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Immunology > 4th test > Flashcards

4th test Flashcards

1
Q

What is Type I HSR

A

true, classic allergies

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2
Q

What can potentially occur with Type 1HSR

A

anaphylactic shock

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3
Q

what type of antigens cause Type 1 HSR

A

non-immunogenic
small, highly soluble
recurrent expostures

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4
Q

How do small highly soluble antigens cause Type 1 HSR

A

small as haptens, soluble, recurrent low does exposures that stimulate TH2

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5
Q

What does stimulating TH2 do

A

cause humoral immune response

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6
Q

How are the antigens of Type 1 HSR delivered

A

transmucosally to contact IS

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7
Q

What do recurrent exposures cause

A

the antigens to appear as hard to remove, stimulates IgE production which stimulates inflammation

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8
Q

What is inflammation needed for

A

call for reinforcements to eliminate the antigens

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9
Q

What is the initial immune response

A

inconsiquential, stimulate production of igG and minor inflammation

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10
Q

What is the minor inflammation from

A

C’ activation

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11
Q

At some point what occurs to the production of IgG

A

it switches class to IgE

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12
Q

What is a critical step in type I HSR

A

IgE attaches to mast cells’ Fc receptors even in the absense of the antigen

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13
Q

Why can IgE attach to mast cell receptors

A

no hinges

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14
Q

What does this attaching of IgE cause

A

nothing because there is no antigen attached to the antibody at this time

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15
Q

Where are mast cells located

A

ISS

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16
Q

What are mast cells loaded with

A

cytoplasmic granules containing VFs and CFs

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17
Q

What causes the response to be set of with the IgE and mast cell bonded to

A

antigen binds during next exposure

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18
Q

What occurs when the antigen binds

A

single of binding is transduced to the cell interior and mast cells degranulate

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19
Q

What do the mast cells degranulate

A

vesicles containing VFs, CFs, C’ proteases and kinis

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20
Q

What contributes to inflammation when mast cells release

A

arachidonic acid of mast cells converted into prostaglandins and leukotrienes, esinophil chemotactic factor, CFs and VFs

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21
Q

What does the eosinophil chemotactic factor cause

A

migration of eosiophils

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22
Q

When does inflammation occur in Type I HSR for second exposure

A

minutes of exposure to antigen (faster than primary response)

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23
Q

What are the 4 major symptoms of allergies

A

bronchoconstriction
excess mucus production
vasodilation and vascular permeability
not localized inflammation

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24
Q

How does bronchoconstriction occur

A

smooth muscle cells of air passages contract

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25
Q

What does excess mucus cause

A

lungs to fill and diarrhea

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26
Q

Why is inflammation systemic

A

mast cells throughout the body were cocked by igE spread

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27
Q

How long is IgE produced

A

continues during this exposure and recocks the mast cells for even larger next exposure

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28
Q

what is systemic anaphylaxis

A

sudden body wide inflammation

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29
Q

When does anaphylaxis occur

A

when large amount of antigen gains access to the blood stream with IgE already present on mast cells

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30
Q

What is an example of HSR Type I

A

penicillan allergy

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31
Q

How does penicillin allergy occur

A

penicillin in bloodstream attaches to RBC, forms a hapten carrier conjugate which is immunogenic. Conformation occurs. Binds to IgE on mast cells and immediate systemic inflammation occurs

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32
Q

What can occur with anaphylaxis

A

systemic vasodilation and bronchoconstriction

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33
Q

What can systemic vasodilation lead to

A

sudden, fatal drop in blood pressure

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34
Q

What is the sudden, fatal drop in blood pressure lead to

A

anaphylactic shock

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35
Q

What can bronchoconstricion lead to

A

asphyxiation

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36
Q

With each exposure to penicillin, what occurs

A

increase in Ab titer which can lead to greater problems

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37
Q

What is allergy testing

A

small amount of allergin placed beneath skin

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38
Q

If allergic to an allergin, what occurs

A

1cm diameter red and swollen area

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39
Q

What does the 1 cm inflammation tell you in allergen testing

A

that IgE is present on mast cells

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40
Q

What is treatment for HSR Type I

A 
avoid allergens
treatments aimed at mast cells
treatments aimed at smooth muscle
corticosteroids
long-term treatments
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41
Q

What 3 signals do mast cells have receptors for

A

Fc receptor for IgE
apha adrenergic R
beta adrenergic R

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42
Q

What does alpha adrenergic R bind

A

adrenaline like hormone that increases degranulation

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43
Q

What does beta adrenergic R bind

A

adrenaline like hormone that inhibits degranulation

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44
Q

How can beta adrenergic R predispose someone to asthma

A

if excess hormone or defective receptor

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45
Q

What treatments could be aimed at mast cells

A

alpha adrenergic R antagonists
beta adrenergic R agonists
Fc receptors for IgE

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46
Q

What do alpha adrenergic R antagonists cause

A

inhibit degranulation

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47
Q

What do beta adrenergic R agonists do

A

inhibit degranulation

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48
Q

What do beta adrenergic R agonists mimic

A

hormone

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49
Q

Which type are most allergy medications

A

beta adrenergic R agoinists

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50
Q

What are examples of beta adrenergic R agonists

A

albuterol or isoproternol inhalers

epinephrine injections

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51
Q

What do all treatments for mast cells block

A

release of CF and VF

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52
Q

What are treatments aimed at smooth muscle

A

beta adrenergic R agonists

antihistamines

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53
Q

What do beta adrenergic R agonists do to smooth muscle

A

relaxation and bronchodilation

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54
Q

What do antihistamines do

A

competitive inhibitors of histamine binding to smooth muscle cells

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55
Q

What are antihistamines

A

histamin antagonist

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56
Q

What does histamine lead to

A

bronchoconstriction

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57
Q

What do antihistamines lead to

A

bronchodilation

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58
Q

What do corticosteroids do

A

inhibit inflammation and immune system

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59
Q

What are some long term treatments for HSR type I

A

densitization therapy- induce tolerance to the allergens

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60
Q

What are Type II cytotoxic HSR

A

antigens are on foreign human RBCs in the recipients bloodstream

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61
Q

What size are Type II antigens

A

large

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62
Q

What is the immune response for type II

A

humoral, not CMI
IgG or IgM attach to the foreign antigens on RBCs
activate C’ which leads to inflammation
MAC lyses donor- breakdown of arachidonic acid, release of enzymes which activate kinis
possible opsonation of donor cells and frustrated phagocytosis lead to enzymes and oxidizing agents released by phagocytic cells
inflammation is systemic

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63
Q

What are the types of blood group antigens

A

proteins and polysaccharides on RBCs

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64
Q

Why are proteins and polysaccharides on RBCs and antigens

A

have normal function as receptors and carrier proteins

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65
Q

Why do RBCs cause immune response in another person but not self

A

vary between individuals b/c of alleles inherited, antigenic to another individuals IS

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66
Q

How many proteins and polysaccharides on RBC

A

atleast 20

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67
Q

The proteins and polysaccharides on RBC can be what

A

more or less immunogenic

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68
Q

What is the most immunogenic protein/ polysaccharide

A

ABO

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69
Q

What is the second most immunogenic on RBC

A

Rh

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70
Q

For each system what does every individual have

A

blood “type” due to many alleles of each 20 system

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71
Q

How do ABO blood group system antigens vary

A

by a single sugar

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72
Q

How can they vary by sugar if no genes for sugar

A

genes for sugar-adding enzymes

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73
Q

What is sugar adding enzyme

A

glycosyltransferases

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74
Q

What does all blood types have

A

glycolipid with sugar chains ending in the sugar fucose

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75
Q

What does type O have that both A and B don’t have

A

both inherited enzymes but due to frameshift mutations the proteins are truncated.

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76
Q

What does type A individual have

A

functional gene coding for a GTase enzyme that attaches GalNAc sugar to the end of glycolipid

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77
Q

What does Type B individual have

A

functional gene coding for a GTase enzyme that attaches galactose o the end of glycolipid

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78
Q

What does Type AB individuals have

A

both genes so both modifications are made

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79
Q

How do some individuals have antibodies to some blood group antigens naturally

A

-transfused blood earlier
Abs produced against bacterial antigens that cross reacted
mismatched transfusion mediates hypersensitivity reaction

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80
Q

How many alleles for the Rh blood group antigen

A

38

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81
Q

How many of the Rh alleles happen to be agglutinated by Abs

A

32

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82
Q

What do the remaining 6 alleles of Rh TMP

A

non immunogenic/ don’t agglutinate

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83
Q

Are there natural antibodies to Rh antigens

A

no

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84
Q

What can be produced to Rh+ antigens on RBCs

A

antibodies if the IS is exposed to immunogenic non self RBCs

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85
Q

What is a Rh mediated type II HS

A

hemolytic disease of the next newborn (HDN

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86
Q

HDN is what

A

the most common type II HSR

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87
Q

How does HDN occur

A

fetal RBCs enter the mothers circulation during delivery
stimulate a primary IR if Rh antigens are different
IgG is produced to the fetal RBCs
during next pregnancy, maternal IgG crosses the placenta and destroys RBCs

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88
Q

How does IgG destroy RBCs of baby

A

with C’

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89
Q

Why is there no inflammation in C’ of the fetus

A

inflammatory cells not yet mature

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90
Q

What does IgG destroying RBCs of fetus cause

A 
no inflammation
anemia
jaundice
brain damage
possible death and miscarriage
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91
Q

Why does jaundice occur

A

buildup of the toxic RBC breakdown product bilirubin (too much for immature liver to remove)

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92
Q

Why does brain damage occur

A

bilirubin buildup and oxygen shortage

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93
Q

what factors influence the risk of HDN

A

baby’s father is Rh+ and mother is Rh- the baby might be Rh+

whether father is homozygous or heterozygous

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94
Q

An Rh+ mother is tolerant to what

A

all Rh+ alleles

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95
Q

An Rh- baby stimulates what in the mother

A

no immune response whether RH+ or RH-

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96
Q

If the mother and baby have different blood types ABO what occurs

A

natural maternal Abs to fetal ABO antigens, usually IgM will destroy the baby’s RBCs immediately upon entering maternal circulation

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97
Q

What occurs to fetus if ABO don’t match mother

A

fetal RBCs will not last long enough to stimulate an IR to their Rh antigens

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98
Q

WHat is the total risk of HDN

A

1:300 births

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99
Q

How can one prevent HDN

A

if high risk, passive immunization with IgM to the bab’s Rh antigen at mid pregnancy and within 72 hours after delivery will destroy RBC before IR to the Rh antigen

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100
Q

How much is the risk lowered with passive immunization

A

1:20,000 births

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101
Q

What type of antigens cause Type III immune complex HSR

A

large amounts of soluble antigen with non repeating epitopes

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102
Q

How are antigens of Type III exposed

A

intravenously-directly to the blood

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103
Q

What are some examples of Type III

A

viral antigens, antigens secreted from some tupors

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104
Q

What is limited

A

allgutionation by IgG

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105
Q

WHy is agglutination by IgG limited

A

epitopes do not repeat, only 1 per cell

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106
Q

What also occurs to the immune complexes that leads to them not being phagocytosed

A

attachment to endothelial cells

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107
Q

What are the consequences to Type III HSR

A

large amounts of C’ and inflammation
MAC lyse nearby blood cells and inflammation
neutrophils release enzymes that damage cells and inflammation

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108
Q

Where do these immune complexes become trapped

A

in basement membranes where blood is being filtered

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109
Q

What still occurs even though the complexes are trapped

A

inflammation is stimulated

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110
Q

Where do complexes commonly get trapped

A

kidney basement membrane filters
synovial joints
choroid plexus in the brain

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111
Q

What occurs when complexes get in kidney basement membranes

A

glomerulnephritis
clogged kidenys that don’t filter blood properly leading to proteinuria and bilirubin toxicity
inflammation
damaged kideny cells

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112
Q

What occurs when complexes trapped in synovial joints

A

arthritis

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113
Q

What do chorioid plexus form

A

CSF

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114
Q

What are some examples of Type III HSR

A

serum sickness
rheumatoid arthritis
idiopathic

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115
Q

What is serum sickness

A

passive Ab and AG

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116
Q

What is rheumatoid arthritis

A

Ab and idiotypic Ab

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117
Q

What is idiopathic

A

Ab and viral proteins

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118
Q

What type of antigens cause Type IV delatyed HSR

A

large prticles containing antigens

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119
Q

What is the immune response for Type IV

A

T lymphocytes, esp TD cells and macrophages

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120
Q

The IR is what independent

A

antibody

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121
Q

What does the inflammation solely depend upon

A

accumultion of cells that takelonger to develop than Ab-dependent HS reactions so it is delayed

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122
Q

What causes the inflammation

A

TD cells recruit macrophages
large particles cannoth be phagocytosed
macrophages release enzymes and oxidizing agents
HS is chronic b/c macrophages are unable to remove the antigen due to its structure and size

