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ODDR > Immunology > Flashcards

Immunology Flashcards

1
Q

What does the inmate immune system do?

A

This stops the proliferation of pathogens and kick starts the inmate immune system.

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2
Q

What does the active immune system do?

A

Irradiates pathogens and creates a positive feedback loop to the inmate immune system

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3
Q

How do epithelial cells create a barrier?

A

They create biochemical barriers like mucus etc and they also mechanicals seeps away these trapped bacteria.

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4
Q

What is the microflora?

A

Barrier of bacteria that live on out surface membranes causing no harm but inhibit pathogenic bacteria.

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5
Q

What is lysosome most effective against and how does it work?

A

Gram positive
Cleaves bonds between the sugars in peptidoglycan:
N-acetylglucosamine
N-acetylmuramic acid

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6
Q

What are antimocrobrial peptides (3 forms)?

A

Defensin
Cathelicidins
Histatins

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7
Q

What is a zymogen?

A

Inactive form of an enzyme usually needs proteolytic cleavage to become active

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8
Q

Defensins?

A

Amphipathic Meaning they have hydrophilic and hydrophobic portions allowing them to insert into exposed lipid membranes forming a pore.

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9
Q

Cathelicidins?

A

Amphipathic cause membrane disruption (LL-37)

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10
Q

Histatins?

A

Produced by parotid gland, they are histadine (type of amino acid) rich and have antifungal properties.

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11
Q

Which is faster the innate or adaptive?

A

Innate (mins hours)

Adaptive (days/weeks)

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12
Q

How does the inmate arm recognise pathogens?

A

They recognise common foreign structures, it’s not pathogen specific.
This is encoded in the DNA

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13
Q

How does the adaptive recognise pathogens?

A

Random generation of recognition improving the recognition. These receptors are not encoded in DNA but memory cells are formed for years

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14
Q

When did the adaptive immune system form?

A

In the agnathans recent in evolutionary terms

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15
Q

How is the compliment system so rapid?

A

Lots of zymogens are already made and in the blood and just need to be cleaved in a reaction cascade amplifying the response

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16
Q

What are the three compliment system activation pathways?

A

Lectin pathway
Classical pathway
Alternative pathway

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17
Q

What is the classical pathway

A

C1 complex interacts with pathogen surface and leads to the generation of C3 convertase activity which converts C3 into 2 products

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18
Q

What is the alternative pathway?

A

C3 undergoes spontaneous hydrologists leading to the deposition of C3 convertase onto a cells surface.

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19
Q

What is the lectin pathway?

A

Mannose binding lectin bonds to pathogen surface creating cascade leading to C3 convetase activity.

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20
Q

What do all the compliment pathways do?

A

Activate C3 convertase, which cleaves C3 leaving C3b bound to microbe surface and releasing C3a

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21
Q

What do C3a and C3B do

A

Mediate the release of C5a and C5b from the cutting of C5

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22
Q

What do C3a and C5a do?

A

the recruit phagocytise cells at infection sites and promote swelling

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23
Q

What does C3b do?

A

It is bound to the pathogen surface and it causes pathogens with a C3b receptor to engulf and destroy the pathogen

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24
Q

What does C5b do?

A

Forms a complex with C6, C7, C8 which recruits lots of C9 molecules which join together and punch a hole in the cell membrane causing it to be lysed. MAC (membrane attack complex)
MAC also stands for macrophage depending on context

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25
Q

Lysosomes are more effective at gram positive because?

A

Gram posative don’t have an extra lipid layer meaning in gram positive the peptidoglycan layer is more accessible

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26
Q

Where do all immune cells come from?

A

Hamatapoetic bone marrow cells because immune cells are in the blood
(Pluripotent)

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27
Q

What do luckocytes mean?

A

All of the white blood cells

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28
Q

What cells make up the adaptive immune system?

A

T cells and B cells and there derivatives

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29
Q

What cells are part of the innate immune system?

A 
NK cells 
Dendritic Cells 
Granulocytes 
Macrophages
Mast cells
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30
Q

Where are macrophages found what do they do (monocytes->macrophage)?

A

Immature monocytes circulate in the blood macrophages are found in sub mucosal layers
They have a long life span and are phagocytic (kill infected/dead cells and clear debris)
Present antigen to T cells and induce immune cells

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31
Q

What do granulocytes (specifically neutrophils) do?

A

They are in the blood and move to infection sites. They are phagocytic bactericidal numerous and have a short life span. Contain lots of vesicles with deadly enzymes.
Puss is mainly neutrophils

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32
Q

What are dendritic cells?

A

They are immature under surface epithelium in organs. When they take up antigen they move to lymph nodes and mature. Here they digest antigen and present it to adaptive immune cells and kick start active immune system.

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33
Q

What are natural killer cells (NK)?

A

In the blood move to tumours and infection sites. That are lymphocytes but are considered part of the inmate arm. They release toxic material extra cellulary killing pathogens and our own cells that are mutated.

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34
Q

What are opsonins?

A

Flags pinned on things suggesting it needs to be digested in phagocytosis

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35
Q

What are pattern recognition receptors (PRRs)?

A

These recognise pathogen associated molecular patterns

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36
Q

What are Fc receptors?

A

They recognise antibody molecule (self molecules) saying this needs to be engulfed.

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37
Q

What are the 3 pattern recognition receptors? What do they do?

A

Lectin like detectin 1
Scavenger receptors
Toll like receptors
They recognise particular structures (broad range)

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38
Q

How does phagocytosis work?

