Immunology Flashcards

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1
Q

2 examples of self-reactivity in the immune system

A
  1. cancer

2. autoimmune diseases

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2
Q

what types of immune cells are located in the blood?

A

leukocytes, WBC

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3
Q

what types of immune cells are present in the lymphatic tissue?

A

lymphocytes

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4
Q

lymphocytes are a type of __

A

leukocytes

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5
Q

there is as much lymphatic tissue in the ___ as in the rest of the body combined

A

GI tract

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6
Q

what structures are involved in the immune system? (4)

A
  1. lymph drainage
  2. lymph nodes
  3. spleen
  4. distributed lymphatic tissue
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7
Q

the innate immune system acts ___ (before/after) the adaptive immune system

A

before

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8
Q

what is unique about the adaptive immune system?

A

it is specific to a pathogen / infection

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9
Q

in the innate immune system, a cut in the skin results in a neurological response, causing stimulation of ___

A

neuropeptides

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10
Q

neuropeptides stimulate __

A

mast cells

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11
Q

mast cells are often found near ___ and always near ___

A

nerves; blood vessels

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12
Q

mast cells that have been stimulated by neuropeptides release___ into blood vessels

A

mediators

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13
Q

in the innate immune response, once mediators have been released into BV, what are released and what is their effect?

A

clotting factors and platelets; direct effect on bloodstream

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14
Q

clotting factors can cleave the ____

A

complement

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15
Q

what is the “complement”? What does it break down into?

A

group of proteins in the blood; C3A and C3B

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16
Q

which part of the complement has an effect on mast cells?

A

C3A

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17
Q

which part of the complement has an effect on the macrophages?

A

C3B

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18
Q

what is the receptor for C3A protein?

A

C3aR

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19
Q

what is the receptor for C3B protein?

A

C3R

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20
Q

the complement is a cascade of ___

A

serum proteins

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21
Q

how many proteins made up the complement cascade?

A

9 (C1-C9)

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22
Q

what are the 4 most important proteins in the complement cascade?

A
  1. C1
  2. C3 (a + b)
  3. C5 ( a + b)
  4. C5b–C9
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23
Q

C5b–C9 are involved in __

A

complement destruction

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24
Q

the lipopolysaccharide is used largely for __

A

protection

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25
Q

what happens to LPS to cause an immune response?

A

being shed off surface

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26
Q

what are CPG motifs and in whom are the common?

A

runs of cytosine and guanine in DNA; common in bacteria (not humans)

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27
Q

CPG motifs stimulate ___

A

inflammatory response

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28
Q

what are DAMPs?

A

Damage Associated Molecular Patterns

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29
Q

LPS and CPG motifs make ___

A

Pathogen associated molecular patterns (PAMPs)

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30
Q

DAMPs are ___ proteins with ___ fragments

A

heat shock; hyalouronic

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31
Q

DAMPs stimulate __

A

inflammatory response

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32
Q

TLR (Toll-Like Receptors) are receptors for __ (3)

A

LPS, CPG, DAMPs

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33
Q

TLR are a type of ___ recognition receptor

A

pattern

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34
Q

TLR recognize molecular patterns associated with __

A

infection / inflammation

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35
Q

T/F TLR recognize specific antigens

A

false

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36
Q

presence of LPS/CPG may indicate a ___ infection

A

bacterial

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37
Q

structure of mast cell

A

very large, contains many different granules

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38
Q

mast cells are found only in the __

A

tissues

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39
Q

precursors to mast cells are found in the __

A

blood

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40
Q

mast cell precursors are tissue basophiles (T/F)

A

false

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41
Q

mast cells are involved in the ___ response

A

allergic

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42
Q

mast cells have a lot of ___ and ___ and the ____ cause it to stain purple

A

nucleus and cytoplasm; granules

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43
Q

structure of monocytes/macrophages

A

curved nucleus, plenty of cytoplasm but not a lot of granules

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44
Q

monocytes / macrophages are important early responders to infection because they are ___

A

phagocytic

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45
Q

monocytes/macrophages are involved in acute and chronic __

A

inflammation

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46
Q

monocytes are found only in the __

A

blood

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47
Q

macrophages are found only in the

A

tissue

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48
Q

when stimulated, monocytes/macrophages release ___

A

histamine (prostaglandins)

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49
Q

histamines are released ___ because they are produced in what way?

