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Module 2 vet med > Immunology > Flashcards

Immunology Flashcards

1
Q

Why is immunology important to vet med

A

Recovery from infection
Vaccination to prevent infection
Allergy and autoimmunity
Inflammation

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2
Q

What happens when we are infected with a microorganism

A

Detect the microorganism
Capture/ phagocytose the microorganism
Destroy the microorganism

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3
Q

Innate immunity has what factors

A

Physical barriers
Secretions
Enzymes
Complement
Phagocytose cells
Nk cells
Interferons

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4
Q

Intrinsic immunity has what factors

A

Restriction factors- TRIM5, APOBECs, Tetherin, SAMHD1

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5
Q

Adaptive immunity has what factors

A

Antibody
Helper T cells
Cytotoxic T cells

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6
Q

What does adaptive immunity develop

A

Develops in response to antigens on the invading organism

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7
Q

What are the two key attributes to the immune response

A
  1. Specificity
  2. Memory
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8
Q

What can macrophages detect

A

Lipids
Sugars
Other molecules unique to invading organisms

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9
Q

What can invading organisms be destroyed by

A

Engulfing by phagocytosis

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10
Q

What can be trapped in nets

A

Neutrophils

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11
Q

Phagocytosis cells kill microbes by

A

Oxygen dependent mechanisms
Oxygen independent mechanisms

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12
Q

What is oxygen dependent killing

A

Oxygen is needed to kill pathogens
Protective mechanism in macrophage through hydrogen peroxide to water using catalase

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13
Q

What is oxygen independent killing

A

Low molecular weight defending
Cathepsin G
Cationic proteins
Bacterial permeability increasing protein

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14
Q

Lysozyme function

A

Destruction of bacterial cell wall

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15
Q

Lactoferrin function

A

Chelation of iron

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16
Q

Proteolytic enzymes and hydrologic enzymes function

A

Digestion of ingested organisms

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17
Q

Microbicidal activity involves

A

Oxygen dependent killing
Oxygen independent killing

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18
Q

Inflammation and fever involves

A

IL-6, TNFa, IL1
Prostaglandins
Complement
Clotting factors

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19
Q

Lymphocyte activation involves

A

Antigen processing
Antigen presentation
IL1 production

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20
Q

Tissue reorganisation involves

A

Elastase, collagenase, hyaluronidisc
Fibroblast stimulating factors
Angiogenesis factors

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21
Q

Modulation of the immune response involves

A

IL12
Th1
Il10
TH2

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22
Q

What does complement do

A

Targets the immune response to the invading organism

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23
Q

What does triggering complement contributes to

A

The rejection of xenotransplantation organs

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24
Q

What is the pathway of complement activation pathway

A

Microbe enters the body
Complement C3b binds to microbial surface and is stabilised
C3bBb complex forms and splits more C3 into C3a and C3b
Cleavage products C3a and C5a promote local inflammation
C3a and C5a attract leukocytes to the site of infection
C3b coated microbe is phagocytosed
Assembly of the membrane attack complex on the microbial surface triggers lysis

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25
Q

Structure of an antibody

A

Fc receptor binding site
Complement fixation
Antigen binding at either end

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26
Q

When do the hormones peak at Primary response to antigen

A

IgM peaks at 7 days
IgG peaks at 14 days

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27
Q

Hormones involved in response to an antigen

A

IgM
IgG

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28
Q

Secondary response involves

A

A sharp increase of IgG
Steady increase of IgM

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29
Q

What happens with hormones in antigen response

A

IgM is released first followed by IgG

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30
Q

Secondary response features

A

Takes less time to respond
Larger response to the recovery threshold

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31
Q

Allotypic variation is

A

Variation in the amino acid sequence between light and heavy chains

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32
Q

Isotypic variation is

A

The heavy chain a certain way or light chain a certain way

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33
Q

Idiotypic variation is

A

Variation in the antigen binding domain

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34
Q

Immunoglobulin structure

A

Light chain and heavy chain is where an antigen binds
Then there is a hinge region which is flexible and can rotate
They are symmetrical
CL shows allotypic variation
Variable domain at VDJ

