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Exam 1 Flashcards

1
Q

What is an innocuous antigen?

A

should not illicit an immune response

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2
Q

What are atopic individuals?

A

predisposed to allergies (IgE)

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3
Q

What is the Hygiene Hypothesis?

A

lack of early childhood exposure to innocuous, increases the susceptibility to allergic diseases

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4
Q

What is responsible for allergies?

A

Type 1 HSR

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5
Q

When is gut microbia established?

A

at birth

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6
Q

Type 1 HSR is mediated by what isotype?

A

IgE

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7
Q

What receptors recognize pathogens and communicate and provide signals to TH cells?

A

pattern recognition receptors

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8
Q

What are the 3 steps to choosing a Th subset?

A
  1. APC binds to antigen + polarizing cytokines
  2. transcription factors induced
  3. production of effector cytokines
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9
Q

Biased Th subsets are required to eliminate a pathogen/allergen. How are these subsets chosen?

A

pattern recognition receptors on APCs

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10
Q

What are the polarizing cytokines for Tregs?

A

IL-2
TGF-B

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11
Q

What are the polarizing cytokines for TH17?

A

IL-1
IL-6
IL-23
TGF-B

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12
Q

What is the polarizing cytokine for TH2?

A

IL-4

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13
Q

What are the polarizing cytokines for TFH?

A

IL-6
IL-21

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14
Q

What are the polarizing cytokines for TH1?

A

IL-2
INF-g
IL-18

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15
Q

What are the effector cytokines for Treg?

A

IL-10
TGF-B

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16
Q

What are the effector cytokines for TH17?

A

IL-17A
IL-17F
IL-22

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17
Q

What are the effector cytokines for TH2?

A

IL-4
IL-5
IL-13

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18
Q

What are the effector cytokines for TFH?

A

IL-4
IL-21

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19
Q

What are the effector cytokines for TH1?

A

INF-g
TNF

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20
Q

What cytokine regulates immune supression?

A

TGF-B

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21
Q

When in development (fetal–>adult) are Tregs and TGF-B the highest?

A

fetal stage

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22
Q

When is immune tolerance the highest in development (fetal–>adult)?

A

fetal stage (lots of Tregs TGF-B present)

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23
Q

When is protective immunity the highest in development (fetal–>adult)?

A

adult stage (low Tregs and TGF-B because immune system has developed)

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24
Q

What is intrauterine IPEX?

A

inactivation of FOXP3 causing no Treg production = no tolerance developed

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25
Q

What is the fetal immune system controlled by?

A

Tregs

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26
Q

Atopic individuals have a ______ bias towards TH2 cells (overactivated)

A

skewed

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27
Q

What are some examples of factors that can cause immune skewing?

A

age
sex
obesity
pre-disposition
prior exposure
microbiome

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28
Q

What are the 5 mucosal surfaces the microbiome colonizes?

A
  1. oral epithelium
  2. airway epithelium
  3. intestinal epithelium
  4. reproductive epithelium
  5. skin epithelium
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29
Q

What is the largest mucosal surface with the most microbiome?

A

intestinal epithelium

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30
Q

What 5 ways are intestinal microbiome help to the host?

A
  1. enhances nutrion
  2. provides competitive growth
  3. produces metabolites
  4. regulates local immune response
  5. regulates immune homeostasis
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31
Q

What are 4 mucosal protection stratagies?

A
  1. tightly packed epithelial cells
  2. limited immune response to host bacteria
  3. antimicrobial peptides
  4. production of IgA
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32
Q

What is immune homeostasis?

A

balance between Tregs and Teffectors

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33
Q

What does immune imbalance look like =? (Tregs v. Teffectors)

A

More T effectors that T regs

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34
Q

What is tonic signaling?

A

immune system skewing above baseline set by barrier surfaces and other factors (like age or sex)
- more bad bacteria than good bacteria

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35
Q

What is an example of how pathology doesn’t always describe the mechanism?

A

weak and excessive immune responses result in immunopathology (wrong response)

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36
Q

What does K means?

A

equilibrium constant
- strength of non-covalent interactions between 2 molecules

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37
Q

Are covalent or non-covalent interactions irreversible?

A

covalent

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38
Q

Are covalent or non-covalent interactions sharing of electrons with extensive orbital overlap?

A

covalent

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39
Q

What is an example of covalent interactions in immunology?

A

C3b binding to pathogen surface

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40
Q

Are covalent or non-covalent interactions weaker?

A

non-covalent

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41
Q

What are 4 examples of non-covalent interactions?

