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Immunology Block 4 > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

type I hypersensitivity

A

immediate - following rexposure to antigen they are hypersensitive to the response is immediate, can detect within minutes

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2
Q

type I hypersensitivity is mediated by Ig

A

E

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3
Q

type II hypersensitivity are mediated by Ig

A

M or IgG

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4
Q

type II hypersensitivity is result of

A

antibody eing generated against a cel surface antigen

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5
Q

type III hypersensitivity is mediated by Ig

A

usuallyu IgG

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6
Q

type III hypersensitivyt

A

formation of immune complexes b/c it is soluble antigen, deposition of antibody antigen complexes at particular sites in body that gives rise to symptoms

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7
Q

Type IV hypsersensitivity is mediated by

A

t cells

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8
Q

type IV hypersensitivity

A

delayed reaction, will take two or more days, mediated by T lymphocytes

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9
Q

type IV hypersensitivity is similar to

A

type I response

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10
Q

what t cell type is involved in DTH response

A

Th1

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11
Q

inhaled antigens generally give rise to what hypersensitivity response

A

type I

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12
Q

materal into circulation (injection, drugs, etc.) generally gies rise to what hypersensitivity response

A

I or III

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13
Q

ingested materials generate what hypersensitivity response

A

type I

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14
Q

result of allergins, especially chemicals and metal ions in contact with skin, like poison ivy or nickel generate what hypersensitivity response

A

type IV

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15
Q

type I hypersensitivity response results form allergin rexposure binding to

A

IgE coated on surface of mast cells

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16
Q

IgE response against alergin than what Th response is involved

A

Th2

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17
Q

to get type I hypersensitivity response you need

A

IgE

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18
Q

IgE is found in very low concentrations inserum, majority is foudn bound to

A

high affinity receptors Fcepsilon RI on mast cells

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19
Q

once allergin is reintroduced into individual sensitized to the allergin, the allergin can crosslink

A

Fcepsilon receptors

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20
Q

for alergin to cross link Fcepsilon receptors there has to be at least

A

two antibodies specific for that antigen bound to that mast cells

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21
Q

type I response has two phases:

A

early stage and late stage

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22
Q

Type II HRS is with antibody produced against

A

surface antigen

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23
Q

once antibody binds to antigen in type II HRS

A

destruction of cell, drug induced hemolytic anemia

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24
Q

type III HRS

A

antibody produced against soluble protein, antibody produced by B cell specific for foreign protein will form immune complexes that can be in walls of blood vessels, which will activate complement, so anything downstraem is initaited by activation of classical pathway of complement, including neutrophil of netrophil

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25
Q

what from complement recruits neutrophil

A

C5a

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26
Q

type IV HRS

A

not antibody mediated, response by Th1 cells, normal self proteins beingind to surface protein, so self peptide presented by DC or langerhans going to regional lymph node and it will be recognized as foreign by t cell and they will migrate back to site of exposure and activate macrophages to do classic cell mediated response

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27
Q

soluble anigen being recongized by IgE and mast cell activation and degranulation is

A

Type I HRS

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28
Q

most serious result of type I HRS

A

anaphylatic shock

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29
Q

mediated by IgG or IgM, directed against moleculs on surface of cell, that can result in destruction of cell

A

Type II HRS

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30
Q

what is IgM best at activating

A

complement

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31
Q

IgG directed aginst soluble antigen resulting in formation and deposition of immune complements to compelent activation and recruitment of phagocytes is

A

Type III HRS

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32
Q

serum sickness is result of

A

type III HRS

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33
Q

drug allergies usually result of

A

Type II HRS

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34
Q

cell mediated, Th1 and CTL component

A

Type IV HSR

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35
Q

antigen that gives rise to allergic response is called

A

allergen

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36
Q

allergic response is

A

an undesirable physical reaction, or a state of hypersensitivity. “Allergy” is generally synonymous with HSR I

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37
Q

most serious case of Type I HSR can result in

A

anaphylaxis

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38
Q

anaphylaxis is

A

is a serious, life-threatening allergic reaction. The most common anaphylactic reactions are to foods, insect stings, medications and latex.
Anaphylaxis can cause you to go into shock (blood pressure drops suddenly and airways narrow) and if untreated can be fatal.