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123
Q

What are non chronic example of Type III HSR

A

poinson ivy: allergic contact dermatitis causes

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124
Q

What are the antigens in non chronic case

A

chemicals fro the plant adsorb onto skin cells forming huge haten carrier conjucates

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125
Q

What cells are stimulated

A

CD4+ TD cells because skin cells not easily phagocytosed; they recruit macrophages

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126
Q

Why does inflammation continue

A

the sheets of skin cells are difficult to remove

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127
Q

What does vasodilation cause

A

redness

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128
Q

What does increased vascular permeability cause

A

fluid accumulation in blisters and itchiness

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129
Q

WHy is the second exposure larger and more rapid

A

memory T cells are produced

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130
Q

What is the origin of immune deficiencies

A

inherited from parents
congenital-problem during development/ present at birth
acquired by infection
degenerative-result of aging

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131
Q

What immune system cells are involved

A 
APCs
T cells
T helper cells
B cells
pluripotent stem cell
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132
Q

Why do T cells generally contribute to immune system deficiencies

A

thymus is defective or absent, causing biggest impact on CMI

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133
Q

What do the loss of B cells cause

A

biggest impact on humoral and bacterial infections

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134
Q

In immune system deficiencies, what cell defects can occur

A 
missing or mutated receiptors
mutated links in signal transduction chains
missing or mutated MHC proteins
failure to secrete interleukins
failure to switch Ig classes
SCID
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135
Q

What is SCID stand for

A

severe combined immunodefieciency

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136
Q

What is SCID

A

one subunit of the IL (in general 6-8) receptor missing leading to no CMI

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137
Q

What does HIV primarily kill

A

helper T cells

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138
Q

What does the loss in helper T cells lead to

A

lack of B cell and CTL proliferation

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139
Q

What shirft occurs in HIV

A

helper T cell shift

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140
Q

What is the helper T cell shift

A

TH1 (CMI) is shifted to TH17 (humoral)

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141
Q

What does this shift and killing in helper T cell cause

A

inability to resist any infection, rare-infections and cancers that lead to death

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142
Q

What are the possible origins of AIDS

A

unknown

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143
Q

What are possible cases of AIDS

A

HIV

General Immune System or Innate suppressors

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144
Q

Does HIV mean Aids

A

no just a coorelation, HIV in presence is circumstantial

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145
Q

How could the general immune system be cofactors to AIDS

A 
another infection
nutritional deficiency
gay life style
promiscity
HIV coreceptor CCR5
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146
Q

How can another infection lead to AIDS

A

immune system is suppressed or the infection causes open wounds on the skin that allow HIV direct access to bloodstream

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147
Q

What transmission type is needed for HIV

A

blood to blood

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148
Q

How likely is another infection leading to AIDS going to occur

A

pretty rare

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149
Q

What are the high correlations mentioned in outline

A

STDs and AIDS

promiscuity and STDs

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150
Q

How can nutritional deficiency lead o AIDS

A

leads to other chronic infections

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151
Q

How does gay lifestyle lead to AIDS

A

anal sex tears the membrane, direct access to bloodstream, heavy drug use suppresses immune system

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152
Q

How does HIV co-receptor CCR5 contribute to AIDS

A

needed to be present in order for AIDS to occur. Not eliminated from Africa or Asia by the black plague centuries earlier

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153
Q

What is implied about the contraction of HIV

A

it is second but critical step in getting AIDS. First step of contracting AIDS can vary

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154
Q

What cells become infected by HIV

A 
helper T cells
macrophages
endothelial cells
neurons
GI tract epithelium
multiple receptors and spike proteins
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155
Q

How are helper T cells infected by HIV

A

lack of IL 2 and 4 (loss of CTL and humoral)

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156
Q

How are macrophages infected by HIV

A

leads to loss of APCs- immunosuppressive
infected macrophages bud self MHC II viruses–hides attack
naive lymphocytes to antigen exposure without interleukins leads to deletion or anergy

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157
Q

endothelial cells infected by HIV can lead to

A

reinfections

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158
Q

What do neurons infected by HIV lead to

A

dementia

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159
Q

What is difficult for the neurons to receive treatment

A

neurons are inaccessible to IS so virus is never killed

can’t reach with drugs do to blood brain barrier

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160
Q

What occurs with GI tract epithelium HIV infection

A

multiple viral infections and widespread IS activation

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161
Q

What receptors and spike proteins are infected by HIV

A

CD4
CCR5
CXCR4
others

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162
Q

To prevent infection, what must occur to these receptors

A

all must be blocked

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163
Q

How is HIV kept in cells

A

first reverse transcribed into DNA
spliced into host cell chromosome
forward transcribed to make new viruses

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164
Q

What type of nucleic acid is HIV

A

RNA

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165
Q

What are the consequences of HIV being spliced into chromosome

A

permanent
spreads to daughter cells without IS detection
can’t be removed by drugs
latent infection

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166
Q

What drugs have been tried but unsuccessful

A

CRISPR

shock and kill

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167
Q

What does the latent viral in chromosomes provide and opportunity for

A

internal reservoir for re-infection

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168
Q

What may prevent initial infection of HIV

A

strong NK cell response

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169
Q

If NK cell response is not strong enough, what occurs

A

HIV multiplies rapidly

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170
Q

What could HIV be eliminated by if strong enough

A

CTL response

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171
Q

Why could CTL response elimate HIV

A

primary IR is faster than the 6-8 weeks needed for HIV incubation/ replication

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172
Q

Does the B cell work

A

impotent, counter productive

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173
Q

If not CTL response occurs, what occurs instead

A

HIV multiplication remains rapid throughout infection

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174
Q

initially what is common between CTL and HIV

A

net amount of free virus in bloodstream is nearly zero

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175
Q

Even though the net is zero where is the HIV count high

A

in lymph nodes, neurons

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176
Q

At this stage even though the net is zero, HIV is not

A

latent

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177
Q

Gradually what occurs between CTL and HIV

A

HIV gains upperhand and the helper T cell count drops

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178
Q

How long does it take for HIV to gain the upper hand

A

10 years

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179
Q

What level does the HIV gain up to

A

where IRs against other pathogens is unable to occur

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180
Q

What results from no protection against other pathogens

A

secondary infections and full blown AIDS

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181
Q

Why is HIV hard to detect within those 10 years

A

mild symptoms, general

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182
Q

What are the symptoms of HIV

A

fatigue, swollen glands, fever

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183
Q

Since HIV is hard to detect, what occurs within those 10 years that makes it hard to eliminate HIV