A
  1. hydrogen bonds
  2. ionic bonds
  3. hydrophobic interactions
  4. van der Waal interactions
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42
Q

What does hydrogen bonding require?

A

donor
acceptor
hydrogen

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43
Q

What is a hydrogen bond?

A

2 electronegative atoms compete for the same hydrogen

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44
Q

What amino acids do hydrogen bonds occur between?

A

polar AA

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45
Q

What is an ionic bond?

A

bond between a cation and anion

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46
Q

What amino acids do ionic bonds occur between?

A

charged AA

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47
Q

What is a hydrophobic interaction?

A

hydrophobic molecules are attracted to one another

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48
Q

What amino acids do hydrophobic interaction occur between?

A

uncharged non-polar AA

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49
Q

What is a van der Waal interaction?

A

packing of atoms together

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50
Q

What amino acids do van der Waal interactions occur between?

A

all amino acids

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51
Q

What is Ka?

A

association constant

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52
Q

What is Kd?

A

disassociation constant

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53
Q

What is Ka measured in?

A

M-1

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54
Q

What is Kd measured in?

A

M

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55
Q

What is the equation for Ka?

A

[RL] / [R][L]

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56
Q

What is the equation for Kd?

A

[R][L] / [RL]

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57
Q

What is the relationship between Ka and Kd?

A

they are inverses of each other
Kd = 1/Ka

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58
Q

What does it mean for the [RL] formation if the Ka is large?

A

more RL formed

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59
Q

What does it mean for the [RL] formation if the Kd is small?

A

more RL formed

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60
Q

What is the equation for (f)?

A

f = Ka [L] / 1+Ka[L]

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61
Q

What does f tell us?

A

the fraction of RL complexes formed at a given [L]

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62
Q

Which axis is f and [L] on in a binding curve?

A

f = y axis
[L] = x axis

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63
Q

Using a binding curve, Kd = [L] when?

A

50% of RL complexes are formed

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64
Q

If 10% of RL is formed, ____x Kd

A

0.1 x Kd

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65
Q

If 50% of RL is formed, _____x Kd

A

1 x Kd

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66
Q

If 90% of RL is formed, ______ x Kd

A

10 x Kd

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67
Q

If 100% of RL is formed, _______ x Kd

A

100 x Kd

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68
Q

Kd or Ka is a constant?

A

Ka

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69
Q

If Ka is a constant, why does the binding increase with increasing concentrations?

A

there is a higher chance of R and L interacting if there is more ligand

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70
Q

How can you tell if a ligand has a stronger affinity than another?

A

If it can reach Kd (50% saturated) with less [L] then its stronger
* smaller Kd = stronger

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71
Q

If affinity or avidity stronger?

A

avidity

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72
Q

What is apparent Kd?

A

(avidity) when expected Kd is different from ther actual Kd

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73
Q

Why is avidity stronger?

A

grabbing 2 ligands at once is much stronger (multivalent/multiple binding interactions)
* like doing a pull up with both hands instead of 1

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74
Q

What 2 things are required for avidity?

A
  1. R or L to be attached to a surface
  2. other component has to have multiple binding sites
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75
Q

Does avidity or affinity have a smaller Kd if its the same interaction?

A

avidity (stronger)

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76
Q

What is responsible for the different affinities between molecules?

A

non-covalent interactions

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77
Q

What is the most important interaction for specificity?

A

van der Waal

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78
Q

How can antibodies disrupt non-covalent interactions to neutralize a microbe?

A

antibody will have higher affinity (lower Kd) for receptor where microbe wants to bind and blocks it

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79
Q

What is a hypersensitivity reaction?

A

when the immune system responds inappropriately to innocuous antigens

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80
Q

What does anaphylaxis stand for?

A

against protection

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81
Q

What is the recognition molecule for type 1 HSR?

A

IgE

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82
Q

What is the effector mechanism for type 1 HSR?

A

granulocytes degranulation

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83
Q

What are the 3 phases of type 1 HSR?

A
  1. sensitization phase
  2. early effector
  3. late phase
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84
Q

What happens during the sensitization phase of type 1 HSR?

A

exposure to antigen

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85
Q

What happens during the early effector phase of type 1 HSR?

A
  • mast cell degranulation mediated by IgE–FcERI
  • release of primary and secondary mediators
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86
Q

What happens during the late phase of type 1 HSR?

A
  • cytokine production
  • granulocytes recruitment
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87
Q

What are the steps of the early effector phase of type 1 HSR?