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35
Q

What is hinge region

A

Flexible and can rotate

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36
Q

Passive transfer is through what

A

The colostrum and properties are species specific

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37
Q

What is an epitope

A

Binding site on antibody that antigen binds to

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38
Q

Epitopes can either be

A

Linear
Conformational

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39
Q

In humans what amount of polymeric IgA is translocated to the gut daily

A

40mg per kg

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40
Q

What is estimated daily production of IgG

A

30mg per kg

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41
Q

IgG in response to antigen

A

Secondary response

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42
Q

IgG with receptor binding what

A

Fc

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43
Q

What does IgG do

A

Neutralises antigen
Fixes complement

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44
Q

Is IgG high affinity

A

Yes due to affinity maturation

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45
Q

What structure is IgM

A

Pentameric

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46
Q

What response is IgM

A

Primary response

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47
Q

Is IgM a low affinity

A

Yes

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48
Q

What does IgM do

A

Neutralises antigen
Fixes complement

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49
Q

How many binding sites does IgM have

A

10

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50
Q

In IgA what is special about the hinge region

A

Heavy glycosylation

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51
Q

In IgA what component is present which isn’t in other immunoglobulins

A

J chain

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52
Q

What type of structure is IgA

A

Dimeric or tetrameric

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53
Q

Features of IgA

A

Secreted immunoglobulin, resistant to proteolytic degradation
Secretory component mediates transport across epithelial surfaces

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54
Q

IgD is expressed on the surface on what type of cell

A

B cell during developmental phase

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55
Q

What is IgD use

A

Facilitator of immunity to respiratory bacteria

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56
Q

What are antibodies produced by

A

B cells

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57
Q

Where are B cells produced

A

Bone marrow
Foetal liver
Bursa of fibricus- birds

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58
Q

IgE triggers the release of what

A

Histamine

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59
Q

What does histamine release

A

Mast cell degranulation

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60
Q

Is IgE is expressed on what cells

A

Mast cells
Basophils
Monocytes

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61
Q

B cells derive from where

A

Hematopoietic stem cells

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62
Q

What are virgin B cells

A

Newly formed B cells

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63
Q

Features of virgin B cells

A

Short lived
75 percent leaves the BM

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64
Q

What antibodies are present on B cells

A

IgM
IgD

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65
Q

Where do gene rearrangements occur in BM

A

Variable region rearrange to generate VDJ and VJ

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66
Q

Where do gene rearrangments occur in lymphoid tissue

A

Isotype- class switching- occurs following stimulation of virgin B cell with antigen

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67
Q

What are the lymphoid organs

A

Lymph node
Spleen
Bone marrow
Thymus
GALT

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68
Q

Vaccination mimics what

A

Re exposure to a pathogen

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69
Q

Where do B cells encounter antigens

A

B cells and T cells traffic to lymphoid organs

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70
Q

Where are B cells made

A

Bone marrow

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71
Q

Where are T cells made

A

Thymus

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72
Q

How are antigens carried to lymphoid tissues

A

Lymphatic systems

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73
Q

B cell trafficking pathway

A

Bone marrow then B cells leave BM and enter blood vessel to the medulla

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74
Q

What parts are involved in the lymph node

A

Afferent lymphatic
High endothelial venue
Germinal centres
Efferent lymphatic
Medullary chords
B cell area
T cell area

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75
Q

What causes travel of lymphatic fluid

A

Simple act of motion

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76
Q

What direction is the movement of lymphatic fluid

A

Unidirectional

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77
Q

What does vaccine need to come into contact with in draining lymph fluid

A

B and T cells

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78
Q

Where can u vaccinate in the body

A

Everywhere

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79
Q

Lymphatic circulation pathway

A

Interstitial fluid
Lymph capillaries
Collecting lymph vessels
Lymph node
Lymph duct
Lymph trunks
Venous system

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80
Q

What vessels have a beaded appearance

A

All vessels except lymph capillaries

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81
Q

What do semilunar valves do

A

Ensure flow in one direction

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82
Q

Germinal centre consists of what

A

Helper T cell- producing cytokines
Dendritic cells
Some of these cells will make memory cells

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83
Q

Pathways of germinal centres

A

B cell to encounter with antigen to secondary lymphoid follicle to germinal centres

84
Q

Pathway of centroblast

A

Centroblast
Centrocyte
Lymphoblasts
Memory B cells or plasma cells

85
Q

What are B cells competing for

A

Antigen

86
Q

What happens when antigen levels decrease

A

Affinity increases

87
Q

If affinity increases what happens

A

More likely to survive the cells

88
Q

Times of vaccination selects for what

A

Best affinity

89
Q

How is the thymus formed

A

Gene is switched on and then cells congregate and the thymus forms

90
Q

What happens to your thymus as you get older

A

Decreases in size and you become more immune deficient

91
Q

Cells within the thymus are called

A

Thymocytes

92
Q

What do the cells go into the thymus as and leave as

A

Go in as precursors and leave as T cells

93
Q

Thymus structure and components

A

Cortex- cortical epithelial cell, trabeculae, thymocyte
Medulla- macrophage, medullary epithelial cell, hassals corpuscle, dendritic cell