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39
Q

anaphylaxis if atal if

A

untreated

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40
Q

atopy definition

A

similar to allergy, but this refers to genetic predisposiiton to generate allergic response

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41
Q

central feature of Type I HSR

A

IgE

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42
Q

sensitization phase is (of Type I HSR)

A

initial part where you will produce IgE from the first contact with allergen

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43
Q

allergens that gives rise to type I HSR are usually

A

small soluble polypeptides delivered at low doses

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44
Q

common inhaled allergens

A

pollens, dander from animals, mold spores, house dust mite

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45
Q

common ingested materials that act as allergens

A

food, orally administered drugs

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46
Q

two major components to deveopment of type I HSR

A

genetic factors

enviornmental factors

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47
Q

hygiene hypothesis

A

exposure to bacteria as a child generates a Th1 response, if not you will generate a Th2 response and could be more susceptible to develop allergies

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48
Q

what is the enviornemnt part of type I HSR

A

thought to be about hygeiene and whether you have been exposed to bacteria at a young age

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49
Q

with a high genetic susceptibilitybackground and in hygenic enviornment you will develop:

A

atopic or allergy

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50
Q

if you are raised in less hygienic enviornemnt (exposed to micro-organisms) and genetic susceptibility is lower, you will not generate

A

atopic or allergic response

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51
Q

MHC II is associated with the development of

A

type I HSR

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52
Q

why is MHC II associated w/ type I HSR

A

need to isotypte sitch so need t cell help and CD4 cell help

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53
Q

TLR and their polymorphisms are associated w/ developmen tof

A

Type I HSR

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54
Q

polymorphisms associated with overproduction of ceratin

A

cytokines, leading to heightened response

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55
Q

to enhacne presentation to allergins for type I HSR are what genes

A

MHC class II genes & TCR alpha locus (pg 14)

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56
Q

type I hypersensitivity push you toward

A

Th2 response

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57
Q

increased expression iof IL _ are associated with increase type I HSR

A

IL-4

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58
Q

describe hygiene hypothesis

A

lack of exposure to microbes as a child, can be overuse of antibiotics and over-clean enviornmen
you want Th1 response, so following allergen exposure they will not have hypersensitivity. if enviornment is more sterile, you will generate more Th2 resopnses, following allergen exposure will generate Th2 response and Type I hypersensitivity

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59
Q

features of Th2 response are mediators important for dealing with

A

helminth parasites

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60
Q

Th2 response, what components?

A

Th2 cells
IL: 3, 4, 5, 9, 10, 13
IgE

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61
Q

wherever you are likely to be exposed to parasitic infections you are less lieklyk to have

A

allergy

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62
Q

majority of IgE is found hwere

A

surface of mast cells, not in circulation, also basophils

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63
Q

for most Fc receptors the antibody has to be bound to antigen, but the exception is

A

IgE

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64
Q

IgE will bind to high affinity of epsiolon receptor in absense of

A

antigen

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65
Q

if allergen gets into blood stream it can cause

A

anaphylaxis

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66
Q

site of allergen exposre in IgE mediated allergic reactions

A

inhalation

defect in skin barrier

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67
Q

essential antibody in Type I HSR is

A

IgE

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68
Q

IgE bound to Fc epsiolon recptors on mast cells are crosslinked which causes release from

A

mediators from granules that gives rise to type I HSR

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69
Q

IgE has extra

A

constant domain: 4

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70
Q

how many constant domains does IgE have

A

4

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71
Q

IgE normally has very ___ concentratoin in serum

A

low

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72
Q

Fc portion binds to what on mast cells

A

Fc epsion receptor, very tightly

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73
Q

granules released from mast cells contain

A

histamine, some TNF alpha, leukotrienes

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74
Q

release of mediators by mast cells cause what of Type I HSR

A

early or immediate phase of type I HSR

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75
Q

what enzymes are released from mast cells

A

enzyme: tryptase and chymase

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76
Q

what toxic mediator is released in mast cells

A

histamine & heparin

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77
Q

what cytokines are released from mast cells

A

TNF alpha

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78
Q

what does TNF alpha do

A

pomotes inflammation

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79
Q

what response does TNF alpha contribute to in Type I HSR

A

late stag

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80
Q

what lipid mediator are rleased from mast cells

A

prostaglandins, leukotrines, platelet activating factor

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81
Q

essential first step of Type I HSR is activation of

A

Th2 cells by allergen presented by antigen presented cells which will promote IgE

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82
Q

what is sensitization phase of Type I HSR

A

Allergen activated Th2 cells promote IgE production by production of IL-4 and IL-13

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83
Q

in sensitization phase the pt will not have ____

A

symptoms

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84
Q

eotaxin is

A

chemoattractant for eosinophils

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85
Q

Th2 cells secrete what cytokines

A

IL-5 and eotaxin to recruit eosinophils to site of reaction

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86
Q

cyokines produced in Type I is what phase

A

late phase

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87
Q

what do eosinophils release

A

enzymes and toxic protein & lipid mediators

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88
Q

what cytokine is needed to differentaite from Th0 to Th2

A

IL-4

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89
Q

IL-4 induceses expression of TF

A

GATA3

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90
Q

sensitization of Type I HSR involves class switching to

A

IgE

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91
Q

following rexposure of allergin in Type I HSR

A

get crosslinking, degranulation, early phase

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92
Q

following eposure to antigen (Type I HSR) you generate a primary response which is the