A
  1. IgE binds to FcERI
  2. free antigen (multivalent) binds to IgE-FcERI
  3. receptors cluster and induce degranulation signaling
  4. mediators released
88
Q

What T cells promote IgE class switching?

89
Q

Where does somatic hypermutation occur on an antibody?

A

Fab region

90
Q

Where does isotype switching occur on an antibody?

91
Q

What is unique about IgE?

A

3 domain Fc structure
binds high affinity to FcERI
low in blood

92
Q

What Ig is similar to IgE’s Fc region?

A

IgM (pentameric)

93
Q

Will IgE bind to FcERI even with no antigen present?

A

yes, no signaling will occur though

94
Q

What isotype is low in the serum?

95
Q

Where are mast cells located?

A

tissue (final epithelial layer)

96
Q

Where are basophils found?

97
Q

Where are eosinophils found?

A

blood (migrate to tissue)

98
Q

Where are neutrophils found?

99
Q

What granulocyte is critical for the late phase response of type 1 HSR?

A

eosinophils

100
Q

What type of antigens/molecules can bind to IgE’s Fab region?

A

proteins and glycoproteins

101
Q

What does it mean when an allergen has proteolytic activity?

A

can cut through the epithelial cell barrier

102
Q

What are the steps of the IgE SIGNALING cascade?

A
  1. allergen binds to IgE–FcERI
  2. FcERI clusters = activated Lyn
  3. Lyn phosphorylates ITAMs
  4. Syk recruits SH2 domain to ITAMs
  5. Syk autophosphorylates
  6. PLC-g is activated
  7. degranulation, PLA activation, cytokine production
103
Q

What is the difference between primary and secondary mediators?

A

primary: already stored in granules
secondary: must be synthesized

104
Q

What are 2 examples of primary mediators?

A

histamine
heparin

105
Q

What are primary mediators derived from?

A

decarboxylated histidine

106
Q

How many histamine receptors do humans have?

107
Q

Which histamine receptor do anti-histamines target?

108
Q

What are 3 examples of secondary mediators?

A

Leukotrienes
Prostaglandins
IL-1/TNF-a

109
Q

Degranulation activates PLA which will generate ____________ to produce leukotrienes and prostaglandins

A

Arachidonic acid (AA)

110
Q

What enzyme pathway synthesizes leukotrienes?

A

lipoxygenase

111
Q

What enzyme pathway synthesizes prostaglandins?

112
Q

What are the steps of leukotriene synthesis?

A
  1. PLA + phospholipids
  2. AA
  3. LOX
  4. cys-LTR1 (receptor)
113
Q

What are the steps of prostaglandin synthesis?

A
  1. PLA + phospholipids
  2. AA
  3. COX 1&2
  4. DP1 & CRTH2 (receptors)
114
Q

How does Montelukast (Singulair) prevent asthma symptoms?

A

prevents leukotrienes from binding to their cys-LTR

115
Q

What is TNF-a?

A

inflammatory cytokine

116
Q

Where is TNF-a stored?

A

mast cell granules

117
Q

What increases in expression when TNF-a is expressed?

A

selectin and integrins

118
Q

What ROS do eosinophils produce?

A

major basic protein (MBP)

119
Q

What ROS do neutrophils produce?

A

myeloperoxidase (MPO)

120
Q

What enzyme turns hydrogen peroxide into hypochlorous acid in ROS?

A

myeloperoxidase (MPO)

121
Q

What enzyme turns L-arginine into nitric oxide in (RNS)?

122
Q

What happens to nitric oxide if its high in concentration?

A

combines with superoxide anion and become peroxinitrite

123
Q

What happens to nitric oxide if its low in concentration?

A

its a signaling molecule

124
Q

What induces iNOS?

A

epithelial cell damage
TH2 inflammatory cytokines

125
Q

What are the 3 effects of peroxinitrite

A
  1. inactivates mitochondria (apoptosis)
  2. oxidizes proteins (inactivates enzymes)
  3. DNA damage (necrosis)
126
Q

What is a systematic reaction of type 1 HSR?

A

anaphylaxis

127
Q

What is a localized reaction of type 1 HSR?

A

hives, asthma, eczema

128
Q

What 4 things affect the severity of clinical symptoms of type 1 HSR?

A
  1. route of allergen
  2. concentration of allergen
  3. prior exposure
  4. host pre-disposition
129
Q

How does epinephrine prevent anaphylaxis?

A

binds to beta adrenergic receptors which will counteract mediators by relaxing smooth muscles and reducing vascular permeability
andis vasoconstrictive

130
Q

What receptor does epinephrine bind to inhibit the allergic response?

