast cell

52
Q

during primary infection what is made

A

IgE

53
Q

IgE binds what on eosinophils

A

FcERI

54
Q

what happens in secondary infection

A

preloaded eosinophils will bind the parasite using IgE-> degranulation

55
Q

when IgG binds during IgE parasite infection what does it do

A

decrease inflammation

56
Q

Fc gamma RII B2->

A

mast cells

57
Q

Fc gamma RII B1->

A

macrophages, neutrophils, eosinophils

58
Q

maternal antibodies are transferred to

A

fetus/ newborn

59
Q

what crosses the placenta

A

IgG

60
Q

how does IgG cross the placenta

A

FcRn

61
Q

what is secreted into breastmilk

A

IgA

62
Q

once IgA is secreted into breastmilk it is transferred to

A

new born

63
Q

steps for neutralization of virus immune

A
  1. virus enters
  2. IgA will bind virus
  3. virus can’t interact with receptor-> doesnt enter cell-> no infection
64
Q

steps for neutralization of non-immune cell

A
  1. virus enters
  2. attachment protein binds to receptor
  3. virus enters-> infection
65
Q

what binds bacteria in immune cells

A

IgA

66
Q

what interacts with non-immune cells

A

bacteria

67
Q

what happens when IgA binds bactera in immune cells

A

bacteria cant bind cells to infect issues

68
Q

what happens when bacteria binds non-immune cells

A

replication and cause infections

69
Q

when a toxin binds receptor what happens

A

endocytosis of toxin

70
Q

when the toxin is endocytosed what happens

A

active part of toxin is released into cytoplasm and there is a bad outcome

71
Q

is there is neutralization of the toxin what happens

A

Ab binds toxin and prevents the toxin from binding cells which results in no diseases

72
Q

IgM binding to antigen on a pathogen surface initiates the

A

classical pathway of complement activation

73
Q

planar form of IgM is

A

flat

74
Q

staple form of IgM is

A

bent at hinge region

75
Q

C1 binds to only what form of IgM

A

staple

76
Q

the binding of C1 to staple IgM initiates

A

classical pathway

77
Q

outcomes of classical pathway

A

phagocytosis
inflammation
pores

78
Q

phagocytosis expresses

A

C3b

79
Q

inflammation expresses

A

C3a

80
Q

pores express

A

C5b

81
Q

multiple IgGs are bound to

A

microbe and C1

82
Q

steps for clearing immune complexes

A
  1. Ab bind Ag (not whole microbes)
  2. C1q bind to start complement
  3. C3b deposited on Ag and Ab
  4. Ab/ Ag-C3b complex binds CR1 on RBCs
  5. complexes filter out in spleen and liver
  6. macrophagaes will phagocytose complex
83
Q

Ab-mediated opsonization

A
  1. Ab binds to microbe
  2. Ab binds Fc receptor
  3. signaling
  4. phagocytosis
  5. microbe destroyed
84
Q

what Fcy receptors are for inhibitation

A

FcyRIIB2 and B1

85
Q

Ab dependent cell-mediated cytotoxicity steps

A
  1. tumor cell binds Ab
  2. Ab binds FcyRIII on Nk cells
  3. NK cells release granules (perfornin and granzyme)
  4. tumor cell dies by apoptosis

Immunology (14 decks)

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