A

sensitization stage

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93
Q

in sensitization stage there will not be any

A

symptoms

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94
Q

what is elicitation stage of Type I HSR

A

secondary response

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95
Q

what happens in eliciatation stage of Type I HSR

A

symptoms

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96
Q

allergen sensitization is very similar to

A

parasite Ag sensitization

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97
Q

what cytokines are needed to swith to IgE

A

IL4 and IL13

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98
Q

rexposure of allergin with Type I HSR is what phase

A

elicitation

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99
Q

immediate phase of Type I HSR happens within

A

minutes

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100
Q

late phase of Type I HSR happens in what time

A

up to 24 hours after exposure

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101
Q

why does late phase take so much longer in Type I HSR

A

recruitment of inflammatory cells and recruitment of cytokines

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102
Q

immediate response being so quickly is due to release of

A

release of histamine, serotonin, heparin, tryptase

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103
Q

what is wheal

A

fluid filled itchy bump - edema

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104
Q

what is flare

A

redness - erythema

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105
Q

what are second wave mediators, in late response (Type I HSR)

A

prostaglandins, leukotrienes, heparin, cytokines (pg 33)

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106
Q

inhaled allergins give rise to

A

hay fever

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107
Q

seasonal rhinoconjuctivitis is

A

hay fever

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108
Q

what is the response to hay fever

A

edema of conjunctiva and nasal mucosa, sneezing

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109
Q

food allergins most commonly give rise to what symptoms

A

vomitting and diarrhea, can be more serious: systemic anaphylaxis

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110
Q

wheal and flare rxn symptoms:

A

hives

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111
Q

actute uticaria is

A

hives on skin

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112
Q

systemic anaphylaxis, route of entry of allergin is

A

intravenous

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113
Q

what is respnse of systemic anaphylaxis

A

systemic mass cell degranulation, drop in blood pressure, can be fatal, collapse of blood vessels, most serious form of type I hypersensitivity

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114
Q

most serious response of type I HSR

A

systemic anaphylaxis

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115
Q

inhaled allergins, if not confined to upper respiratory tract, that can go to bronchi, etc (like cat dander) can give rise to

A

allergic asthma

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116
Q

effects of mast cell degranulation depends on

A

where and how antigen is encountered

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117
Q

where can antigen be encounteredfor mast cell degranulation

A

GI tract
eyes, nasal, airways,
blood vessels

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118
Q

route of encounter with allergin determins what of type I HSR

A

symptoms

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119
Q

most serious form of type I HSR response

A

intravenous in injection of high dose of allergin

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120
Q

allergin via injection and high does,e, what happens

A

fluid moving from circulation into tissues, collapse of blood vessels

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121
Q

inhalation f allergin at low does gives rise to

A

hay fever, asthma

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122
Q

subcutaneous low dose response with Type I HSR

A

local release of histamine, wheal and flare rxn

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123
Q

ingestion of allergin at low dose, symptoms type I HSR

A

vomiting, diarrhea, if in circulation more systemic affects like anaphylactic shock

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124
Q

inhaled allergins is due to what kind of antigen inhaled

A

solublw

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125
Q

soluble inhaled antigen activates

A

protein
MHC II
CD4 T cells

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126
Q

what t cell response necessary for type I HSR

A

type 2

Th2

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127
Q

inhaled antigen results in production of what binding to mast cells

A 
B cells
Th2
IL-4, IL-13
IgE
Mast cells
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128
Q

important features of inhaled allergens:

A

low dose

proteins, because that’s what t cells can recognize & need to be able to bind to MHC II

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129
Q

low dose promotes differentation of Th0 to

A

Th2

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130
Q

high dose promotes diferentiation of Th0 to

A

Th1

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131
Q

main features of type I response in respiratory tract in upper tract

A

allergic rhinitis

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132
Q

main features of type I response in respirtatory lower tract

A

bronchial asthma

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133
Q

allergic asthma is more serious b/c it ca be associated with

A

difficulty breathing

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134
Q

chronic ashtma can be caused from bronchial asthma due to

A

eosinophils, toxic to host cells

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135
Q

allergens associated w/ respiratory type I HSR:

A

pollen, dust mites, fungal hyphae, spores, animal dander

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136
Q

large particles for respiratory type I HSR are limited to

A

upper airways

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137
Q

large particles for respiratory type I HSR are associated with what response

A

hay fever

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138
Q

smaller particles inhaled allergens for typw I HSR respiratory can be associated with