A

Compliment receptor 1 recognised C3b and then this binds to the receptor. Endocytosis of the bacterium forming a membrane bound vesicle which fuses withy lysosome forming phagolysosome

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39
Q

What are toll like receptors (TLRs)?

A

There are 10 human one and the each recognise a specific characteristic. Not all are expressed in cell surface some intracellulary which help detect viral infection. They trigger expression of antimocrobrial peptides and cytokines.

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40
Q

How do macrophages kill bacteria?

A 
Acid
Toxic oxygen derived products
Toxic nitrogen oxides 
Peptides
Lysosome
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41
Q

How do neutrophils destroy bacteria?

A 
Acid
Toxic oxygen products 
Nitric oxide
Defensins 
Lysosomes 
Lactoferrin (binds iron ions)
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42
Q

What is a cytokine?

A

A small protein that affects the behaviour of other types of cell (only if the cell has the correct receptor).

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43
Q

What is a chemokine?

A

A small protein that stimulates the migration and activation of cells

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44
Q

What releases cytokines and chemokines? What do they do at infection site?

A

Macrophages
Change blood vessel permeability And diameter (increase) allowing neutrophils and plasma to exit.
Additionally it can clot micro vessels to stop infection spreading

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45
Q

What is colonal expansion and deletion?

A

T and B cell binds to antigen and then multiples then once pathogen removes they delete and produce memory cells

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46
Q

How do we ensure that antigen cells aren’t created that attack self cells?

A

When developing in the bone marrow of the bind to a cell here then they die via apoptosis because they know it’s a self cell

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47
Q

What do B cells mature into

A

Plasma cells and memory cells

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48
Q

What is the T cell receptor and how is it different to the B cell receptor?

A

B cell is antigen bound to surface T cell is a more specific receptor and will only bind to the antigen if it is coupled with a major histocompatability complex

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49
Q

What is an epitope?

A

(Antigenic determinant) this is the actual part of the antigen that binds to the antibody

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50
Q

What is a continuous/linear epitope?

A

Fragment of polypeptide chain one amino acid after another

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51
Q

What is a conformational/discontinuous epitope?

A

Binds to amino acids at different points in the protein

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52
Q

What epitopes do B cells recognise?

A

Surface antigens

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53
Q

What do T cells recognise

A

Epitopes buries writhing antigen structure presented by MHC molecule

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54
Q

What is a multivalent antigen?

A

Has more than one epitope

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55
Q

How many pollypeptides is an antibody made from?

A

Heavy chains and light chains 2 of each so 4 chains in total held together by 4 disulpide bonds.

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56
Q

What regions does and anybody have?

A

Variable and constant regions

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57
Q

What drains does a light chain have?

A

1 variable and 1 constant

58
Q

What regions does a heavy chain have?

A

1 variable and 3 constant

59
Q

What is affinity?

A

Strength of binding of one molecule to another

60
Q

What is avidity

A

The sum total strength of two molecules binding at multiple sites

61
Q

What does papain digestion produce?

A

2 Fab fragments and an Fc fragment

62
Q

What does pepsin digestion produce?

A

One F(ab)2 fragment and peptide fragments

63
Q

What are the two different types of antibody light chain in humans?

A 
K and (upside down Y)
Any particular antibody will have one or the other of these chains in its structure
Ratio 2:1 K:Y
64
Q

What are the different sub types of heavy chains and what do they create (classes of antibody)

A

IgG IgA IgM IgD IgE

65
Q

What is the immunoglobulin fold?

A

This is a loop on the heavy and light chains
Light - 2
Heavy - 3
They are made of 2 anti parallel beta pleated sheets held together by a disulphides bond. The b strand is linked by flexible loops allowing strands to change direction

66
Q

what is a complementary determine region?

A

These are regions ( 3 in heavy and 3 in the light) 12 total. They are located at the tip of the Fab fragment in the loop and combine from the heavy and light chain to make he antigen binding site

67
Q

Where is the antigen binding site

A

N terminal domains of heavy and light chains

68
Q

What alter antigen antibody binding affinity?

A

Salt concentration
Detergents
pH
Epitope concentration

69
Q

What is neutralisation?

A

They block the antibody from interacting with cells and our body
Opsonisation= coating pathogen with antibody
Phagocytes recognise Fc region triggering phagocytosis

70
Q

What does trim 21 do?

A

This is and Intracellular receptor that detects anyibody that will be bound to a virus that the recruits proteozome to digest the virus

71
Q

What is the estimated number of antibodies we can make?

A

4 x 10 to the 11

72
Q

What is germline diversity?

A

This is the idea that there are multiple choices for each gene

73
Q

What is combinational diversity

A

That the segments are randomly selected and brought together in different combinations

74
Q

What gene fragments are the heavy and light chains made of?

A

Variable joining constant - light

Variable diversity joining and constant - heavy

75
Q

How is the light chain rearranged?

A

L and J brought together by somatic recombination in DNA.

The VJ is only brought to the C segment in splicing of the mRNA.

76
Q

How is the heavy chain rearranged?

A

Somatic recombination 1 D and J brought together
Somatic recombination 2 the V and DJ segment brought together.
Then after splicing the VDJ is brought to the C.

77
Q

What is a leader sequence

A

This guides the protein to where it needs to be for example presentation or secretion

78
Q

What is the 12 23 rule

A

Recombinant signal sequences have a heptomer and nonomer seperated by 12 or 23 base pairs. