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OLD "MIC 661" > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is the hygiene hypothesis?

A

lack of exposure in early childhood to infectious agents and possible allergens results in a higher likelihood of developing hypersensitivity issues

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2
Q

Type I HSR are mediated by what Ab isotype?

A

IgE

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3
Q

Type ___ HSR is responsible for allergies

A

type 1

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4
Q

What are the polarizing and effector cytokines of Tregs?

A

polarizing: IL-2, TGF-B
effector: IL-10, TGF-B

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5
Q

What are the polarizing and effector cytokines of TH17?

A

polarizing: IL-1, IL-6, IL-23, TGF-B
effector: IL-17, IL-22

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6
Q

What are the polarizing and effector cytokines of TH2?

A

polarizing: IL-4
effector: IL-4, IL-5, IL-13

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7
Q

What are the polarizing and effector cytokines of TH1?

A

polarizing: IL-12, IL-18, IFN-g
effector: IFN-g, TNF

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8
Q

Atopic individuals have a skewed _____ response

A

TH2

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9
Q

What T cell subset is important for type I HSR?

A

TH2

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10
Q

What is tonic signaling?

A

immune skewing above the baseline set by barrier surface microbiome and other factors (sex, age, weight, …)

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11
Q

What are 4 types of non-covalent interactions?

A
  1. hydrogen bonds
  2. ionic bonds
  3. van der Waal interactions
  4. hydrophobic interactions
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12
Q

What unit is the Kd measured in?

A

M

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13
Q

What unit is the Ka measured in?

A

M-1

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14
Q

Kd and Ka are _________ of each other

A

inverses

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15
Q

What is the Kd?

A

concentration of L when 50% of RL complex is formed

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16
Q

When 10% of RL is formed = ____xKd

A

0.1

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17
Q

When 50% of RL is formed = ____xKd

A

1

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18
Q

When 90% of RL is formed = ____xKd

A

10

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19
Q

When 100% of RL is formed = ____xKd

A

100

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20
Q

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

A

increasing concentration increases the probability of an interaction between R and L

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21
Q

The smaller the Kd the better or worse the affinity?

A

better

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22
Q

What is avidity?

A

enhanced affinity interaction due to multiple binding interactions

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23
Q

What 2 things are required for avidity?

A
  1. R of L attached to surface
  2. requires other complement to have multiple binding sites
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24
Q

What non-covalent interaction is important for specificity?

A

van der Waal

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25
Q

What is a hypersensitivity reaction?

A

when the immune system responds inappropriately to innocuous antigens

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26
Q

What is the effector mechanism of type I HSR?

A

degranulation

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27
Q

What are the 3 phases of type I HSR?

A
  1. sensitization phase
  2. early effector phase
  3. late phase response
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28
Q

What happens in the early effector phase of type I HSR?

A

IgE + allergen binds to FCERI on mast cells = release of primary and secondary mediators

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29
Q

What happens in the late phase of type I HSR?

A

TH2 and granulocyte recruitment and cytokine release

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30
Q

What 2 things are special about IgE?

A
  1. low in serum
  2. binds high affinity to FCERI
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31
Q

Mast cells, TH2 cells, and eosinophils produce _____ to induce IgE class switching

A

IL-4

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32
Q

What high affinity receptor does IgE bind to?

A

FCERI

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33
Q

Where are mast cells found?

A

tissue

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34
Q

Why are mast cell usually the first granulocyte to encounter IgE bound to an allergen?

A

they are stored in the tissue close to sites of entry

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35
Q

What are the 3 products of IgE–FCERI signaling cascade?

A
  1. degranulation
  2. PLA
  3. cytokine production
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36
Q

What is an example of primary mediator of type I HSR?

A

histamine

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37
Q

What are 2 examples of secondary mediators in type I HSR?

A

leukotrienes
prostaglandins

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38
Q

PLA —> _______ —–> prostaglandins and leukotrienes

A

arachidonic acid (AA)

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39
Q

What pathway does prostaglandin synthesis use?

A

COX2

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40
Q

What pathway does leukotriene synthesis use?

A

lipoxygenase

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41
Q

What is the product of leukotriene synthesis?

A

cys LTR1

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42
Q

What is the product of prostaglandin synthesis?

A

DP1 and CRTH2 receptors

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43
Q

Montelukast (Singulair) blocks synthesis of ________ which aids in asthma symptoms

A

cys LTR1 (leukotrienes)

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44
Q

Eosinophils produce ______ in their granules

A

MBP

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45
Q

ROS in granulocytes produce _________

A

myeloperoxidasee

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46
Q

Neutrophils produce ______ in their granules

A

MPO

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47
Q

RNS combined with ROS in granulocytes produce ________

A

peroxynitrite

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48
Q

What are the 3 results of iNOS exposure?

A
  1. apoptosis
  2. protein damage
  3. necrosis
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49
Q

RNS in granulocytes produce _________

A

iNOS

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50
Q

What cytokine initiates the transition to the late phase response of type I HSR?

A

TNF-a

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51
Q

What are some things that affect the severity of type I HSR?

A

route
concentration
prior exposure
predisposition

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52
Q

Epinephrine binds to ___________ to counter act meditators and improves cardiac output

A

a+B adrenergic receptor

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53
Q

Steroids inhibit _______ signaling to stop inflammation

A

NfkB (pro-inflammatory transcription factor)

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54
Q

What is the goal of SCITs?

A

divert the TH2 response in atopic individuals

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55
Q

How do SCITs divert the TH2 response?

A
  1. induce IL-10 signaling to inhibit IL-4 (TH2)
  2. shifts IgE–>IgG which can bind to inhibitory receptor = block degranulation
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56
Q

What is SHIP phosphatase?

A

inhibits IgE-Lyn phosphorylation and blocks mast cell activation
* uses ITIMs

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57
Q

beta-2 agonists use the same receptor as __________

A

epinephrine (a+b adrenergic receptor)

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58
Q

What is FEV?

A

forced expiratory force

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59
Q

What is PEF?

A

peak expiratory flow

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60
Q

What are 2 biomarkers for asthma?

A

FeNO (nitric oxide)
eosinophil levels

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61
Q

What are anticholinergics?

A

allows acetylcholine to bind to M2 in airways (inhibitory receptor) instead of eosinophil MBP

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62
Q

Type II IL-4/13 receptors are found on _________, __________, ________

A

epithelial cells, smooth muscles, and endothelial cells

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63
Q

What happens when acetylcholine is not able to bind to M2 in airways and MBP from eosinophils take place?

A

bronchial spasms and hyper reactivity

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64
Q

Type I IL-4/13 receptors are found on _________

A

lymphocytes

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65
Q

Type I IL-4/13 receptor is made of what chains?

A

IL-4R a
gc

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66
Q

Type II IL-4/13 receptor is made of what chains?

A

IL-4R a
IL-13R a

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67
Q

Is type I or II IL-4/13 receptor unique for IL-4?

A

type I

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68
Q

Atopic dermatitis is IL-___ dominant

A

IL-13

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69
Q

Asthma is IL-_____ dominant

A

IL-4

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70
Q

What is the genetic mutation in AD?

A

FLG gene

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71
Q

What does the FLG gene do?

A

crosslinks epidermal layer so its strong

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72
Q

FLG mutation is common in what race?

A

europeans and asians

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73
Q

What race has higher IL-17/TH17 levels in AD?

A

asians

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74
Q

FLG mutation is less common in _____________ but their AD is just as severe

A

african americans

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75
Q

What race has the highest IgE/Th2 response and a very low Th17/22 response?

A

african americans

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76
Q

Why is it important that AD is mediated differently in different races?

A

AD is not just mediated by TH2 but also TH17 due to polymorphisms

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77
Q

What is the polymorphism in AD regarding races?

A

(Q576R) IL-4 Ra gene mutation

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78
Q

What does atopic mean?

A

predisposition to allergic responses involving IgE

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79
Q

What is the atopic march?

A

AD showing up early in life opens the door for food allergies –> asthma —> rhinitis

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80
Q

What are the 3 distinct features of AD?

A
  1. epithelial barrier dysfunction
  2. susceptibility to infections
  3. atopic features (rhinitis and asthma)
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81
Q

What is the role if IL-5 in type I HSR?

A

eosinophil activation

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81
Q

What is the role if IL-4 in type I HSR?

A

IgE class switching

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82
Q

What are the 4 major steps in the primary immune response?

A
  1. antigen–DC
  2. DC–T cell
  3. antigen–B cell
  4. T cell – B cell
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83
Q

MHC class 1 is presented on _______ cells

A

all cells

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84
Q

MHC class II is presented on _____, _____, _____ cells

A

macrophages, DC, B cells

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85
Q

What 3 protein interactions are required for T cell–DC?