A

asthma

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139
Q

IL-4 and IL-13 promote

A

IgE production

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140
Q

IL5 activates

A

recruits activated eosinophils

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141
Q

allergin cross links receptors on surface of mast cells whch causes

A

degranulation of mast cells

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142
Q

after degranulation of mast cells what will be released

A

cytokines and eosinophils

IL-5 will activate eosinophils

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143
Q

allergic asthma is example of what kind of asthma

A

extrinsic asthma

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144
Q

intrinsic asthma caused by

A

unknown, thought to be stress, exercise, cold temperatures, drug induced (aspirin)

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145
Q

look at chart

A

pg 41

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146
Q

hives are example of what response from type I HSR

A

wheal and flare response

147
Q

dermatitis is a form of

A

eczema

148
Q

atopic urticaria is

A

hives

149
Q

what is basic for skin test to diagnose type I HSR

A

atopic uticaria (wheal and flare)

150
Q

usually atopic urticaria will resolve and not leave a

A

mark/trace

151
Q

usually atopic urticaria will resolve itself, if not can give

A

steroids

152
Q

in chronic form of atopic dermatitis what happens to epidermis

A

it thickens

153
Q

Atopic dematitis (eczema) is the epidermal equivalent of

A

chronic asthma

154
Q

what allergens give rise to Atopic dematitis

A

a lot unknown, can be food, inhalant

155
Q

a person who has type I response to an allergen will often have multiple

A

responses to different alelrgens

156
Q

what is lichenification

A

thickening of skin b/c of scratching

157
Q

biopsy of skin with atopic dermattitis, wil find

A

activated CD4+ memory Th ceols and elevated serum IgE

158
Q

for majority of time with not severe food allergies the symptoms happen

A

in GI tract

159
Q

most food allergies are what kind of HSR

A

type I HSR

160
Q

most common food allergens

A

nuts (especially peanuts), shellfish, eggs, cow’s milk and soy proteins, (gluten not Type I HSR).

161
Q

response against gluten is what kind of HSR

A

type IV HSR - triggers celiac disease

162
Q

what is sytemic anaphylaxis

A

Bronchial and tracheal constriction, complete vasodilation.

Shock, multi-organ system failure and death are possible outcomes

163
Q

penicillin acts as a

A

hapten

164
Q

penicillin (hapten) in itself will not enduce

A

immune response

165
Q

how does penicillin induce type I HSR resopnse

A

Penicillin modifies self protein and presented by macrophages
T cell helps activated B cell to switch to IgE
Mast cells are armed with IgE
Armed mast cells degranulate

166
Q

site of exposure determines

A

what symptoms you get

167
Q

tryptase is enzyme released

A

upon degranulation of mast cells

168
Q

elevated serum tryptase is indication of recent

A

anaphylactic rxn

169
Q

when is peak of serum tryptase

A

30-70 min following antigen exposure

170
Q

individuals w/ serious allergies are advised to carry EPI pen b/c EPI will

A

counteract drop of blood pressure during systemic anaphylaxis

171
Q

how you diagnose if someone has a type I HSR

A

skin test to detect if pt has wheal and flare rxn -they will generate hive if they are allergic

172
Q

what is only test that will determine if someone is allergic to something

A

wheal and flare rxn test

173
Q

IgE can tell you if somebody has response but

A

other people can have high levels of IgE and not have allergy

174
Q

basis of wheel and flare response

A

increase in vascular permeability alowing seapage of fluid and proteins into tissue

175
Q

positive control of wheel and flare response

A

histamine

176
Q

what is wheal

A

raised patch of skin in the center

177
Q

what is the flare

A

red flush around the outside of response on skin

178
Q

wheal and flare response aginst someone who has type IV response what would happen

A

you would get similar looking response as with the type I but it would take two hours to happen

179
Q

individuals with type I hypersensitive responses are often allergic to multiple

A

allergins

180
Q

can test if indiviaul has IgE against allergin, what does this tell you

A

it can indicate if they have allergy, but is not definitive b/c you can have IgE and not be allergic

181
Q

what test is used to do IgE test

A

RAST

182
Q

RAST STANDS FOR

A

RADIOALLERGOSORBENT TEST

183
Q

describe RAST

A

allergin coated onto disk, add serum from pt, if they have antibodies specific for allergin the antibodyies will bidn to allergin immobilized on disk, so have disk with allergin and allergin specific antibody. you aren’t interested in IgG, you want to detect IGE specific for allergin. use radiolabeled anti-human IgE antibody, if you add it to disk and disk have IgE antiallergin added to it it will bind and you can detect by putting the disk into counter

184
Q

what is often used instead of rast

A

ELISA

185
Q

ELISA, DESCRIBE

A

wells coated w/ allergin, then add pts serum, so fi pt has IgE specific it will bind to allergin on wells, then detect if IgE has bound to allergin, so have another layer that is commercially antibody that will bind to human IgE with enzyme attached, then add substrate and if it is bound then you will either get color change or fluorescence

