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CP - JL > Core Immunology - Part 1 > Flashcards

Core Immunology - Part 1 Flashcards

1
Q

What makes you more likely to get an autoimmune disease

A

Women
Elderly
Sequestered antigens
Environemntal triggers - infection, trauma-tissue damage, smoking

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2
Q

What is the most common genetic susceptibility in autoimmune diseases

A

In the HLA region aka the MHC protein

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3
Q

What does the ACPA antibody in rheumatoid arthritis attach to

A

MHC

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4
Q

Where is MHC I found

A

on all cells

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5
Q

Where is MHCII found

A

On T cells and APCs

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6
Q

Failures in what can cause autoimmune disease

A 
Central tolerance (where self-recognises T cells are destroyed in the thymus)
Peripheral tolerance (where sclf-recogniseing T cells are removed in the lymph nodes by T-reg cells)
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7
Q

How do T cells cause inflammation

A

Inflammatory Cytokines

Helping B cells make autoantibodies

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8
Q

How do auto reactive T cells cause clinical disease

A

Directly cytotoxic

Inflammatory cytokines

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9
Q

How do auto reactive B cells cause clinical disease

A

Directly cytotoxic
Activate the complement system (antibodies bind to C1q)
Interfere with normal physiological function

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10
Q

What is organ specific autoimmune disaese

A

Auto-immunity restricted to that organ
Overlap with other organ specific diseases
Typically autoimmune thyroid

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11
Q

What are non organ specific autoimmune diseases

A

Affects several organs
Auto-immunity assocaited with antigens found on most cells in the body
Overlap with non-organ specific diseases
Typically connective tissues disaeses

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12
Q

What is Hashimotos Thyroiditis

A

Destruction of thyroid follicles
Auto-antibodies to thyroid peroxidase and thyroglobulin
Results in hypothyroidism

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13
Q

What is Grave’s diseases

A

Anti-TSH autoantibodies

Cause hyperthyroidism

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14
Q

What is myasthenia gravis

A

Auto antibodies to the ACh receptor in the NMJ

Quickly fatigued muscles, difficulty keeping eyes open, speaking, swallowing

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15
Q

What is pernicious anaemia

A

Antibodies to parietal cells or intrinsic factor
Cant absorb B12
Get pernicious anaemia (macrocytic anaemia), decreases Hb levels

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16
Q

Example of sequestered angtigens

A

The nuclei of cells

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17
Q

How does the nuclei of cells becomes in contact with the immune system

A

Defective apoptosis or necrosis means the DNA is not destroyed

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18
Q

How does SLE occur

A

Get anti-nuclear antibodies (ANA) due the sequestered nuclei being exposed
The ANA and their antigens form immune complex that bind to complement factors and cause inflammation in any tissue

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19
Q

How do ANA cause inflammation

A

Bind to complement factors causing inflammation in any tissue

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20
Q

Common features of SLE

A

Photosensitivity, malar rash, mouth ulcers, arthralgia, arthritis, fatigue, alopecia

Organ invovlement

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21
Q

Organ involvement of SLE

A

Kidneys - Lupus Nephritis
Lungs - pleural effusion/pleurisy
CNS - Cerebral lupus, seizures, comas

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22
Q

Testing for SLE

A

ANA

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23
Q

Treatment of SLE

A

Immunosuppression

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24
Q

What are ANCAs

A

Anti-neutrophil cytoplasmic antibodies

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25
Q

What are the 3 forms of vasculitis

A

Microscopic Polyangiitis
Granumaltosis with polyangiitis (wegeners granulomatosis)
Eosinophilic granulomatosis with polyangiitis

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26
Q

What is a granuloma

A

mass of inflamed tissued - often get lesion in the URT dance an be destructive leaving cavities

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27
Q

What is polyangiitis

A

Inflammation of many small vessels in the skin, kidney, lungs and gut

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28
Q

Treatment of ANCA Vasculitis

A

Immunosuppression

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29
Q

Test for ANCA Vasculities

A

ANCA antibodies

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30
Q

What is primary Raynauds

A

Common in young women
Runs in family
ANA negative

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31
Q

What is secondary Raynaud’s

A

ANA positive

May be associated with scleroderma, SLE and other diseasesa

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32
Q

What is scleroderms

A

Autoimmunity leading to ischaemia and fibrosis

ANA antibodies - particular anti-centromere and anti Scl-70 (look for these in diagnosis)