94
Q

What mutation do nude mice have

A

FOX1 gene

95
Q

Do nude mice have a functioning thymus

A

No- virtually no T cells

96
Q

The impact on nude mice FOX1 gene the impact on this acquired immune response is

A

Defective antibody formation
No cell mediated response
No delayed type hypersensitivity
No killing of malignant or virus infected cells
No graft rejection

97
Q

Thymic selection pathway

A

Nurse cell
Blast cell
Thymocytes
Gene rearrangement
To CD4/CD8
TCR expression
Interdigitating cell
Macrophage
Naive T cells

98
Q

What is positive selection

A

Interaction with MHC class 1 or MHC class 2 on cortical epithelium

99
Q

Do T cells kill parasites

A

Yes

100
Q

what does CD4 do

A

Stabilise interactions with receptors

101
Q

Helper T cell uses what CD

A

CD4

102
Q

Cytotoxic T cell uses what CD

A

CD8

103
Q

Dendritic cells instruct what

A

Helper T cells to respond in an appropriate way

104
Q

T cells promote what

A

Cellular response

105
Q

Once activated what can T helper cells do

A

Interact with B cells and support their expansion

106
Q

Humoral immunity

A

B cell proliferation
Class switching
Increase Ig production

107
Q

Th17 promotes

A

Neutrophil response

108
Q

What do TH2 cells favour

A

Humoral response
Induce mast cell production

109
Q

What happens when neutrophils kill a cell

A

Neutrophil

110
Q

Cytotoxic T cells do what

A

Kill cells as they tigger cell death

111
Q

What are granules

A

Modified lysosomes that contain effector proteins in an active form

112
Q

What do NK cells recognise

A

Stress signals

113
Q

natural killer cells have a high number of what on their surface

A

Fe receptors

114
Q

Pattern recognition receptors

A

Pathogen associated molecular patterns- PAMPS
Damage associated molecular patterns- DAMPS

115
Q

What does PAMPS and DAMPS do

A

If something is dangerous and recognising a foreign body

116
Q

What is antigen presentation

A

Display of processed peptide fragments to T cells for recognition by their T cell receptor

117
Q

What mechanisms have macrophages developed with which they can sense danger

A

Mannosyl fucosyl receptor
CD14
Fc receptors
Complement receptors
MHC class 2

118
Q

What is the function of mannosyl fucosyl receptors

A

Bind to sugars on the surface of microorganism

119
Q

CD14 function

A

Bind to lipopolysaccarhide receptor

120
Q

Fc receptor function

A

Bind to immunoglobulin and triggers phagocytosis

121
Q

Complement receptors function

A

Bind to complement factor on surface of microbe

122
Q

MHC class 2 function

A

Antigen presentation to T cells

123
Q

In histology the red is

A

Dendritic cells

124
Q

What is MCH class 1 responsible for

A

Peptide binding groove- non covalent

125
Q

What is MCH class 2 responsible for

A

Alpha and beta chains

126
Q

What are peptides recognised by

A

Human MCH class 1

127
Q

Anchor residue function

A

Holds the peptide

128
Q

Cheetahs affect with the MCH system

A

Cheetahs are inbred and have less genetic MCH diversity this causes a lessened immune response

129
Q

A killed vaccine doesn’t have what type of cell

A

Cytotoxic T cells

130
Q

What does live attenuated vaccine route of antigen processing

A

Make cytotoxic T cell

131
Q

Why do we need the MCH system

A

If we all had the same MHC molecules then we would have a limited ability to protect ourself against antigens
Allow infinite diversity against different pathogens
Diversity of MCH molecules means more immunity
Small tight population means that there is not enough MCH

132
Q

What happens when we loose MCH expression

A

CTCV cells down regulate MCH and secrete immunosuppressive cytokines
Deregulates MCH so we cant see it on the surface and means tumour cells can grow and develop

133
Q

What did vaccination start with

A

Smallpox vaccine

134
Q

Killed vaccines

A

No longer able to replicate following treatment
Protection is short lived
Booster needed

135
Q

Killed vaccine examples

A

Rabies
Lepto

136
Q

Live attenuated vaccines

A

Usually more potent than killed vaccines as limited viral replication
Antigen is produced by exogenous and endogenous pathways- stimulate cytotoxic T cells
More potent so selects for high affinity B cells so higher affinity maturation which causes a longer immune response