186
Q

what is the best way to treat type I HSR

A

avoid allergen

187
Q

how do you block mediators for type I HSR

A

block mediators - Antihistamines, leukotriene inhibition, corticosteroid inhibition of NF-kappaB

188
Q

NF kappa B is required for production of

A

pro-inflammatory cytokines

189
Q

desensitization as treatment for type I HSR

A

injection into skin of minute quantities of allergen and then gradually increase over two year period, can convert response into IgG response

190
Q

prevent IgE mediated degranulation as treatment for type I HSR, describe

A

binds to Fc portion of Ige and prevents IgE from binding to mast cell

191
Q

describe monoclonal antibody as a treatment for Type I HSR

A

IgE binding to mast cells is blocked

192
Q

when desensitization works you get production of what

A

IgG and IgG

193
Q

how does desensitization work

A

IgG will be made and it will bind to allergen so that IgE doesn’t get a chance to

194
Q

draw chart of type I hypersensitivty rxns

A

pg 65

195
Q

what is tie frame of Type I HSR following re-exposure

A

minutes, it is immediate

196
Q

what is the immunologic mechanism? (Abs, or T cells? INnate cells? cytokines?) type I HSR

A

IgE is the ab
Th2
innate: mast cells, eosinophiles, basophils
cytokines: IL-4 & 13, IL-5, eotaxin

197
Q

the immune response elicited in type I HSR is usually directed to which pathogens?

A

parasitic infections

198
Q

name the two stages of type I HSR

A

early and late (sensitization & elicitation)

199
Q

describe the immediate and late phase responses in type I HSR

A

immediate: degranulation products of mast cell (eesp histamine)
late phase: leukotrienes and prostaglandins and cytokines, and cells attracted like eosinophils

200
Q

name some allergens for type I HSR

A

cat dander, ragweed

201
Q

what feature do allergens ahre? type I HSR

A

proteins - they have to be able to be recognized by t cells

202
Q

type II HSR mediated by

A

IgM or IgG

203
Q

type III HSR mediated by

A

IgG - directed against soluble antigen

204
Q

in type II IgM or IgG is directed against

A

cell surface antigen

205
Q

type III HSR is directed against

A

soluble protein

206
Q

when antibody binds to antigen (ike type II and III HSR) what can happen

A

ctivation of complement

207
Q

IgG binding to cell surface antigen can do what

A

opsinize that cell and target it for phagocytosis

208
Q

two main type sof type II HSR

A

cytotoxic & non-cytotoxic

209
Q

cytotoxic type II HSR lead to

A

death/destruction of cell

210
Q

non-cytotoxic type II HSR lead to

A

degranulation of mast cells

211
Q

example of non-cytotoxic type II HSR

A

graves & myesthenia gravis

212
Q

type II HSR, what is common cause

A

drugs, like penecillin

213
Q

differences b/w type II and I HSR (4)

A

isotype of Ig, type II is never IgE and type I is only IgE
antigen recognized in type I is soluble, antibodies in type II recognize cell surface or extracellular matrix
antibody binding to self protein leads to classical complement activation in type II (so can result in opsonization, phagocytosis, MAC, phagocytosis)

214
Q

what are particuaily prone to lysis by complement

A

RBC

215
Q

frustrated phagocytosis:

A

neutrophil releases its stuff directly into tissue

216
Q

following binding of antibody in type II HSR what happens

A

recruit inflammatory cells
opsonize or activate complement
interfere w/ cellular functions

217
Q

complememt will recruit and call over what cells

A

neutrophils and macrophages

218
Q

c3b will do what to cells

A

opsonize

219
Q

how is tissue injured in type II HSR

A

complement recruites leukocytes & macrophages
opsonization
hormone receptor signaling (pg 72)

220
Q

describe complement activation of tissue injurty in type II HSR

A

neutrophils recruited and activated, they will engulf or destroy cell or relase their ROS and degrative enzymes into tissue and cause tissue injury

221
Q

describe opsonization & phagocytosis in type II HSR in regards to tissue injury

A

C3b binds due to complement activation leads to phagocytosis

222
Q

myasthenia gravis

A

blocks binding of ACh to receptor, antibody is antagnositc antibody

223
Q

graves’ disease

A

pg 74 notecard

224
Q

hemolytic disease of the newborn is caused by

A

IgG directed against fetus antigen, attacks RBC of fetus and fetus can be still born

225
Q

describe hemolytic disease of newborn

A

IgG directed against fetus antigen, attacks RBC of fetus and fetus can be still born

226
Q

describe transfusion/transplantation reaction

A

Natural antibodies to ABO blood group antigens cause hemolysis of non-matched donor RBCs (or hyperacute rejection of a donor transplant)