A

B7—CD28
MHC—TCR
CD4/8

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86
Q

What cytokine aid in T cell proliferation?

A

IL-2

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87
Q

What 3 protein interactions are required for T cell —-B cell?

A

TCR — MHC II
CD40L—CD40
CD4

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88
Q

Ig___ is highly efficient in complement activation

A

IgM

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89
Q

Ig__ and Ig__ are high efficient in activating NK cells

A

IgG1
IgG3

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90
Q

Ig___ all function as opsins

A

IgG

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91
Q

What is a type II HSR?

A

IgM/IgG recognition of innocuous cell surface molecules as foreign leading to Ab-mediated death

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92
Q

What are the 3 mechanisms of Ab-mediated death in type II HSR?

A
  1. MAC
  2. ADCC
  3. phagocytosis
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93
Q

What binds to IgM first in complement activation?

A

C1q

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94
Q

NK cells express _____ and bind to antibodies Fc region to induce ADCC

A

FCgRIII

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95
Q

Ig___ is the most common isotype promoting ADCC

A

IgG1

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96
Q

What is released when NK cells kill?

A
  1. FASL
  2. granzymes
  3. perforins
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97
Q

How does Ab-mediated phagpcytosis work?

A

Ab binds to antigen on cell surface and Fc receptor on phagocytes detect and engulf it

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98
Q

What are 3 examples of type II HSR?

A
  1. mismatched blood transfusion
  2. hemolytic disease in newborns
  3. drug induced anemia
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99
Q

What is mismatched blood transfusions?

A

IgM binds to blood antigens recognized as foreign resulting in MAC lysis

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100
Q

What is hemolytic disease of newborns?

A

IgG (pass barrier) binds to Rh antigen on fetal RBC (opsonization) resulting in lysis via NK cells of fetus

101
Q

Why do most people possess IgM against blood carb antigens they don’t express?

A

common microbes express similar carb antigens

102
Q

Why is lysis of red blood cells dangerous?

A

hemoglobin metabolizes into toxic billibrubin

103
Q

How does the Rho-gam therapy work?

A

Rh+ fetal cells enter mothers circulation, anti-Rh Ab bind and inactivate fetal Rh antigen before mother ever sees antigens

104
Q

What 2 mechanisms are used in rho gam to prevent detection of fetal Rh+ cells?

A
  1. inhibit B cell signaling via FCGRIIB
  2. Anti-D Ab binds to fetal RBC and is phagocytosed
105
Q

In hemolytic disease in fetus, Ig___ is responsible for the primary response while Ig___ is for the secondary response

106
Q

Why is a mother’s secondary exposure of D+ easier to achieve with fewer D+ RBC than the first exposure?

A

she has memory B cells which have a lower threshold for activation

107
Q

What are delayed type 4 HSR?

A

skin permeable antigens activate CD4+/Th1 cells resulting in sensitization followed by DT4H on second exposure

108
Q

What HSR is mediated by only T cells?

109
Q

Why is type 4 HSR “delayed”?

A

recruitment and activation of macrophages requires time

110
Q

What are the antigens for delayed type 4 HSR?

A

contact/skin permeable antigens

111
Q

What happens during the sensitization phase of DT4 HSR?

A

recognition, presentation, activation via IL-2, TH1 cells created, memory T cells made

112
Q

What T cell subset controls delayed type 4 HSR?

A

TH1 (CD4+)

113
Q

What are the 3 memory T cells?

A
  1. central
  2. effector
  3. resident
114
Q

Where are central memory T cells located?

A

circulation/SLT

115
Q

Where are effector memory T cells located?

A

circulatioon/SLT, tissues

116
Q

Where are resident memory T cells located?

117
Q

What is a marker for naive T cells?

118
Q

What is a marker for central, memory, and effector T cells?

119
Q

What is a marker for naive T cells and central memory T cells?

120
Q

What is a marker for resident T cells?

121
Q

Where are monocytes located?

122
Q

Where are macrophages located?

123
Q

What is the most important cell in delayed type 4 HSR?

A

macrophages

124
Q

What 2 cytokines activate and recruit macrophages?

A

IFN-g and TNF

125
Q

Draw the TH1 inflammatory loop

126
Q

What’s the initiator of the inflammatory loop for DT4 HSR?

127
Q

What’s the function of IL-12 in the inflammatory loop?