A

immediately; pre-formed by mediators

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50
Q

prostaglandins are released ___ because they are produced in what way?

A

later; continually produced

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51
Q

which has longer-lasting effects, histamines or prostaglandins?

A

prostaglandins

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52
Q

release of histamines/prostaglandins causes increase in ___ and ___ that is localized to the area

A

vascodilation and vascular permeability

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53
Q

what are the 4 hallmarks of acute inflammation?

A

swelling, pain, redness, heat

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54
Q

vascodilation is responsible for which of the 4 hallmarks of acute inflammation?

A

swelling and pain

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55
Q

vascular permeability is responsible for which of the 4 hallmarks of acute inflammation?

A

redness and heat

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56
Q

swelling in acute inflammation is caused by increased __

A

plasma to intersitial fluid

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57
Q

increased plasma that causes swelling in inflammation carries ___ and ___ that are meant to kill the bacteria

A

antibody and complement

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58
Q

the antibody is useful in killing the infection if __

A

the bug has been seen before

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59
Q

the complement is useful in killing the infection if ___

A

always, because it can kill the bug all by itself

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60
Q

what are the 3 ways to activate the complement?

A
  1. classical
  2. alternate
  3. lectin
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61
Q

what is the classical way to activate the complement?

A

involves antibody (bug has been seen before)

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62
Q

what is the alternate way to activate the complement?

A

spontaneous cleavage of C3 protein ( C3b binds to bug and pokes holes in it)

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63
Q

what is the lectin way to activate the complement?

A

lectin directly activates C

64
Q

what are the 4 functions of the complement?

A
  1. target lysis
  2. target neutralization
  3. enhance phagocytosis
  4. inflammation
65
Q

what is the role of target neutralization by the complement?

A

prevents infectivity

66
Q

how does the complement enhance phagocytosis?

A

C3b bound to a bacteria makes macrophages bind to C3b by their receptors and then phagocytize

67
Q

inflammation is mostly caused by which part of the complement?

A

C3A

68
Q

C3A is known as the ___ factor for other immune cells

A

chemotactic activating

69
Q

(T/F) The complement will bind directly to the bug regardless of if it has been seen before or not

A

true

70
Q

only if the bug has been seen before, ___ will bind and activate a number of killing pathways

A

antibody

71
Q

what 2 pathways are activated by the antibody?

A
  1. antibody-mediated complement pathways

2. antibody-mediated phagocytic pathways

72
Q

what makes macrophages different from mast cells?

A

they phagocytize bacteria

73
Q

what is the benefit of macrophages phagocytizing bacteria?

A

helps in activation

74
Q

what are 2 phagocytic enhancers?

A
  1. antibody

2. complement

75
Q

why do antibodies enhance phagocytosis?

A

macrophages have Fc receptors for antibodies and the antibodies act like a “candy coating”

76
Q

why does the complement enhance phagocytosis?

A

macrophages have receptors for C3, so if C3b is on the bacteria it makes the macrophage more likely to bind

77
Q

what is the first thing to happen once a bacteria has been phagocytized?

A

vesicle acidification

78
Q

what are 2 benefits of vesicle acidification?

A
  1. harder for bacteria to survive

2. some enzymes work better at lower pH, so they will only harm the pathogen, not the host

79
Q

a lysosome merges with the phagosome and secretes ___

A

digestive enzymes

80
Q

bacteria get broken down in the __

A

phagolysosome

81
Q

what is done with the bits of bacteria that are not digested in the phagolysosome?