227
Q

blood group antibodies are all

A

IgM

228
Q

HDNB stands for

A

Hemolytic Disease of the Newborn

229
Q

when does HDNB occur

A

RhD negative mother and RhD positive fetus

230
Q

consequence of HDNB and blood mixing

A

mother is immunized against RhD antigen

231
Q

what is sensitization phase of HDNB

A

mixing of mom and baby blood and mom develops antibodies against RhD

232
Q

what happens with second pregnancy for mom who was sensitized to RhD positive if she has a second RhD positive baby

A

it would attack baby blood

233
Q

what is treatment for HDNB

A

prevent antibody forming against IgG (RhD positive)

234
Q

what is Rhogam

A

antibody to protect against HDNB

235
Q

when is other treated with Rhogam

A

28 weeks, 36 weeks, at birth

236
Q

what does rhogam do

A

prevents b cell activation and memory cell formation by blocking Rh antigen from activating maternal b cells
it is specific for b cells that would bind the RhD
it prevents activation of RhD positive by signaling through the negative co-receptor on b cells

237
Q

would IgM anti-Rh work?

A

no, because the constant region of IgM is not gamma, it’s mu, so IgM cannot bind to gama receptor

238
Q

review pg 81

A

81

239
Q

notecard

A

pg 82

240
Q

type A recipient, type B donor, what antibody

A

anti-B antibody that will attack the transfused RBC from donor

241
Q

penicillin rxn b/c penecillin can bind to

A

glycoproteins on our cells, generates antibody against the protein, leading to hemolytic anemia

242
Q

how does penecillin act as hapten

A

it can modify proteins to create foreign epitopes, which leads to destruction of the RBC either by phagocytosis or ADCC, the drug modified penecillin protein is presented to Th2 leading to production by B cell of high affinity isotype switched

243
Q

myasthenia gravis

A

autoantibody against Ach

244
Q

graves disease

A

autoantibody against thyroid stimulating hormone

245
Q

certain compounds that can give rise to all 4 HSR

A

like penecillin, hapten

246
Q

how do you determien what HSR it is with something like penecillint hat can give rise to all 4 HSR

A

timing & symptoms

247
Q

Type III HSR are

A

immune complex diseases

248
Q

Type III HSR, where will immune complex deposit

A

skin, joints, blood, kidney

249
Q

antigen component of Type III HSR immuen complex is

A

poorly catabolized antigen

250
Q

antibody most commonly involved in Type III HSR

A

IgG

251
Q

just like type I HSR the antigen recognized by antibody for Type III HSR

A

soluble

252
Q

immune complex deposited where in blood in Type III HSR

A

vessel walls

253
Q

why do immune complexes deposit in blood vessels in Type III HSR

A

FC gamma dnc omplement receptors

254
Q

when complement is generated in response to Type III HSR what happens

A

C3a and c5a, which will attract neutrophils, damage to endothelial cells: tissue factor, coagulation cascade, so occlusion of blood vessels

255
Q

how do you distinguish Type III HSR from type II?

A

type II: antibody binds to anitgen of surface of cel or ECM, so specific damage
type III: deposition can occur throughout body, not due to specific interaction b/ antibody and immune complex, so bystander destruction

256
Q

what do type II and III HSR have in common

A

never IgE

257
Q

Type III HSR result from

A

immune complex that are poorly handeled/poorly eliminated

258
Q

why are Type III HSR poorly eliminated

A

their size - they are usually small circulating immune complexes

259
Q

3 main types of immune complexes depnging on ratio of

A

antigen to immunogen (?)

260
Q

in antigen excess will only form

A

small immune complexes

261
Q

small immune complexes at beginning of response will not activate

A

complement

262
Q

zone of equivalents:

A

ratio of antibody to antigen is roughly the same

263
Q

what happens when ratio of antibody to antigen is roughly the same

A

large complexes that are efficienty removed

264
Q

antibody excess stage in ratio of antibody to antigen is roughly the same

A

medium sized immune complexes that are efficiently removed from circulation

265
Q

how are immune complexes normally removed from body

A

RBC have CR1 receptor

so RBC ahdn off the complexes to splenic macrophages and cooper cells

266
Q

CR1 is receptor for

A

C3b

267
Q

CR1 on RBC & WBC

A

RBC have much less receptor on their surface, but b/c there are so many RBC compared to WBC theya re most important for delivering immune complexes to liver and spleen for their removal