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33
Q

What does scleroderma affect

A

Raynaud’s phenomenon
Skin thickening and tightening in fingers and face
Fibrosis may affect lungs, gut and kidneys

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34
Q

How to treat myasthenia gravis

A

Acetycholinesterase inhibitors

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35
Q

How to treat pernicious aneamia

A

Replace B12

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36
Q

How to treat Hashimotos Thyroiditis

A

Give thryoxine

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37
Q

How to treat Grave;s diseases

A

block thyroid function

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38
Q

How to treat SLE and ANCA Vasculitis

A

Immunosuppresions
Glucocorticoids
B cell depletion

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39
Q

How to treat scleroderms

A

Vasodilating drugs
Stem cell transplant
Cyclophosphamide

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40
Q

What is positive predictive value

A

The proportion of people who test positive who have the disease

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41
Q

What is negative predictive value

A

the proportion of people who test negative who do not have the disease

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42
Q

What is the likelihood ratio

A

likelihood of finding in disease patient/likelihood of finding in healthy patient

tells us how discriminate the test can be between patients with the disease and healthy patients

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43
Q

What is CRP produced in response to

A

Produced by the liver in response to IL-6

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44
Q

ESR in infection

A

Longer due to the higher viscosity due to increased good proteins

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45
Q

What happens to albumin in chronic inflammation

A

decreases

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46
Q

How do we measure complement activation

A

Measure using C3 and C4 levels particlarly

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47
Q

What are the precise targets of ANA

A

Extractable Nuclear Antigens

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48
Q

What is destroyed in SLE

A

the nuclei of cells by neutrophils/macrophages due to the ANAs to the ENAs

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49
Q

How do we test for ANAs

A

Large fibrocyte cells with antigen On
Add FITC-conjugated antibody –> fluoresces showing positive result

BUT positive ANA doesn’t necessarily mean you have lupus

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50
Q

What is a micro-bead immunoassay

A

Multiplex assessment of non-organ specific autoantibodies

Attach patients serum to bead - if autoantibody is present beads will fluoresce

Can test unto 20 at a time - but only measures diseases specific and only autoantibodies against the nucleus

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51
Q

What is rheumatoid factor

A

Autoantibody against the Fc portion of IgG

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52
Q

When if rheumatoid factor found

A

Often in rheumatoid arthritis

But only 70% sensitivity/specificity

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53
Q

Where else is rheumatoid factor found

A

In other disease with high polyclonal B cell stimulation e.g. chronic infection

High levels can be pathogenic in vaculitis

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54
Q

What is a more specific way for rheumatoid arthritis

A

ACPA (Anti-CCP) antibody
95% speicific but similar sensitivity to rhuematoid factor

ACPA positive patients tend to have a more severe and erosive disaeses

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55
Q

When is CCP made

A

Made when cells die –> but in rheumatoid arthritis we make antibodies against it

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56
Q

Detection of dsDNA

A

Crithidia lucillae assay (protozoa)
Farr Assay
ELISA (enzyme linked immunosorbent assay)

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57
Q

Detection of ENA’s

A

Immunoblots

Individual ELISA

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58
Q

Cytoplasmic and perniculear targets of ANCA

A

Cytoplasmic - PR3

Perinuclear - MPO (MPO is an enzyme used by neutrophils to kill bacteria)

59
Q

What is MPO

A

MPO (MPO is an enzyme used by neutrophils to kill bacteria)

60
Q

Is ANCA clinically useful

A

Positive ANCA good at positive diagnosis BUT histology is gold standard
Negative ANCA does not exclude it

61
Q

Do we need to treat positive ANCA with no clinical conditions

A

No

62
Q

What does the re-currence of ANCA in a patient who was ANCA negative in remission suggest

A

Risk of diseases flare

But poor temporal correlation between ANCA return and disease flare

63
Q

What do you have i primary biliary sclerosis

A

Anti-mitochondrial antibodies

64
Q

What causes autoimmune hepatities

A

auto-antiboides to smooth muscle and to liver/kidney/microsomal (LKS) antiboides

Detect these by IF screening using rodent tissue block and antigen specific ELISA

65
Q

Negative predictive value of ICA and IAA in type I diabetes

A

almost 99%
Increased risk of development of type 1 diabetes with greater number of different autoantibodies and younger age of patient