A

induces more TH1 cells

128
Q

What’s the function of TNF/IFN-g in the inflammatory loop?

A

activates macrophages

129
Q

What’s the function of IL-8 in the inflammatory loop?

A

neutrophil recruitment

130
Q

What’s the function of IL-6 & IL-1 in the inflammatory loop?

A

inflammation/fever

131
Q

What’s the function of CCL2 in the inflammatory loop?

A

recruits monocytes

132
Q

The inability of macrophages to clear a pathogen results in _________

A

granuloma formation

133
Q

What 2 things can cause granulomas?

A
  1. silica
  2. sutures
134
Q

What 2 cytokines are important for granuloma formation?

A

TNF-a and IFN-g

135
Q

If granuloma cannot clear pathogen blood vessel and tissue damage occurs how?

A

persistent activation of ROS/RNS

136
Q

What is in a TB skin test that induces a pure TH1 response?

137
Q

TB skin test is CD___/TH__ mediated

138
Q

What is the antigen in poison oak?

139
Q

Poison oak is CD___/TH___ mediated

140
Q

What 2 ways can CD8+ activate DCs?

A
  1. sequential activation
  2. cross presentation
141
Q

What is sequential activation?

A

DC —CD4 T cell interaction increases B7 levels, then DC interacts/activates CD8 T cell

142
Q

TB skin tests and poison oak are both types of ….

143
Q

DT4 HSR are CD___ T cell mediated

144
Q

What is cross presentation of CD8 T cells?

A

DC—-CD4 T cell interactions, then changes their antigen processing to present on MHC I which can activate CD8 T cells
(present extracellular antigen on MHC I)

145
Q

What is it called in cross presentation when DC switches thier antigen processing to present on MHC I?

A

cytosolic diversion

146
Q

CD4 T cell engagement help CD8 T cells activate by providing paracrine _____ in cross presentation

147
Q

TCRs recognize just the peptide presented?

A

No, interact with the MHC as well

148
Q

NKT cells recognize ____ presented by ____ on APCs

A

glycolipids
CD1d

149
Q

NKT cells DO NOT recognize…

A

MHC—peptide complex

150
Q

What is different about NKT cell’s TCRs?

A

no memory or diversity

151
Q

How does CD1a present lipids differently than how MHC presents peptides?

A

lipid is buried in CD1d and the A’ roof is what is recognized

152
Q

Is CD1a activated on LC cells when the A’ roof is blocked or unblocked?

153
Q

What causes A’ roof to be blocked in CD1a?

A

healthy skin lipid head causes steric hinderance

154
Q

In the interference model of CD1a, binding of TCR is soley based on _____ not _____

A

CD1a not ligand

155
Q

CD1__ is highly expressed on LC DCs

156
Q

CD1__ is expressed on NKT cells

157
Q

What linkage in skin is abnormal in atopic dermatitis?

A

fillagrin linkages

158
Q

What are corneocytes?

A

keratinocytes without nucleus

159
Q

Where are regular LC DCs located?

160
Q

When LC DCs sample a foreign lipid with its CD1a what T cell subset is produced?

161
Q

How does the skin sense PPD from TB skin test?

A

injected directly into dermis by passing LC DCs and being sensed by dermal DCs and macrophages

162
Q

NKT cells use CD1__ and LC DCs use CD1__

A

NKT: CD1d
LC DC: CD1a

163
Q

Only CD1___ has an A’ roof

164
Q

Why is there no diversity for TCR recognizing CD1a—lipids?

A

The A’ roof is the same for all receptors

165
Q

What 2 things are special about NKT cells?

A

Invariant TCR (no diversity)
Only identified glycolipids

166
Q

INF-g and TNF are important for what 2 things?

A

Macrophage recruitment
Granuloma formation

167
Q

What is an autoimmune reaction?

A

immune response to self antigen

168
Q

What is central tolerance?

A

T cell development/selection (removing auto reactive T cells)

169
Q

What is peripheral tolerance?

A

When self-reactive T cells escape into the periphery, peripheral tolerance ensures that they are deleted or become anergic

170
Q

What are the 4 outcomes of Treg–MHC interaction?

A

IL-10 expression
CTLA-4 expression
IL-2R upregulation
linked expression

171
Q

When Tregs and MHC interact, what is the purpose of IL-10 expression?