A

GCRP alpha & beta adrenergic receptors

131
Q

Besides opening the airways what does epinephrine do for the heart?

A

increases cardiac output (increased BP)

132
Q

What drug is a leukotriene antagonist?

133
Q

What 4 things do corticosteroid do to inhibit immune response?

A
  1. anti-inflammatory (block mediators)
  2. immunosuppressant (suppress T cells)
  3. anti-proliferative (inhibit epidermal cell turnover)
  4. vasoconstrictive (inhibit histamine)
134
Q

What does glucocorticosteroids inhibit to stop inflammation?

A

NfkB nuclear factor

135
Q

All pattern recognition receptors activate _________

136
Q

SCITs are a type of _____sensitization therapy

A

hyposensitization

137
Q

What are SCITs?

A

atopic patients are slowly exposed to more and more allergen

138
Q

What is the overall goal of SCITs?

A

divert the TH2 response from pathogenic to tolerant

139
Q

What are the steps of SCITs mechanism?

A
  1. TH2 diverts to Treg via IL-10
  2. IgE is not made and now IgG is
  3. IgG binds to FcGRIIB receptor
  4. SHIP phosphatase is recruited by ITIMS and FcGRIIB and removes the phosphate group from ITAMs
  5. signal cascade is blocked
140
Q

What is the inhibitory version of FcERI?

141
Q

Which cytokine induces IgE class switching?

142
Q

Which cytokine induces IgG class switching?

143
Q

What does SHIP phosphatase inhibit?

A

Lyn phosphorylating ITAMS

144
Q

Beta-2 agonists use the same receptor as?

A

epinephrine

145
Q

What does FEV stand for?

A

force expiratory volume

146
Q

What does PEF?

A

peak expiratory force

147
Q

What type of TH cells may promote tolerance?

148
Q

What immune homeostasis?

A

balance between activation and suppression on barrier surfaces

149
Q

How do you find Kd on a binding curve?

A

go to 50% on y axis and and move down to [L] on x axis

150
Q

The relationship between _____ and RL formation is the same for all interactions

151
Q

Why are molecules repulsed from one another in van der Waal interactions?

A

steric repulsion

152
Q

What cytokine initiates the transition to the late phase response?

153
Q

What is the mechanism of anti-IL5Ra therapy?

A

blocks IL-5 receptor and induces AMCT

154
Q

What is the mechanism of anti-TSLP therapy?

A

prevent CD4 cells from commiting to the Th2 lineage

155
Q

What is the mechanism of anti-IL4 AMG317 therapy?

A

blocks IL-4Ra receptor because IL-13 or IL-4 both use it
- doesn’t work well because its outcompeted
- TYPE2 IL-4R

156
Q

What is the mechanism of IL-4Ra therapy?

A

blocks IL-4Ra receptor because IL-13 or IL-4 both use it
- worked

157
Q

What is the mechanism of anti-IL13 therapy?

A

blocks IL-13 or its receptor
- doesnt work very well because IL-4 picks up the pace

158
Q

What is the mechanism of anti-IgE therapy?

A

bind to IgE Fc region and prevents it from binding to FcERI

159
Q

What does SHIP phosphatase do for FcGRIIB?

A

removes phosphate from ITAMs to inactivate them

160
Q

Does FcGRIIB use ITAMs or ITIMS?

161
Q

What is unique about IgE?

A

low in serum
binds high affinity to FcERI

162
Q

Why did anti-IL5 therapy initially not work?

A

Patients with asthma were chosen not eosinphil asthma

163
Q

How do you choose what therapy is right for a certain diseae?

A

target the most important cytokine or its receptor

164
Q

What are 3 examples of biomarkers?

A

blood eosinophil levels
FeNO
serum IgE

165
Q

What increases the level of FeNO in the breath?

A

inflammation that causes epithelial cell damage

166
Q

What does IgE bind to with high affinity?

167
Q

When does atopic dermatitis onset usually?

A

early in life

168
Q

What makes AD atopic?

A

elevated IgE
family history (genetics)

169
Q

What 4 things affect AD?

A
  1. environment (pollution or diet)
  2. skin microbes
  3. epithelial barrier dysfunction (FLG mutation)
  4. immune response (core Th2 response)
170
Q

What is the mutation in AD patient?

171
Q

What cytokine is AD most reliant on?

172
Q

What cytokine is asthma most reliant on?

173
Q

What is the FLG gene important for?

A

cross linking epithelial layer making it strong

174
Q

What does the mutation in the FLE gene cause?

A

disruption of skin layers causing microbiome to get where it shouldn’t

175
Q

The FLE mutation is most common in what race and less common in what race?