66
Q

Where are blood group substances found

A

On the surface of all vascular endothelial cells and certain epithelial cells

67
Q

What are MHC

A

Set of genes found in all vertebrate species

68
Q

What do MHC have roles in

A 
Immune function
Disease susceptibility
Reproductive success (females choose their partners based on their HLA profile)
69
Q

What disease has a strong association with HLA

A

ankylosing spondylitis

70
Q

What do MHC present to T cells

A

self or non self antigens

71
Q

Where is the MHC on the chromosome

A

6p21.3

72
Q

What is the role of Class I HLA

A

Found on all nucleated cells
Present endogenous antigens
Present antigens such as in viral infections

73
Q

What is the role of Class II HLAs

A

Primarily expressed on B lymphocytes

Expression can be induced on T lymphocytes and other cells

74
Q

Composition of class I HLA

A

45d heavy chain non-covalenently associated with a polymorhpic B2 microglobulin

75
Q

Composition of class II HLA

A

31-34kd alpha chain non covalently association with beta chain

76
Q

Peptide binding domain in Class I

A

alpha 1 and 2. alpha 3 is proximal

77
Q

Peptide binding domain in class II

A

alpha 1 and beta 1

78
Q

What is the expression type of HLA genes

A

Co-dominant - all of the inherited antigens are displayed on the cell surface

79
Q

Why is HLA polymorphic

A

Survival advantage - means if there is a new infection it is likely that we have an MHC suitable to that antigen

80
Q

DIrect recognition in transplantation

A

WBC’s from the donor move to the T cells of the recipient

These cells move back to the transplant causing damage

81
Q

Indirect recognition in transplantation

A

Graft peptides recognised by recipient immune system

T cells activated and migrate to the graft in a normal immune response

82
Q

Semi-direct recognition

A

Recipient and donor APC interact - these form a new APC and migrate to the lymph node
T cells activated
Causes immune response to transplant

83
Q

What is sensitisation

A

Any event that elicits a HLA directed immune response e.g. pregnancy, blood transfusion, transplantation

84
Q

How to prevent transplant rejection

A

Serum screening and cross matching

85
Q

What is sensitisation calculation

A

HLA antigens made into a cRF (calculated reaction frequency) –> describes the amount of time in the past 10000 that a donor would have been inaccessibly to the recepient

86
Q

What would a cRF of 0% indicate

A

They can receive virtually any donor as you have not been sensitised against them

87
Q

What is the likelihood of a transplant based on

A

Blood group
Rarity of HLA type
Extent to which they are sensitised

88
Q

How does cross matching occur

A

T cell from donor - will express its HLA antigens
Add donor lymphocytes to patients serum
Add reporter molecules that bind to antibodies and fluoresce if they have minded
Add a lineage marker to tell the specific cell antibodies have bound to
Pass through a flow cytometer

89
Q

What happens in hyper-acute rejection

A

Activation of complement and clotting casacde

Coagulation
Lose integrity of vascular endothelium –> organ become engorged with blood–> DIC–> tissue becomes necrotic

90
Q

Antigen in type II allergy

A

Occurs at cell surface

91
Q

What type of allergy does penicillin trigger

A

type II

92
Q

Good pastures nephritis, erythroblastosis and fetalis associated with wchih type of allergy

A

type II

93
Q

What is SLE associated with allergy wise

A

type III

94
Q

Contact dermatitis is which type of allergy

A

type IV

95
Q

Mould hay and farmers lung in which type of allergy

A

type III

96
Q

Onset time of type III

A

3-8 hours

97
Q

Onset time of type II allergy

A

minutes to hours

98
Q

HIstology in type i allergy

A

basophils and eosinophils

99
Q

Histology in type II allergy

A

Antibody and complement

100
Q

Histology in type III allergy

A

Neutrophils and complement

101
Q

Histology in type IV allergy

A

Monocytes and lymphocytes

102
Q

What occurs in cytotoxic allergy

A

IgG/IgM response to self or foreign antigen at the cell surface
Get complement activation, phagocytosis

Can occur in pregnancy

103
Q

Type III is a reaction against what type of antigens

A

soluble

104
Q

Type IV is a reaction against what type of antigens

A

tissues or organs

105
Q

Traditional cause of type III reaction

A

Serum sickness

106
Q

Where does arthurs reaction occur

A

It is a type III reaction that affects the perivascular space when drugs given IV