A

inhibits MHC on APCs
inhibits B7/CD28
inhibits TNF-a and IL-6

172
Q

When Tregs and MHC interact, what is the purpose of CTLA-4 expression?

A

binds with B7 on APC to induce anergy

173
Q

When Tregs and MHC interact, what is the purpose of IL-2R (CD25) being up regulated?

A

binds IL-2 = outcompetes for T cell activation

174
Q

When Tregs and MHC interact, what is the purpose of linked expression?

A

Treg can bind and inhibit 2 T effectors bound to an APC

175
Q

What is the steps of central tolerance for T cells?

A

HSC
blood
double negative
thymus cortex (positive selection)
double positive
thymus medulla (negative selection)
single positive
blood

176
Q

Where does positive selection happen?

A

thymus cortex

177
Q

Where does negative selection happen?

A

thymus medulla

178
Q

What is positive selection?

A

T cell is functional and equipped to make a response against foreign antigens

179
Q

What is negative selection?

A

deletes T cells with high affinity for self-peptides via apoptosis, thus ensuring self tolerance

180
Q

What presents to double positive T cells in positive selection?

A

cTEC/DC/macrophage

181
Q

What presents to single positive T cells in negative selection?

A

AIRE + mTECs

182
Q

Transport of single positive T cells out of thymus is mediated by ________

A

Transport of single positive T cells out of thymus is mediated by ________

183
Q

What does the drug FTY720 prevent autoimmune T cells?

A

binds to S1PR on T cells to prevent them from leaving the thymus (prevents auto reactive T cells from leaving the thymus)

184
Q

What is the disorder APECED?

A

mutation in AIRE causing there to be not presentation of self during negative selection

185
Q

Why are people with APECED prone to yeast infections?

A

IFN-a and IL-17 activity id blocked which is important for Th17 functions of protection against fungi

186
Q

What are 3 trademarks for APECED?

A

reduced expression of self-antigen
reduced IFN-a (due to anti-cytokine Ab)
reduced IL-17 (due to anti-cytokine Ab)

187
Q

APECED patients also have loss of B cell tolerance, how does this happen?

A

B cells depend on T cells for SHM
auto-reactive T cells make conjugate pair with B cells = auto-reactive Ab

188
Q

What T cells mediate psoriasis?

189
Q

What are 3 alterations of skin in psoriasis?

A

redness
skin thickening
white scales

190
Q

What causes the redness in psoriasis?

A

vasodilation and inflamed endothelial cells

191
Q

What causes the skin thickening in psoriasis?

A

hyper-proliferation of keratinocytes

192
Q

What causes the white scalees in psoriasis?

A

parakeratosis (top layer of keratinocytes won’t loose nucleus and die)

193
Q

Because of the dysfunction of skin in psoriasis what 3 things occur making it a skin barrier dysfunction disease?

A

improper skin stacking
improper secretion of lipids
improper adherence of keratinocytes

194
Q

What is psoriasis area and severity index (PASI) score?

A

observational score determined by severity and amount covering skin

195
Q

What are the 4 histological changes in psoriasis?

A

corneum becomes thick and broken
epidermis is much larger than normal
dermis has enlarged blood vessels
immune infiltrates (DC and T cell clusters)

196
Q

Are keratinocytes or T cells the driving force of psoriasis and why?

A

T cells
IL-2R on T cells is important for T cell proliferation

197
Q

What molecule produced by keratinocytes causes formation of new blood vessels?

198
Q

What 2 cytokines heavily affect keratinocytes?

A

IL-17
IL-22

199
Q

Immune signaling in psoriasis…
neutrophils produce ______

200
Q

Immune signaling in psoriasis…
pDCs produce __________

A

lots of INF-a

201
Q

Immune signaling in psoriasis…
TH1 cells produce _____ and recruit ______

A

TNF-a

macrophages

202
Q

Immune signaling in psoriasis…
keratinocytes produce _____, ____, and ______

A

IL-1
IL-6
TNF-a

203
Q

What is the specific antigen for psoriasis?

204
Q

The basic dysfunction of psoriasis is _________ imbalance

205
Q

IL-___ is the most important cytokine for psoarisis

206
Q

What are the 2 types of IL-2 receptors?

A

type I: low affinity
type II: high affinity

207
Q

What is type I IL-2 receptor made of?

A

low affinity
IL-2R beta + IL-2R gamma

208
Q

What is type II IL-2 receptor made of?