268
Q

once immune complexes in liver and spleen the phagocytes have

A

CR1 & FC gamma receptors

269
Q

how do phagocytes bind and take the immune complexes from RBC

A

they have much higher affinity

270
Q

review pg 94

A

94

271
Q

small immune complexes do not efficiently bind to

A

RBC

272
Q

class places small immune complexes accumulate

A

small blood vessel
renal glomerulus
skin and joints

273
Q

when level of immune complexes exceed disposal mechanisms, then

A

IC can deposit

274
Q

what are the most systemic autoimmune disease

A

immune complex disease

275
Q

IC stands for

A

immune complex

276
Q

IC deposit in cell wall which attracts

A

neutrophils, IL-8, tissue factor, C3bR and (pg 96)

277
Q

characteristics of ratio of antibody to antigen is roughly the same

A

directed against self or foreign soluble antigens
caused by deposition of antigen/antibody complexes (immune complexes) in tisue and blood vessels
tissue damage by neutrophils and possible generation fo MAC and complement mediated lysis
clotting cascade and so ischemic damage to tissues and scarring

278
Q

arthus reaction

A

localized inflammatory response

279
Q

intravenous delivery of high doses of antigen can give rise to (Type III HSR)

A

serum sickness

280
Q

subcutanous route of Type III HSR can give irse to

A

arthus reaction

281
Q

inhaled route of Type III HSR can give rise to

A

farmer’s lung

282
Q

farmer’s lung

A

deposition of IC in alveoli

283
Q

faermer’s lung has same mechanism as

A

arthus reaction

284
Q

serum sickness:

A

any soluble protein, antigen usually Immunoglobulin from passive immunization

285
Q

antibody generated against streptococcal will form

A

small complees wnad deposit in kidney

286
Q

Post-streptococcal glomerulonephritis can be caused by

A

streptococcal antigens

287
Q

staining pattern of glomerunoephrits

A

lumpy/bumpy

288
Q

if serum sickness is a response against what foreign antigen what happens

A

antigen will be removed

289
Q

if intravenous injection is anti-venom (passive immunization), draw out serum sickness graph

A

pg 101

290
Q

associated w/ inflammation you will have

A

fever

291
Q

post-streptococcal glomerulonephritis want to see if there are

A

IC deposited

292
Q

stain biopsy with antibody against IgG to see if pt has IC deposited following streptococcal

A

will see granular or lump-bumpy pattern (pg 103)

293
Q

arthus rxn is

A

localized visualized resposne

294
Q

what test can you do to see if pt has Type III HSRs

A

arthus rxn test - skin test

295
Q

what is timing for Type III HSRs for skin test (or any repsonse)

A

hours

296
Q

describe arthus rxn for Type III HSRs

A

local injection w/ antigen
local immune complexes form, c5a binds which attracts neutrophilsdegranulation of mast cells due to binding of FcgammaR
mast cells activated them formation of lesion that looks like what it does in type I HSR, it just takes longer than with type I
essentially wheal and flare response, timing is very different from type I

297
Q

minimum timing for Type III HSRs rxn

A

2 hours

298
Q

tetanus booster can give rise to what response

A

Type III HSRs

299
Q

inhaled allergens from spores can give rise to arthus rxn at what site

A

alveoli

300
Q

chronic farmer’s lung is what type of HSR

A

IV

301
Q

cwhat cells required for Type IV HSR

A

th1 cells

302
Q

Th1 clls activate

A

CD8 cytotoxic t cells

303
Q

how long does Type IV HSR take

A

48-72 hours, so about 2 days after antigen exposure

304
Q

what cytokine important for activating macrophage

A

IFN gamma

305
Q

Type IV HSR symptoms

A 
contact dermititis (poison ivy, nickel)
most common form of transplant rejection
306
Q

type Type IV HSR are inappropriate manifestation of

A

normal Th1 response against intracellular bacterial and fungal infection

307
Q

delayed-type hypersensitivity response describe

A

redness, swelling, induration, cellular infiltrate, so it is hard bump

308
Q

what is antigen in delayed type hypersensitivity

A

protein

309
Q

what is antigen for contact hypersensitivity

A

haptens

310
Q

what are examples of antigens for contact hypersensitivity Type IV HSR

A

nickel, poison ivy

311
Q

describe Type IV HSR tiem course

A

antigen injected into subcutanous tissue
Th1 effector cell recognizes antigen and releases cytokines, they act on vascular endothelium
recruitment of phagocytes

312
Q

what causes swelling in Type IV HSR

A

infiltration of t cells

313
Q

Th1 cells release

A

chemokines: CXCL2 especially

IFN gamma

314
Q

CXCL2 recruits

A

monocytes

315
Q

IFN gamma activates

A

macrophage and promotes differentiation from monocytes into macrophages

316
Q

IFN gamma induces expession of adhesion molecules on

A

vascular endothelial cells

317
Q

LT stands for

A

lymphotoxin

318
Q

TNF beta new name

A

lymphotoxin

319
Q

TNF alpha and LT can induce

A

local tissue destruction

320
Q

local Th1 cells secrete

A

GM-CSF

321
Q

GM-CSF promote

A

production of monocytes by bone marrow

322
Q

persistnet stimulation of Type IV HSR can give rise to

A

granuloma & contact hypersensitivity

323
Q

test for Type IV HSR

A

put some on skin to see if there is rxn

324
Q

tuberculin response

A

ejection of TB into skin to see if there is response (TB test)