A

sexual activity leads to extensive spread

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184
Q

During viral replication what is the rate of mutation

A

10 mutations per 9200 nt per cycle ( 1/920)

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185
Q

What is the rate of mutation of general somatic cell replication

A

1/ 1 million

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186
Q

How many distinc strains of HIV do we have now

A

three

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187
Q

What is within those three strains of HIV

A

different subtypes

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188
Q

Can only 1 HIV infect a person

A

no multiple forms within one infected person

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189
Q

Between the different forms what is difficult to treat them

A

some are more likely to spread, some more resistant to drugs, some escape from IS, ones used for vaccine may not be relevant to real world experience

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190
Q

WHat is the ratio of infected to dead TH cells

A

1:100

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191
Q

What percent is killed by lysis

A

1%

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192
Q

What factors lead to 99% not killed by lysis

A

-deleted by lack of presentation with stimulus to proliferation
-some deleted by superantigen attaching to their TCRs
-secreted viral gp120 attaches to CD4 on unifected cells
without stimulation CD4+ cells die
-B cells and CTLs deleted by lack of helper cells
-HIV not responsible for killing TH cells????

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193
Q

What are the treatments for HIV

A 
treat symptoms with heavy doses of drugs
administer IL-2
antiviral drugs
protease inhibitors
HAART
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194
Q

What drugs are used to treat symptoms

A

antiviral, atibiotics, antifungal

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195
Q

What is the downfall of using these drugs to treat symptoms

A

side effects and no substitute for IS

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196
Q

Why would IL-2 be administered

A

TH cells are missing and this could be compensation

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197
Q

What is the problem with IL-2 administer

A

too dilute

if increase dose side effects occur

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198
Q

What causes the side effects with an increased IL-2 dose

A

stimulation of all CTLs

199
Q

What do antiviral drugs do

A

block replication of viral DNA> host cell DNA

200
Q

What does the viral reverse transcriptase more prone to use

A

base analogs

201
Q

What results with using antivirals

A

side effects from blocking host cell, lymphocyte multiplication

202
Q

What is a failed chemotherapy drug

A

AZT

203
Q

What did AZT lead to

A

diabetes, heart attacks, muscle and nerve toxicity

204
Q

What occurs with antiviral drugs to resistant viruses

A

emerge rapidly

205
Q

What do tandem genes lead to

A

tandem mRNAs and polyprotein

206
Q

What do viral protease aid

A

separating members of polyprotein

207
Q

What occurs when proteiase inhibitors are used

A

side effects appear, resistant viruses emerge rapidly

208
Q

WHy do side effects appear

A

numerous proteases within and outside of cells are also blocked

209
Q

What is HAART stand for

A

highly active anti retroviral therapy

210
Q

What does HAART include

A

all the previous treatments combined

211
Q

What is the goal of preventions

A

to eliminate reservoir of HIV

212
Q

How would elimination of the reservoir occur

A

not actively but passively

213
Q

How would you passively eliinate HIV

A

HIV would disappear withit last victims if they didn’t pass it on to someone else

214
Q

What does HIV depend on for its survival

A

promiscuity

215
Q

How could prevention occur with blocking route of transmisttion

A

avoid contact with reservoir; avoid promiscuous sex

216
Q

Why can’t condoms be used

A

30% failure rate and are ineffective

217
Q

How could prevention occur with vaccinating

A

use recombinant gp120 vaccines
attentuating viruses
vaccine with non-self MHC I and II proteins
CCR5 vaccine

218
Q

Why is using recombinant gp 120 vaccine not work

A

soluble, poorly phagocytosed, may cause clonal deletion
promotes humoral immunity
shifts away from CMI by promoting IgG not IgA
antigenic variation is high in HIV

219
Q

Why is humoral immunity not favored in AIDS

A

patients already have HIV antibodies

220
Q

Why would IgA be more favored

A

need Ab in mucus of vaginal or rectum

221
Q

What does the high antigentic variation lead to

A

antigenic drift and shift

222
Q

What is antigenic drift caused by

A

frequent mutations

223
Q

What is antigenic shift caused by

A

recombination of viral RNA strands when 2 different strains infect the same cell

224
Q

What leads to antigenic shift once 2 strains infect same cell

A

swapping of strands and crossing over of the strands

225
Q

Attenuated virus shouldn’t be used why

A

too risky

226
Q

What do attenuated viruses stimulate

A

CMI response

227
Q

How do you attenuate HIV

A

delete multiple genes or splice HIV genes into canary pox virus

228
Q

If you splice naked HIV genes what does this lead to

A

less prone to mutation

retain CMI response

229
Q

What would vaccinating with non self MHC I and II proteins lead to

A

attack on transfused virus infected cells or enveloped viruses

230
Q

What is the problem with vaccinating with self MHC i and II proteins

A

generate attack on future transplant

too many MHC proteins to vaccinate against them all

231
Q

What would be a CCR5 vaccine

A

neutralize the co-receptor making people resistant

232
Q

What are the problems of vaccine testing

A

time consuming and expensive

233
Q

Why is vaccine testing time consuming

A

long delay before symptoms actually appear

234
Q

What are surrogate markers

A

other levels of other cell markers that decline and are used to assess decline of IS

235
Q

What is the amount of decline in CD4+ cells that indicates decreased immune system

A

below 200/ul

236
Q

You could test CTL repsonse in vitro but what is the problem

A

Which strain or subtype of HIV do they have or not have

237
Q

WHat would be the best method of prevention

A

change behavior and to avoid the cofactors

238
Q

What is auto immunity

A

production of antibodies of T cells to epitopes on self proteins

239
Q

What does production of antibodies or T cells to epiotpes on self proteins lead to pathologically

A

disease

240
Q

What does production of antibodies or T cells to epitopes on self proteins lead to physiologically

A

removal of worn out cells
cells that die by apoptosis
identify worn out cells

241
Q

How does anibodies remove worn out cells

A

when RBCs become aged, new epitopes appear due to bond breakage. This stimulates Abs, obsonization of the RBCs and phagocytosis

242
Q

Where does phagocytosis of RBCs occur

A

spleen

243
Q

Why do cells that die by apoptosis get Ab produced

A

presents new antigen on them

244
Q

What antigen is expressed on apoptosed cells

A

eat me protein

245
Q

What are the three functions of the immune system

A

defense against invasion by microorganisms
policing for cancers
garbage disposal and recycling center

246
Q

what is the difference between the pathological and the physiological functions of auto immunity

A

loss of control over the process, may not be the formation of Ab that is the problem