137
Q

Live attenuated vaccine examples

A

Kennel cough

138
Q

Subunit vaccines

A

Protective virus neutralising antibodies tend to be directed against surface proteins of the virus

139
Q

Examples of subunit vaccine

A

Canine herpes virus
Strangles

140
Q

Vectored vaccine function

A

Using attenuated virus to deliver gene encoding

141
Q

Examples of vectored vaccine

A

Feline leukaemia virus

142
Q

Advantages of inactivated vaccine

A

Safety- no reversion to virulence
Do not induce disease
Induce response against multiple viral proteins
Inexpensive
Antigen consistence
Stable at room temperature

143
Q

Disadvantages of inactivated vaccine

A

Need to ensure complete inactivation
Response may require adjuvant
Cellular components may cause side effect
Cold chain required for storage and transport
More than one injection is usually required as antigen does not persist

144
Q

Live attenuated advantages

A

Antigenic epitopes are preserved
Antigen persists, response may be long lived
Inexpensive
Administration across mucosal surfaces

145
Q

Live attenuated vaccine disadvantages

A

May revert to virulent form
May induce disease in weakened immune system
Cellular components may cause side effects

146
Q

Sub unit advantages

A

Safe
Focussed immune response
No hazards associated with production
No cellular contaminants

147
Q

Sub units disadvantages

A

More than one injection may be required as antigen does not persist
Cold chain required for storage and transport
Response may require adjuvant

148
Q

Advantages of vectored vaccines

A

Single gene
Mostly safe
Focused immune response
No hazards associated with production
No cellular components
Oronasal delivery possible
Endogenous and exogenous antigen presentation

149
Q

Disadvantages of vectored vaccines

A

May not induce response to tertiary structures
May cause mild pox virus symptoms
Response to vaccine may be weak
Response to vector may affect subsequent doses

150
Q

What is the perfect vaccine

A

A good safety profile
Highly efficacious
Induce both Humoral and cellular immunity
Minimal requirement for boosting
Goofed breadth of immunity against diverse viral stains
Stability and ease of administration

151
Q

What is an adjuvant function

A

Enhance immune response

152
Q

How does an adjuvant work

A

Danger hypothesis takes something non dangerous and switch on antigen presentation by promoting uptake of antigen presenting cells or by switching on macrophages

153
Q

Autoimmune reaction represents what

A

A breakdown of self tolerance

154
Q

What is tolerance

A

State of unresponsiveness that is specific for a particular antigen and which is induced by prior exposure to that antigen

155
Q

Dizygotic twin calves in tolerance. What happens

A

They can exchange haemotopoietic stem cells as a result of placental fusion.
The twins are thus tolerated to each others MHC molecules

156
Q

In peripheral tolerance, the endothelial barrier segregates what

A

T cells from self antigens

157
Q

In peripheral tolerance, what triggers an immune response

A

Self antigens that present in insufficient quantities

158
Q

What is clonal deletion

A

When high levels of self antigen is present which causes destruction of B cells

159
Q

Autoimmunity arises through bypass of the control of

A

Autoreactivity

160
Q

Autoimmune conditions

A

Addisons disease- adrenal glands
Rheumatoid arthritis
Myasthenia gravies
Immune mediated haemolytic anaemia
SLE

161
Q

What is the full name of an ELISA

A

Enzyme linked immunosorbent assay

162
Q

Method of ELISA

A

Add test sample to well of ELISA plate
Wash well to remove unbound antigens
Add antibody enzyme conjugate
Wash well to remove unbound conjugate
Add chromogenic substrate for enzyme
Read absorbance on microplate reader

163
Q

What does monoclonal antibody grab onto in ELISA plate

A

Antigen

164
Q

Pathway of ELISA

A

Monoclonal antibody grabs onto antigen and anchors it on the ELISA plate.
Then remove unbound antigen then add second antibody.
This will recognise a different epitopes in order to detect that second antibody, the antibody is coupled with an enzyme

165
Q

What is the amount of antigen in an ELISA well directly proportional to

A

Amount of conjugated enzyme

166
Q

Amount of antigen is directly proportional to

A

The amount of colour change

167
Q

In immunoassay Less colour has

A

More progesterone

168
Q

Immunoassay using labelled competitor method

A

Add test sample- 10ml to well of elisa plate
Progesterone in the sample bins to coating antibody
Add progesterone enzyme conjugate 200ml
Wash well to remove unbound progesterone enzyme complex
Add chromogenic substrate for enzyme