A

removed and recycled, and then the message is taken to the lymphocytes

82
Q

what are the 4 reactive oxygen intermediates?

A
  1. superoxide (O2-)
  2. hydroxyl radicle (OH-)
  3. hydrogen peroxide (h2O2)
  4. hyperchlorite anion (ClO-)
83
Q

what are the 2 reactive nitrogen intermediates?

A
  1. nitric oxide (NO)

2. nitrous acid (HNO2)

84
Q

nitrogen intermediates require ___ (which is made by Tcells)

A

IFNy

85
Q

why do nitrogen intermediates require control by IFNy?

A

they are very potent and can damage tissues

86
Q

what 3 things are involved in phagocytic effector cell function?

A
  1. reactive oxygen intermediates
  2. reactive nitrogen intermediates
  3. lysosomal enzymes
87
Q

macrophages contribute to local immune/inflammatory response by producing ____ and ___

A

cytokines and chemokines

88
Q

what cytokines are produced by macrophages?

A

IL-1 and TNF

89
Q

what chemokines are produced by macrophages?

A

IL-8

90
Q

what are cytokines?

A

produced by one cell and have an effect on another (way immune system communicates)

91
Q

what are interleukins?

A

a particular type of cytokine with a particular molecular structure

92
Q

what does TNF stand for?

A

tumour necrosis factor

93
Q

what are the effects of TNF? (3)

A
  1. kills tumours
  2. potentially inflammatory
  3. effect on vascular system
94
Q

what is interleukin 8?

A

a chemokine that activates neutrophils

95
Q

neutrophils are involved in __

A

fighting bacterial infection

96
Q

Interleukin 8 causes changes in ___ that cause neutrophils to be ___

A

CAMs; attracted

97
Q

what does CAM stand for?

A

cell adhesion molecules

98
Q

____ change, allowing neutrophils to leave vasculature and get to macrophage

A

CAMs of vasculature

99
Q

neutrophils are also known as ___

A

polymorphic nuclear cells

100
Q

what is the most common type of WBC?

A

neutrophils

101
Q

___ are an important first responder to bacterial infection

A

neutrophils

102
Q

neutrophils are highly ___ in tissues

A

phagocytic

103
Q

neutrophils are involved in tissue ___

A

remodelling

104
Q

what is trans-endothelial migration?

A

neutrophils come into tissue from blood due to attraction to CAM

105
Q

____ of neutrophils bind to CAM to cause rolling

A

selectins

106
Q

what is the purpose of selectins binding to the neutrophil?

A

the rolling slows down the neutrophil

107
Q

once the neutrophil has rolled, it releases ___ and produces ___ that will bind to another ___

A

selectin; integrin; another selectin

108
Q

neutropils binding to the endothelial cell, leading to ___ and ___

A

adhesion and diapedesis

109
Q

what is diapedesis?

A

neutrophil forcing its way out of the blood vessel into tissue

110
Q

what are NETs?

A

extracellular structure made of chromatin and specific proteins released by neutrophils after death

111
Q

what is a happens during necrosis of neutrophil?

A

large, sticky strands of DNA (that can stick to bacteria) are released into the local environment

112
Q

cellular proteins associate with NETs to __

A

damage bacteria

113
Q

T/F: neutrophils expel more “garbage” than macrophages

A

true

114
Q

neutrophils “putting out the garbage” is extremely important to __

A

activation of dendritic cells

115
Q

dendritic cells are the bridge between ___ and ___

A

innate and adaptive immune response

116
Q

at the site of infection, dendritic cells have high __ and low __ . Why?

A

uptake; movement. More garbage to uptake

117
Q

further from site of infection, dendritic cells have high __ and low __. Why?

A

movement; uptake. Less garbage to uptake

118
Q

dendritic cells carry “garbage” from ____ site to ___

A

infection; local draining node

119
Q

all lymphatic drainage moves from __ to __

A

periphery to core

120
Q

lymphatic drainage is carried out by a series of ___ that are controlled by ___ contraction

A

one-way valves; muscular

121
Q

what 2 veins have a large role in lymphatic drainage?