247
Q

What occurs to healthy cell that leads to auto immunity dieseases

A

removal of the healthy cells by phagocytosis of the spleen

248
Q

What two reasons may lead to the removal of healthy cells

A

immune system is overactive

immune system is normal but cells are appearing worn out prematurely

249
Q

What occurs when the immune system is normal but cells are appearing worn out prematurely

A

the eat me protein of MICA occurs

250
Q

What mechanisms could lead to auto immune diseases

A 
change in location of self proteins
change in conformation of proteins
cross reactivity
affinity selection
microchimerism
loss of tolerance
pseudo auto immunity
251
Q

How can a change in location of self proteins lead to auto immune diseases

A

proteins from a location where they were never exposed to IS cells to a location where they come into direct contact with IS

252
Q

what are the sites where the IS cannot have access to

A

immunologoically privileged site

253
Q

What proteis in body are in immunologically priviledged site

A

sperm
cornear/lens
mitochondrial and nucleic proteins

254
Q

What blocks IS from interacting sperm

A

blood testis barrier between them

255
Q

What is the blood testis barrier

A

extra thick basement membrane

256
Q

If the blood testis barrier is broken what can occur

A

male infertility

257
Q

What protects the cornea and lens from IS

A

no blood supply to anterior chamber of the eye so no contact with APCs or lymphocytes

258
Q

What protects neurons from IS

A

the blood brain barrier

259
Q

What do neurons lack so IS can’t respond to them

A

no Fas receptors and MHC I proteins

260
Q

What can occur if blood brain barrier broken

A

alzheimers/ breakdown of neurons

261
Q

What can break protective barriers

A

infection, disease, trauma, injury, aging, surgery

262
Q

What occurs if any of the barriers are broken

A

antigens released into the loodstream and IRS to self proteins may occur

263
Q

What protects mitochondria and nucleus proteins

A

plasma membrane

264
Q

What occurs with a heart attack

A

cardiac muscle cells are dying from lack of oxygen, they become lysed releasing mitochondria, antigens in bloodstream

265
Q

What is found after a heart attack

A

anti mitochondrial antibodies

266
Q

Why don’t anti mitochondrial antibodies have negative effects

A

won’t attack intact cells because plasma membrane is still intact

267
Q

WHat is the clinical purpose of anti mitochondrial antibodies

A

diagnosis

268
Q

What can a change in conformation and shape of self proteins lead to

A

new epitopes to appear that the immune system is not tolerant to

269
Q

What can cause the conformation change of self proteins

A

chemical binding to the protein (siilar to hapten)
denaturation of protein (fever)
cleavage and proteolysis
mutation

270
Q

What causes cleavage and proteolysis

A

spontaneously or by enzymes released from damaged cells

271
Q

How can cross reactivity lead to auto immunity

A

Abs made to foreign epitopes on microorganisms may bind weakly to a self epitope

272
Q

What is it called when Abs to foreign epitopes bind weakly to a self epitope

A

molecular mimicry

273
Q

A single foreign epitope on a self protein will

A

NOT stimulate and IR b/c it is a hapten

274
Q

A single foreign epitope on a large foreign protein

A

will stimulate an IR against the epitope which then can cross react with the self protein

275
Q

Cross reactivity may also occur between cancer and

A

normal cells

276
Q

What are the diseases that result when epitopes on cancer react with normal cells

A

paraneoplastic syndromes

277
Q

How can affinity selection lead to auto immunity

A

if poor fitting antibodies are not deleted, it may generate auto reactive antibodies

278
Q

How can micro chimerism result in auto immunity

A

during delivery of baby, RBCs and lymphocytes enter mom bloodstream

279
Q

How many MHC mom to baby or baby to mom

A

50%

280
Q

What does 50% matching mean

A

ASLs can work with recipients immune system but are not tolerant of other proteins and lead to attack

281
Q

There is a strong correlation between micro chimerism and

A

auto immuniity

282
Q

What is micro chimerism

A

small numbers of allogeneic lymphocytes are present in person’s bloodstream

283
Q

How can loss of tolerance lead to auto immunity

A

allow IS to attack self epiotpe it was tolerant to

284
Q

How can loss of tolerance occur

A

Treg cells are killed
sudden proliferation of the B or Th cell
PSC in adult bone marrow

285
Q

How does Treg cells killed lead to auto immunity

A

tolerance is lost

286
Q

What kills Treg cells

A

reactivated latent viral infection
mutation
clonal deletion

287
Q

What would cause sudden proliferation of the B or Th cells

A

cancer

288
Q

What does the sudden proliferation of the B or Th cells cause

A

tip the balance toward auto immunity

289
Q

The tipping of balance toward auto immunity an be what

A

regained

290
Q

How is the tipping of the balance regained

A

recovery from latent viral infection

291
Q

What does regaining balance cause

A

cycles of remission and relapse characteristic of auto immune diseases

292
Q

How can PSC cause auto immune disease

A

adult bone marrow PSC developes into new close of ASLs that recognize self epiope but is not deleted

293
Q

Which methode cuses most adult auto immune

A

PSC developing into new clone during adult life

294
Q

What is pseudo auto immunity

A 
microchrimerism
cells appearing worn out pre maturely
mutual Fas CD95 mediated apoptosis
The IR is the effect not cause
chaperone failure
persisten slow viral infections
B cell activation by virus infection
295
Q

What is the common cause of auto immune troiditis

A

Fas CD95 mediated apoptosis

296
Q

What is chaperone failure

A

chaperone proeins befin to fail to fold protein properly

297
Q

What occurs if proteins don’t fold properly

A

new epidopes appear causing attack

298
Q

How do persistent slow viral infections lead to auto immunity

A

truly foreign viral proteins on the surfaces of host cells elicit an immune response

299
Q

What occurs that slow viral infections don’t get blamed for auto immune disease

A

no viral particles detected

300
Q

How does B cell activation by virus infection cause auto immunity

A

production of programmed antibodies

301
Q

What causes damage to host cells

A

antibodies
CD8+ CTLs
antibodies neutralizing cell surface receptors
antibodies stimulating cell surface receptors