A

common: white/asian
less common: african american

176
Q

In asian people, AD is more mediated IL-__/TH___

A

IL-17
TH17

177
Q

What does it mean that asian people’s AD is more reliant on TH17/IL-17?

A

AD is not just TH2 mediated but also POLARIZING TH17 mediated activation depending on race

178
Q

African americans are higher in TH___ response

179
Q

What is the atopic march?

A

If you have AD as an infant you will likely have food allergies –> asthma –> rhinitis

180
Q

How do anticholingerics work?

A

reduce swelling by binding acetylcholine to the M2 receptor which block ACs function

181
Q

What happens when AC is in the airways?

A

induces bronchial spasms and hyper-reactivity

182
Q

What happens to the M2 receptor when eosinophils in the airway degranulate?

A

the major basic protein released in the granules binds to the inhibitory receptor M2 and now acetylcholine is not inhibited = bronchial spasms and hyper-reactivity

183
Q

Where are type 1 IL-4R found?

A

lymphocytes

184
Q

Where are type 2 IL-4R found?

A

epithelial cells, goblet cells, smooth muscles

185
Q

Type 1 and Type 2 IL-4R share ___________ but have different _________

A

share: IL-4Ra
different: 2nd chains

186
Q

What do all of the Ig isotypes do?

A

neutralize

187
Q

What is IgM responsible for? (chart)

A

complement activation

188
Q

What are all the IgGs responsible for? (chart)

A

opsonization

189
Q

What is IgG1 responsible for? (chart)

A

everything

190
Q

What is IgG2 responsible for? (chart)

A

neutralization
opsonization
complement activation

191
Q

What is IgG4 responsible for? (chart)

A

neutralization
opsonization

192
Q

What is IgE responible for? (chart)

A

mast cell and basophil sensitization

193
Q

What region of IgE binds to FcERI?

194
Q

What cells make IgE?

A

plasma cells

195
Q

What is special about TSLP?

A

epitheial derived cytokine showing that there are different mechanisms of activation

196
Q

How is IL-4 receptor polymorphic?

A

people have differences in the genes encoding IL-4Ra

197
Q

Atopic Dermatitis is an IL-___ dominant disease

198
Q

Psoriasis is an IL-____ /Th___dominant disease

A

IL-23/Th17

199
Q

What cytokines are elevated in AD?

A

IL-36
IL-13
IL-20

200
Q

What cytokines are elevated in psoriasis?

A

IL-17
IL-36
IFN
IL-20

201
Q

What cytokine was surprisingly low in AD?

202
Q

What cytokines were used to differentiate psoriasis skin from AD skin?

A

IL-17
IL-4
IL-13

203
Q

What was the overall goal of the AD paper?

A

comparing AD and psoriasis using RNAseq

204
Q

What are the 3 AD-specific molecular findings reported by this paper?

A
  1. IL-13 as a predominate cytokine and IL-4 as a less significant
  2. more dysregulated long noncoding RNA
  3. heterogeneity
205
Q

What three distinct features are associated with AD?

A
  1. issues involving the integrity of the epidermal
  2. other IgE-mediated immune problems like asthma
  3. increased vulnerability for infection.
206
Q

How strong is the comorbid relationship between AD and Asthma? and why?

A

Very strong, 60%
IL-13 and IL-4 share a receptor

207
Q

The AD paper suggests that chronic AD shares a molecular component with Psoriasis. What is that component?

A

Chronic AD and psoriasis both have over activation of TH1 which secretes INF-g causing the inflammatory response.

208
Q

What is the current optimal therapeutic for AD and Asthma?

A

combo anti-IL4/IL-13 therapies

209
Q

IL-____ and IL-___ encourage the production of IgE

A

IL-4 and IL-13

210
Q

What therapy causes apoptosis of eosinophils?

A

Anti-IL5Ra

211
Q

What drug does not work for asthma therapy?

A

Anti-IL13s

212
Q

List 3 granulocytes and their locations?

A
  1. mast cells - tissue
  2. eosinophils - blood
  3. basophils - blood
213
Q

What is a major primary mediator stored in granules?

214
Q

What drug binds to B adrenergic receptors?

A

epinepherine

215
Q

What are 2 mechanisms of SCITs?

A
  1. Th2 —> Tregs (IL-10)
  2. IgE —> IgG
216
Q

What is a major transcription factors inhibited by corticosteroids?

217
Q

What race had the highest IgE serum levels in AD?

A

african american

OLD "MIC 661" (19 decks)

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