A

high affinity
IL-2R alpha + IL-2R beta + IL-2R gamma

209
Q

What chain in IL-2R type II makes it high affinity?

210
Q

What 3 interactions/signals are required for T cell activation?

A

MHC–TCR
B7–CD28
autocrine IL-2

211
Q

A proposed mechanism of psoriasis is that specific HLA class I alleles are expressed what other mechanism backs up this claim?

A

CD8+ cells (T17 or T1 cells) found in lesions

212
Q

HLA-B___ is a risk factor for psorasis

213
Q

What are 4 characteristics of IFN-a?

A

pleiotropic (multiple functional cytokine)
anti-viral
immunomodulator (up-regulates MHC)
anti-proliferative (shuts down protein synthesis)

214
Q

What signaling cascade does IFN-a R1 and 2 use?

A

JAK/TYK/STAT

215
Q

What are 3 psoriasis therapeutics we talked about that targets IFN-a?

A

TYK2 inhibitor
anti-IFNa R1 Ab
anti BCDA2 Ab

216
Q

How does TYK2 inhibitor prevent psoriasis?

A

blocks IFN-a signaling pathway in cells

217
Q

How does anti BCDA2 Ab prevent psoriasis?

A

prevents pDC from activating and secreting IFN

218
Q

What are 3 ways to measure IFN signaling?

A

measure MHC up-regulation
measure STAT phosphorylation
detect expression of ISG (IFN stimulated gene)

219
Q

What are 3 pieces of evidence what pDCs are important in psorasis?

A

psoriatic skin has active IFN-a signaling pathways
excessive IFN signaling
treatment with IFN-a will make psoriasis worse

220
Q

What are 2 markers for pDCs?

A

BDCA-2/CD123
CD86

221
Q

How do pDCs produce so much IFN-a?

A

pDCs TLR-7 (endosomal receptors) sense DNA/RNA inside of cell endosome (where viral DNA is sensed)

222
Q

How do pDCs recognize self-DNA if its inside the endosome in the cell?

A

LL37 converts self-DNA by binding to DNA, causing it to aggregate and cluster, triggering TLR-7

223
Q

What induces LL37 function?

A

IL-17 mediated keratinocyte damage

224
Q

Entry of LL37/DNA complex induces activation of _____ of pDCs

225
Q

What does IL-17 recruit?

A

neutrophils

226
Q

What are 3 inflammatory cytokines?

A

TNF-a
IL-1B
IL-6

227
Q

What is TNF-a main function?

A

master regulator

228
Q

What is IL-1B main function?

A

fever response

229
Q

What is IL-6 main function?

A

produces acute phase proteins

230
Q

What cell produces the inflammatory cytokines, TNF-a, IL-1B, and IL-6?

A

macrophages

231
Q

______ is required for production of IL-1B and IL-6

232
Q

TNF-a increases what 2 things?

A

vascular permeability
adhesion molecules

233
Q

What inflammatory cytokine activates macrophages?

234
Q

What is an example of an acute phase protein?

235
Q

What 2 things are special about IL-1B?

A

no gene transcription is required to make it
cannot leave the cell unless leakage occurs

236
Q

What are 3 functions of neutrophils?

A

phagocytosis
degranulation
NETosis

237
Q

What do neutrophil nets contain?

A

LL-37 (AMP)
histones
proteases
DNA

238
Q

What does PAD4 do?

A

de-condenses chromatin by changing charge on Arg causing histones to release DNA

239
Q

What is a type III HSR?

A

abnormal immune response mediated by the formation of immune complexes

240
Q

Where does citrullination occur?

A

neutrophils

241
Q

What activates PAD4?

A

pore forming toxins produced by bacteria

242
Q

What are ACPAs?

A

anti-citrullinated protein antibodies

243
Q

What is epitope spreading?

A

Ab recognizes different epitopes on the same protein causing the creation of many types of auto-Abs

244
Q

What is the role if IL-13/4 in type I HSR?

A

promotes eosinophil trafficking

245
Q

What is the antigen for Type I HSR?

A

innocuous/environmental antigens

246
Q

What are the important cytokines for type I HSRs?

A

IL-13
IL-5
IL-4

247
Q

Anti-citrullinated Ab indicates what disease?

248
Q

Anti-dsDNA Ab indicates what disease?

249
Q

Anti-mylein Ab indicates what disease?

250
Q

What activates macrophages?

OLD "MIC 661" (19 decks)

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