302
Q

How can antibodies damage host cells

A

cause complement that leads to MAC formation and slow gradual lysis

303
Q

What leads to antibdies damaging host cells

A

antigens on cells that promote type II HSR

soluble complexes type II HSR

304
Q

how do CD8+ CTls cause damage to host cells

A

recognize self class I proteins and a new epitope

305
Q

HOw do antibodies netralizing cell surface receptors lead to damaging host cells

A

blocking the binding of natural ligands and the cells response

306
Q

What examples do neutralizing cell surface receptors are there

A

insulin receptor leads to diabetes

beta adrenergic receptor leads to asthma

307
Q

What is the precise cause of auto immunity diseases

A

unknown

308
Q

What is the typical onset age of Auto immune disease

A

20-40 years

309
Q

What factors cause auto immune diseases

A

multifactorial

environmental factors

310
Q

What environmental factors contribute to MS

A

colder climates increase risk of MS

311
Q

Auto immune dieases are controlled by how many gene factors

A

polygenic

312
Q

What proteins specifically contribute to auto immune diseases

A

MHC class II proteins

313
Q

What do MHC class II proteins contribute to

A

TH response intensity and the ability to present certain epitopes

314
Q

What do cycles of spontaneous remission and relapse cause

A

resurgence of Treg cells
virus to go latent
surege of C’ or inflammation inhibitors

315
Q

What symptom greatly occurs in auto immune diseases

A

chronic inflammation

316
Q

What may chronic inflammation be a result of

A

delayed type hypersensitivit (TYpe IV)

317
Q

What gender does auto immune typically occur in

A

femalles

318
Q

What percentage of auto immune is females

A

90%

319
Q

Why is auto immune more common in females

A

estrogen
higher antibody titers
more CD4+ cells
TH2>TH17>TH1=pro inflammatory

320
Q

WHat are treatments for auto immune

A 
immunosuppresive drugs
plamaphoresis
thymectomy
statins
oral admisistration of antigens
bone marrow transplant
321
Q

What immunosuppressive drugs are currently used

A 
corticosteroids
low doeses of anti rejection drugs
cemotherapy drugs
cyclosporin
humira
322
Q

What do chemotherapy drugs do

A

block lymphocyte proliferation

323
Q

What does cyclosporin do

A

block IL-2 production and CMI response

324
Q

What is Humira

A

adalimumab=mcAb to TNF

325
Q

What is plasmaphoresis

A

removal of Ab from blood through dialysis and returning blood cells

326
Q

What is thymectomy

A

removal of thymus

327
Q

What are statins

A

reduce cholesterol and C reactive protiens which reduces inflammation

328
Q

What can oral administration of antigens produce

A

tolerance

329
Q

What can be done in the future

A

selectively seplete self reactive cells

330
Q

How can you selectively self deplete reactive cells

A

inject antibodies to auto antibodies (AG)
inject antibodies to IL4/ IL6R
inject antibodies to TCR or CD154 on TH cells and CD20 on B cells
induce tolerance via clonal deletion
immunize patient with own killed auto reactive T cells
block only the MHC III presenting the auto reactive epitopes

331
Q

What is auto immune thyroiditis

A

Abs to thyroid gland cells

332
Q

What is the first stage of auto immune thyroiditis

A

auto Abs to TSH receptor

333
Q

What is the cause of auto immune thyroiditis

A

unknown

334
Q

WHat does the Ab binding do

A

has same effect as TSH binding: TH release and stimulation of cell division of thyroid cells

335
Q

What doesn’t the Ab respond to

A

negative feedback

336
Q

What normally tells anterior pituitart to decrease TSH output

A

TH

337
Q

What does Ab stimulate thryoid cells to do

A

excessive TH concentration and excessive mitosis

338
Q

What does excessive TH concentration cause

A

increased metabolism

339
Q

What does excessive mitosis cause

A

enlarged thyroid

340
Q

What is hyperthroidism

A

Grave’s disease

341
Q

What is the treatment for hyperthyroidism

A

drugs to block TH synthesis
surgical removal of part of the thyroid
radioactive iodine

342
Q

What does radioactive iodine cause

A

concentrates in thyroid and kills many of the cells

343
Q

What may occur with treatments

A

exposure of new epitopes as proteases and other enzymes are released from the dead cells

344
Q

What does the exposure of epitiopes lead to

A

second stage where ABs to other thyroid antigens

345
Q

What do Abs to dead thryoid cells do

A

cross react with normal thyroid cells

346
Q

What does the cross reaction lead to

A

further destruction of thyroid gland

347
Q

What is hypothryroidism

A

Hasimotos disease

348
Q

What is Hasimotos disease

A

decreased metabolism and energy levels

349
Q

What is the treatment for hashimotos disease

A

daily synthethic TH

350
Q

What is MS

A

auto Abs or CTLS to certain alleles of myelin basic protein in the mylein membrane surround CNS nerve axons

351
Q

What is the function of myelin

A

accelerations action potential propagaion

352
Q

What occurs with the accumulation of lymphocytes

A

spill over into CSF

353
Q

What lymphocyte especially spills over into CSF

A

TH17

354
Q

What causes MS

A

unknown

355
Q

What is the effect of MS

A

C’ or CTL mediated lysis or apoptosis of oligodendrocytes leading to slowed AP propagation

356
Q

What are oligodendrocytes

A

cells that produce myelin

357
Q

What does MS lead to

A

inflammation and further damage

358
Q

What are treatments for MS

A

IFN

bone marrow transplant after complete lymphocyte removal

359
Q

What doe IFNs do

A

shift immune response toward CMI, away from humoral

360
Q

What is SLE

A

systemic lupus erthematosus

361
Q

How many cases of SLE are in USA

A

1 million

362
Q

What percentage of SLE cases are female

A

90%

363
Q

WHen does SLE begin

A

during child bearin years

364
Q

What causes SLE

A

generalized loss of tolerance leading to production of Abs to self cells

365
Q

What cells are affected by SLE

A 
RBCs
platelets
cardiac muscle
skin
released DNA
arthritis
oral ulcers
CNS
other organs
366
Q

What does SLE to RBC cause

A

anemia

367
Q

WHat does SLE to platelts cause

A

poor clotting

368
Q

WHat does SLE to cardiac muscle cause

A

myocarditis

369
Q

What does SLE to skin cause

A

butterfly rash in areas exposed to the most sun

370
Q

WHat does released DNA cause

A

glomerulonephritis and arthristis

371
Q

What does SLE to CNS cause

A

seizures

372
Q

What inidicates diagnosis of SLE

A

4 of 11 possible symptoms

373
Q

What is the cause of SLE

A

unknown

374
Q

What possibly causes SLE

A 
genetic predisposition
NOT simple cross reactity
viral infection of multiple colones of Treg
broad microchimerism
antibodies to Treg cells
anti DNA antibodies> normal
375
Q

identical twins have what risk of getting SLE

A

10X

376
Q

What are treatments for SLE

A

oligonucleotides
antiB cell antibodies
C5 inhibitor

377
Q

What do oligonucleotides do

A

neutralize anti DNA abtibodies to prevent large immune complexes from clogging blod filters