325
Q

Tdth is same as

A

Th1

326
Q

tuberculin rxn is an example of what response

A

Type IV HSR

327
Q

sensitization phase in Type IV HSR

A

generation of type of response that will ultimately give rise to symptoms

328
Q

what is generated during sensitaation phase of Type IV HSR

A

Th1 from Th0 cells

329
Q

what is signal to make Th1 from Th0

A

IL-12 & IFN gamma

330
Q

what is lineage specific TF from Th1

A

Tbet

331
Q

elicitation phase of Type IV HSR happens following

A

rexposure

332
Q

are there symptoms in sensitzation phase of Type IV HSR

A

no

333
Q

are there symptoms in elicitation phase of Type IV HSR

A

yes

334
Q

what cytokines are involved in elicitation phase of Type IV HSR

A

IFN-gamma, TNF-beta, IL-2, IL-3 and GM-CSF

335
Q

what chemokines are involved in elicitation phase of type IV HSR

A

IL-8, MCAF and MIF

336
Q

MIF stands for

A

macrophage inhibition factor

337
Q

how do we keep macrophages in area we want

A

MIF

338
Q

describe elicitation phase of Type IV HSR

A

Macrophages are activated by IFNgamma & TNFbeta. They migrate to the site following a trail of IL-8 and MCAF, stop when they get there under the influence of MIF, and are activated to secrete their own cytokines by MCAF & CD40/CD40L interaction.

339
Q

MCAF stands for

A

Macrophage Chemotactic and Activating Factor

340
Q

what usually gives rise to contact dermatitis

A

nickel, rubber, poison ivy

341
Q

how does contact dermatitis from type IV present

A

lymphocytes, later macrophages,edema of epidermis

342
Q

sensitization phase of contact dermitisis for type IV, list all the steps

A 
hapten introduction into epidermis
hapten-carrier complex
taken up by APC in epidermis - langerhans cell (LC)
migrate to lymph node
to paracortex
present antigen to naive CD4 T cell
CD4 T cell differentiate into Th1 cells
343
Q

elicitation phase of contact hypersensitivity type IV HSR list steps

A

antigen specific CD4 Th1 cell
they migrate to epidermis
macrophages migrate to epidermis
macrophages migrate to epidermis

344
Q

following second exposure to contact allergin ( like poison ivy) what happens

A

IFN gamma activates macrophages
MIF keeps macrophages to stay in tissue
IL-8 and MCAF also released
damage caused by release of enzymes from macrophages once they are activated

345
Q

what enzymes to macrophaegs release that cause tissue damage

A

hydrolases & oxidases

346
Q

besides contact hypersensitivty type IV HSR can cause

A

granuloma

347
Q

response against intracellular bacteria that are difficult to control

A

granuloma

348
Q

time frame for generation f granuloma

A

3-4 weeks

349
Q

appearance of formation of granuloma

A

hadening of skin or lung

350
Q

what will you see on histological magnification of granuloma

A

lots of macrophages, some t cells

cells that arise from macrophages: epithelioid cells, giant cells, fibrosis

351
Q

type s of antigens that give rise to granuloma

A

persistent infections that we cannot resolve

352
Q

what are clinical examples that would give rise to ganuloma

A

tuberculosis, sarcoidosis, leprosy, schistosomiasis

353
Q

steps in formation of granuloma (for example with TB)

A

pathogen picked up by M cells and brought o lamina propria
dendritic cells take it
DC to go lymph node
DC present to naive CD4 T cell in paracortex
clonal selection & clonal proliferation
activate macrophages
macrophages proliferate & fuse at center
at very center of macrophages are the ones that contain live TB

354
Q

skin test to test for type IV HSR

A

TB test - inject into skin

355
Q

what is the skin TB test called

A

PPD

356
Q

clinical appearance of rxn to TB test (PPD)

A

localized swelling

357
Q

PPD stands for

A

purified protein derivitive

358
Q

what are the majority of the cells that respond to TB

A

macrophages - less than 5% will be TB specific t cells

359
Q

review pg 130

A

130

360
Q

what is time frame of type IV HSR

A

2-3 days

361
Q

type IV immune mechanism is normally the immune response to what?

A

intracellular pathogens - viruses, bacteria, protosoan, fungi

362
Q

another name for TDTH?

A

Th1

363
Q

review slide 131

A

131

364
Q

review slide 132

A

132

Immunology Block 4 (10 decks)

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