107
Q

Common antigens of type IV reaction

A

metals or tuberculin reaction
Antigen taken up by T cells
T cells produce cytokines and activate macrophages causing damage

108
Q

Development of an allergy

A

Breakdown of barrier
Sensitisation
Changes in T cell substype - predominantly Th2 cells
T cells activated and produce IgE

109
Q

Similarities between parasitic infections and allergiess

A

The same components of the immune system response to both

110
Q

What has driven the rise in allergies

A

The lack of infectious drive

111
Q

Immune response to parasites

A

Increased levels of IgE

Tissue inflammation due to basophils, eosinophils and mastocytosis

112
Q

Method of preventing autoimmuntiy

A

Probiotics given to pregnant women
Stimulation by microbes in protective!
Mechanism: th1/2 deviation, antigenic competition and imunoregulation

113
Q

Defect in FLG gene causes what

A

Eczema

But genetic factors alone are not sufficient for the disease only makes you more susceptible

114
Q

What is an allergen

A

Antigens that initiate an IgE mediated response

115
Q

What does Th1 normally deal with

A

intracellular infections

116
Q

Role of Th17

A

Thoguht to have a protective role

117
Q

Role of Th2

A

These cells produce IL-4 that drives B cells to produce IgE

118
Q

How does IgE cause an allergic response

A

Mast cell and basophil degranulation - released preformed mediators and de novo synthesised mediators that cause the late response

119
Q

What causes the late response in type 1 reactions

A

Eosinophils and central role for th2 T cells

120
Q

What are secondary mediators

A

leukotrienes and prostaglandings

121
Q

Role of TH2 cells in allergy

A

Releases multiple cytokines
Drives immunoglobulin production
Activates the innate immune response

122
Q

What type of allergic reaction is rhinitis

A

Type 1

123
Q

What is rhinitis

A

Allergic response affecting upper airways
Blocked runny nose and eye symptoms

It is perennial/seasonal

124
Q

Treatment of rhinitis

A

Antihistamines and nasal steroids

125
Q

Causes of rhinitis

A

dust mite, animals, pollen

126
Q

What is asthma

A

Inflammation and hyperactivity of the lower small airways

127
Q

What is a key cause of asthma

A

house dust mite

128
Q

How does damage to the airways occur in asthma

A

Due to the late phase response -> damaged air wards are hyperactive to non-allergic stimuli e.g. fumes

129
Q

What types of dermatitis are there

A

Atopic e.g. eczema

Contact e.g. allergic - type IV allergy

130
Q

Features of dermatitis

A

Itching, blistering, weeping and cracking of skin

131
Q

What is IL-31

A

A t cell derived itch mediator

132
Q

Major trigger of contact dermatitis

A

House dust mite

133
Q

What is anaphylaxis

A

IgE mediated systemic hypersensitivity response

Can get hypotension, bradycardia, collapse and cardiac arrest

134
Q

Basophil activation test to diagnose allergy

A

Measure basophils before and after allergen given
Measure the markers present on basophils (they are normally present in low levels which come out when they are activated)

135
Q

Specific IgE tests for allergyn

A

Blood test, looks for specific IgE’s, but lots of false negatives and positives

136
Q

Skin prick test for allergy

A

Add 3 bits: Control e.g. water, histamine/poisitive control and allergen if over 3mm reaction you allergic

BUT risk of false/negatiev/ policies and need antihistamines as risk of major allergy

137
Q

Treatments of allergic reaction

A

Antihistamines
Steroid for late phase
Adrenaline if anaphylaxis
Can sue immunotherapy too –> use if life/threatening reactions to wasp/bee stings

138
Q

What is immunotherapy

A

Decreases tissue number and decreases mediator release and alters cytokines produced

139
Q

What distinguishes anaphylaxis

A

Immediate onset diarrhoea

140
Q

What its he gold standard test of allergies

A

Oral challenge test

141
Q

IgE mediated food allergies

A

Anaphylaxis, urticaria, angioedema, oral allergy sydrome, acute rhinitis and asthma

142
Q

Mixed food allergy

A

Atopic dermatitis, eosinophilic osephagitis, eosinophilic enteritis

143
Q

Non-IgE mediated food allergies

A

contact dermatitis, dermatitis herpetiformis, proctocolitis, FPIES

CP - JL (14 decks)

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