378
Q

what do C5 inhibtors do

A

block MAC formation and lysis

379
Q

What is myasthenia gravis

A

Abs to acetylcholine receptors on skeletal muscle cells

380
Q

What do ABs to acetylcholine receptors cause

A

block Ach from binding to muscle cells which leads to poor contraction, muscle atrophy, C’ mediated lyss of muscle cells lead to weakeining extrme fatigue

381
Q

What is the cause of myasthenia gravis

A

unknown

382
Q

What could cause myasthenia gravis

A

cross reactive with poliovirus capsid protein

thymus tumor

383
Q

What is the treatment for myasthenia gravis

A

AChase inhibtors

384
Q

What is the possible cause of Rheymatoid arthritis

A

EBV (B cell virus) infection

385
Q

What does EBV lead to

A

B cell proliferation and antibody production

386
Q

What are the two results of EBV

A

mono or arthritis

387
Q

What causes mono

A

adequate Ab removal by AGs and C3b R and or moderate Ab protduction

388
Q

What causes arthritis

A

if inadequate Ab removl or excessive production

389
Q

What do immune complex deposition in joint cartilidges cause

A

C’ release of VFs and CFs which lead to neutrophil chmotaxis and enzyme and oxidant release to CGT damage CT repari scar tissue formation orgranuloma formation

390
Q

WHy type of HSR is immune complex deposition

A

type III HSR

391
Q

What are treatments for rheumatoid arthritis

A

mcAB to TNF alpha

392
Q

What is the cause for insulin dependent diabetes mellitus

A

damage to pancrease leading to IFN production to stimulate expression of MHC II proteins that are exogenous antigens and attract TH cells

393
Q

How does the immune system attack the islet cells

A

CMI
DTH
antibodies to C’ mediated lysis

394
Q

THe islet cells though were what

A

not attacked by lymphocytes so not really auto immunge

395
Q

What are the main sources of organs for transplanting

A

sygeneic sources
allogeneic sources
xenogeneic

396
Q

What are syngeneic sources

A

same chromosome pair #6

397
Q

What do syngeneic sorces contain

A

all MHC loci

398
Q

what is the probability of perfect match for syngeneic sources

A

1/4 for sibling

399
Q

What can be problem for syngeneic sources

A

no all genes for other surface proteins are matched unmatched chromosomeswhich can lead to slow rejection

400
Q

What is the only truly perfect match

A

identical twins

401
Q

A parent has what

A

half the same chromosomes and half different as child

402
Q

What are syngenic source example

A

adult stem cells from transplant recipient

403
Q

What are allogeneic sources

A

genetically dissimlar individual of the same species

404
Q

What is the probability of a perfect match at all MHC loci for allogeneic sources

A

astronomical

405
Q

What would be the best way to find a match for allogenic sources

A

prioritze A, B calss I and DR class II loci

406
Q

What does the probability of the match depend upon

A

the number of alleles available for each locus

407
Q

What also needs to be matched with allogeneic sources

A

ABO type because A and B are highly immunogeneic

408
Q

What causes natural antibodies to exist in some people

A

unmatched blood transfusion recipients
repeated pregnancies
promiscuity

409
Q

What is promiscuity

A

exposure to other peoples cells

410
Q

How much time for rejection for allogeneic if natural antibodies present

A

24 hours

411
Q

What can be a treatment for allogeneic sources

A

immunosuppressive druges for life time

412
Q

What do immunosuppressive drugs generally lead to

A

attendant increse in risk of infections and cancers, activation of latent viruses, and epensive

413
Q

how could embryonic stem cells be allogeneic

A

transplant of cells not organs, but allogenic unless a bank of the different ESC lines are available

414
Q

How is fetal tissue allogeneic

A

unless matched

415
Q

What is fetal tissue used for

A

Parkinsons disease, transplant into brain and the brain is immunologically privelged site less susceptible to rejection but not successful

416
Q

What is xenogeneic

A

from an individual of another species

417
Q

What is xenogeneic transplant

A

xenograft

418
Q

What is the chances of matching

A

none

419
Q

What is the risk of using xenogenic transplant

A

zoonotic virus infection

420
Q

What is PERV

A

porcine endogenous retrovirus

421
Q

What is the rejection time due to natural antibodies for xenogeneic antigens and complements

A

10-20 minutes

422
Q

How could xenogeneic sources be used

A

high availability and an engineer the animals to reduc their immunogenicity and immunosuppression from immune system in immunologically priveleged sit

423
Q

What is the physiology of transplant rejecion

A

blood vessels in organ must be attached to recipients blood supply, which travel through organ and come in contact with foreign endothelial cells and their antigens

424
Q

What is the initial IS attack on which endothelilal cells

A

those lining arteriesa and capillaries including lymphocyte and macrophage infiltration beneath the endothelium

425
Q

What is result of endothelial cell death

A

smooth pathway for blood flow becomes rough causing platelters to sick and burst open

426
Q

What do the platelets that burst open cause

A

blood clots

427
Q

What do the bood clots cause

A

block the blood supply to the other cells in the transplant and they ddie from a lack of oxygen and ATP

428
Q

If the transplant is unmatched or poorly matched what causes rejection

A

phagocytosis of cell gragments, dead cells, or secreted MHC proteins by DCs and antigen presentation produces priarily a B cell response

429
Q

What do the transplated organ express

A

highly immunogenic foreign MHC proteins

430
Q

What can be a problem of the frustrated phagocytosis to the transplant

A

type IV HSR and ADCC

431
Q

If the transplant is reasonably well matched what causes rejection

A

self MHC I proteins carrying and presenting foreign endogenous antigens will be recognized by the recipients CTLs initiating CMI attack

432
Q

What is different about unmatched and well matched transplant

A

intenicy of APC attack is reduced because fewer less variable less immunogenic antigens are presented

433
Q

What is the time course steps for rejection

A

primary IR
secondary IR
IR to self MHC proteins

434
Q

What causes primary IR

A

foreign MHC proteins

435
Q

How many days before rejection does primary IR occur

A

7-10

436
Q

What is the secondary IR in response to

A

foreign MHC proteins

437
Q

What occurs with secondary IR

A

antibody left over from the first set reactions immediately attaches to endothelial cells causing complement, clots, oxygen starvation

438
Q

When does rejection occur after secondary response

A

1 day

439
Q

What is IR to self MHC proteins with mHC protein epitopes

A

less rapid less intencse
months before transplant is rejected
helped by immunosuppressive drugs

440
Q

How can you suppress the recipients immune system

A 
ratiation of secondary lymphoid organs
cytotoxic chemotherapy drugs
antilymphocyte serum
mcAB o CD4 or CD28
corticosteroids
cyclosporine
441
Q

What does radiation of secondary lymphoid organs cause

A

new ASLs to be taught to tolerate transpant

442
Q

What do cheotherapy drugs do

A

block cell proliferation, mitosis, purine synthesis

443
Q

What does anti lymphocyte serum do

A

block CMI to neutralize or lyse

444
Q

WHat does cyclosporine do

A

block IL-2 production therefore CMI with side effects

445
Q

What does GVHD stand for

A

Graft vs host disease

446
Q

What is GVHD

A

IS cells in transplant attacking recipient

447
Q

What causes GVHD

A

transplanted organ contining significant numbers of APCs and lymphocytes

448
Q

For bone marrow transplants how many times does GVHD occur

A

50-70% of the time

449
Q

what is GVHD attack on

A

endothelial cells esp skin liver GI tract

450
Q

What is treatment for GVHD

A

immunosuppressive drugs

451
Q

How can the transplanted organ be so severe

A

even though doesn’t contain all the lymphocytes, the ability to proliferate with TH cell help causes significant attack

452
Q

What are tranplants that are not rejected

A

tranplants to immunolocially priviledged sites
females reproductract (sperm)
developing embryo does not cause attack
transplants into babies or infants
cultered cells
PSC transplants of umilical cord blood are less often rejected

453
Q

What are immunologically privileged sites

A

inaccessible to lymphocytes

454
Q

What are common immunologically privileged sites

A

corneoand blood brain barrier

455
Q

Why does female not have IR to sperm

A

seminal fluid is normally immunosuppressive and sperm are normally relatively hypo antigenic

456
Q

If IRs do occur, what could happen

A

cause infertility

457
Q

Can you make male attack his own sperm

A

no because sperm is immunologically privileged

458
Q

What is the way to attack sperm

A

disrupt blood testis barrier and induced auto immunity and sterility

459
Q

Can you make female attack sperm

A

no because hypoantigenic

sperm antigens would vary from one partner to the next

460
Q

Can you make female attack her eggs’ zona pellucida

A

no becaus she is tolerant to glycoproteins, if you could auto immunity to the eggs in ovaries and infertility would occur

461
Q

Can you attack embryo

A

no because it would vary with each pregnancy

462
Q

What needs to be overcome to convince the females IS to produce antibodies to FSH

A

tolerance and neutralizing it

463
Q

What are problems to blocking FSH

A

body needs it elsewhere

464
Q

What is the proposed target for allowing immune response in female reproductive system

A

39kd glycoprotein hormone hCG

465
Q

WHat produces hCG

A

trophoblast cells surrounding the embryo

466
Q

What does hCG signal

A

corpus luteum in the ovary to produce estrogen and progesterone that the uterus needs to maintain the blood rich endometrium that the ebryo needs to survive

467
Q

WHy is hCG not typically cause a problem

A

ignored bc very low doses

468
Q

What could neutralize hCG

A

antibodies the prohibit its binding to the corpus luteum

469
Q

What is the hope that having ntibodies

A

when want to get pregnant the IS would fail

470
Q

What could work the same as antibodies without risk of sterility

A

passive immunization with hCG antibody

471
Q

What could happen if using passive immunization for immunological abortion

A

serum sickness

472
Q

What does the embryos trophoblast form

A

chorionic villi which penetrate deep into the endometrium, in which maternal blood and lymphocytes bath the foreign cells which form th villi

473
Q

What is point of contact for IS is

A

trophoblast cells

474
Q

Why is there normally no attack

A

trophoblast cells reduce immune responses or the cells stimulate a humoral IR to their proteins involve blocking antibodies

475
Q

trophoblast cells express wht

A

non plymorphic class I MHC protein to which is relatively hypoantigenic

476
Q

What does the trophoblast cells secrete

A

a thick layer of non antigenic mucus which physically masks their antigens
locally effective non specific imunosuppressive factors

477
Q

What do trophoblasts inhibit

A

C’ activation

478
Q

WHat do trophoblasts stimulate

A

Treg cells to specific trophoblast antigens

479
Q

What could be imprinted in trophoblast cells

A

maternal chromosome #6

480
Q

What occurs if trophoblast cells stimulate a humoral IR to their proteins that block antibodies

A

attach to trophoblast antigens without activating C’, prevent other antibodies or CTLs from attaching

481
Q

If a transplant can be maintained by immunosuppressive drugs for a long period or time, what may develop

A

tolerance and the drugs may be discontinued

482
Q

Why are transplants into babies or infants less rejected

A

proteins on donor endothelial cells are accepted as self by the baby’s still maturing immune system

483
Q

WHy are PSC transplants of umbilical cord blood less rejected

A

the PSCs proliferade more rapidly than adult PSCs and the T cells are more willing to accept the recipient as self so less GVHD

484
Q

What is the problem of storing cord blood

A

not enough PSCs in one cord to benefit an adult

485
Q

cells in cord blood are less what

A

immunogenic

486
Q

why are cultured cells accepted by recipients IS more readily

A

MHC II positive cells ( becells and dendritic cells) de in culture routine
cells down regulate expression of MHC I proteins
no capillaries to attack
lymphocytes do not adhere to culture flasks and are easily removied

487
Q

How do you get tolerance with solid organ transplant

A

partial bone marrow transplant with solid organ produces mixed chimerism and tolerance

488
Q

What is the tolerance due to

A

regulatory T cell protecting transplanted organ

489
Q

What are types of implants

A

heart valves, artificial joints, teeth, glass eyes, cochlear implants and fasteners and adhesives

490
Q

What types of materials are used or the implants

A

plastic polymers, metal, ceramic

491
Q

Why do most induce inflammation

A

gradual breakdown of biomaterial due to wear and tear making new epitopes. leaking of chemical synthesis by products or excess monomer of material
adsorption of serum proteins to the biomaterial changing their contromateions and revealing new epiotopes

492
Q

What type of inflammation occurs with implants

A

chronic and delayed due to the size and composition of the implant

493
Q

What type of hypersensitivity is implants

A

type four

494
Q

What would be a way to reduce immune response to implants

A

coating them with antiinflammatory chemical, layers of self proteins in their natural conformations, or a stable layer of self cells to hide foreign surfaces

Immunology (4 decks)

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