169
Q

Immunoblotting also stands for

A

Western blotting

170
Q

In electrophoresis proteins are separated firstly by

A

Size

171
Q

Western blotting methods

A

Incubate blot with primary antibody
Wash
Incubate blot with enzyme conjugated secondary antibody
Wash
Incubate blot with substrate

172
Q

Western blotting is washed.WHY

A

So there is no antibody’s left on the slide
No contamination occurs

173
Q

Chromatin will go what colour

A

Completely blue

174
Q

Enzyme catalyses colour change of what

A

No colour to colour

175
Q

Immunodiffusion precipitates test size of ring is what to amount of antigen present

A

Directly proportional

176
Q

Coombs test can be used for what

A

Haemolytic anaemia

177
Q

Allergy is what

A

An overreaction of the immune system to a harmless antigen

178
Q

What type of immune response does an allergy trigger

A

Inappropriate immune response

179
Q

Hypersensitivity can be classed into four different sections

A

Class 1
Class 2
Class 3
Class 4

180
Q

Class 1 hypersensivity

A

Binding of antigen to surface IgE

181
Q

What hypersensitivity class is primarily on mast cells

A

Class 1

182
Q

In class 1 what happens

A

Mast cell degranulation then an inflammatory response occurs

183
Q

Class 2 hypersensitivity

A

Small molecules binding to cell surface components modify the antigency and render it immunogenic

184
Q

In class 2 hypersensitivity b cells response to antigen does what to the cell

A

Destroys the cell

185
Q

class 3 hypersensitivity

A

Soluble protein antigens bind to immunoglobulin forming immune complexes. Complexes are deposited in blood vessel walls and phagocytic cells pick them up and destroy them

186
Q

Where are complexes in class 3 deposited

A

In blood vessel walls and phagocytic cells pick them up and destroy them

187
Q

Class 4 hypersensitivity

A

Antigen specific T cells

188
Q

Reactions to class 3

A

Arthrus reaction eg. Tetanus vaccine
Serum sickness eg. Drugs
Farmers lung
Hypersensitive penumonitis

189
Q

Hypersensitivity type 1 features

A

Antigen- soluble antigen
Effector mechanism- mast call degradation
Reaction- asthma, allergic rhinitis
Granule contents- histamine, hepatin, proteases, enzymes, cytokines

190
Q

What wont work with with an antihistamine present

A

Steroids

191
Q

Antihistamines block binding of

A

Histamine so vasodilation doesn’t occur

192
Q

What is harder to treat a chronic allergy or a acute allergy

A

Chronic allergy

193
Q

Diseases hypersensivity class 1 symptoms

A

Asthma
Flares on skin
Coughing
Diarrhea
Atopic dermatitis- house mites and fleas
Food allergies
In horses- sweet itch- insect bites
Heaves- allergy to mould

194
Q

Sweet itch symptoms

A

Alopecia
Atopical dermatitis
Thickening and ridgening of skin
Due to saliva of insect bites- manifests on horses coat

195
Q

Hypersensitivity class 2 function

A

Can create an epitope
Only binds to rbc when drugs are present

196
Q

Hypersensivity class 2 features

A

Antigen and altered cell surface components
Effector mechanisms- IgE binds to novel antigen, complement cascade triggered.
FcR targeting leukocytes. IgE binds to cell surface receptor- autoimmunity
Reaction- haemolytic anaemia
Drug modification of a protein antigen
Transfusion reaction- neonatal isoerythrolysis

197
Q

Immunodeficiencies

A

Results of a defect in an immune response

198
Q

Hypersensitivity class 3

A

Antigen- soluble antigen
Effector mechanisms- immune complexes, complement, phagocytes

199
Q

How can neonatal isoerythrolysis be detected

A

Erythrocyte agglutination test

200
Q

Hypersensitivity class 4

A

Soluble antigen
Effector mechanisms- macrophages, eosinophils
Reaction- asthma, contact dermatitis
When cells from immune system move into site of allergen exposure.
Delayed hypersensitivity of 1-3 days

201
Q

IgA inherited deficiency

A

Secreted immunoglobulin
Resistant to proteolytic degradation
Secretory component mediates transport across epithelial surfaces
High affinity receptor on monocytes and neutrophils

202
Q

Immunodeficiency is in response to

A

Viral infection

203
Q

Viruses and infections to do with immunodeficiency

A

Lentiviruses
FeLV- thymic atrophy
Distemper
Parvovirus infection
Parasite infection- generalised immunosuppression

204
Q

Atopic dermatitis is in what class of hypersensitivity

A

Type 1

205
Q
A

Module 2 vet med (16 decks)

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