A

2 subclavian veins

122
Q

describe how dendritic cells take up garbage and present it to the lymph nodes (adaptive immunity)

A
dendritic arm picks up garbage and takes it in.
lysozyme then merges to form phagolysosome and breaks garbage into peptides that can be placed into vessicle class 2 MHC and brought to surface of dendritic cell to present to Tcells
123
Q

what is class 2 MHC made of ?

A

alpha and beta chains

124
Q

class 2 MHC is found on the surface of ___

A

dendritic cells

125
Q

class 2 MHC binds with a __ that is presented to the T cells

A

peptide

126
Q

can class 2 MHC present its antigen (peptide) to any T cell?

A

no, the T cell must recognize the antigen

127
Q

____ T cell binds directly to a class 2 MHC

A

CD4

128
Q

the dendritic cells produces ___ to activate the CD4 T cell

A

interleukin 12

129
Q

interleukin 12 signals that it is likely a ____ infection type

A

bacterial

130
Q

B7 on ___ binds to CD28 on __

A

dendritic cell; CD4 Tcell

131
Q

the binding of CD4 with the class 2 MHC and the B7 with CD28 results in ___

A

co-stimulation

132
Q

the signal sent from B7 on the dendritic cell to the CD28 on the T cell promotes the T cell to ___ to respond to the peptide and infection

A

proliferate

133
Q

activating T cells to proliferate is done by activating t-cell ___ factor (interleukin __)

A

growth; IL-2

134
Q

do resting t cells have the receptor for IL-2?

A

no

135
Q

inorder for a tcell to be activated by the IL-2 it is making to proliferate, it must also make __

A

IL-2 receptor and bring it to its surface

136
Q

by resting tcells not having the receptor for IL-2, it creates ___ in activation of t cells

A

specificity

137
Q

IL-2 binding to its receptor results in __ replication of T cells

A

clonal

138
Q

what are the 2 fates of clonal t cells?

A
  1. memory cells

2. effector cells

139
Q

what is the role of effector t cells? (2)

A
  1. the orchestra leaders of the immune response

2. help b cells make antibodies (because t cells cant make them)

140
Q

can b cells make antibodies without the help of t cells?

A

no

141
Q

what surface antibody is found on b cells?

A

IgM

142
Q

what must happen for a b cell to activate?

A

specific antigen must bind to the antibody

143
Q

b cells do not see the peptide in MHC, what do they see?

A

soluble protein

144
Q

once the soluble protein binds to the antibody on b cell, what happens to it?

A

it is taken in by receptor-mediated endocytosis

145
Q

once the protein has been endocytized by b cell, the lysosome forms an endolysosome with the vesicle containing __ and brings ___ to the surface, stuffed in a groove

A

MHC; peptide

146
Q

how do the effector t and b cells interact?

A

if effector t cells see the peptide on the surface of the b cells, it will interact

147
Q

are there naive t cells present in the b cell area?

A

no

148
Q

CD4 t cells produce b cell growth factor (interleukin __

A

IL4

149
Q

T/F: when a b cell clones itself, all the surface antibodies will be the same

A

true

150
Q

what are the 2 fates of cloned b cells?

A
  1. memory cells

2. plasma cells (majority)

151
Q

structure and role of b plasma cells

A

lots of ER, produce and secrete lots of antibodies

152
Q

t cells release ___ that tell b cells what antibody to secrete

A

cytokines

153
Q

in the beginning, most b cells are producing Igm, but t cells what them to produce __. To do this, they must undergo a class __

A

IgG; class switch

154
Q

to perform a class switch, a t cell produces ___ (switch factor)

A

IFN-y

155
Q

antibody is produced in the __ and gets into blood and to site of infection due to increased __

A

vascular permeability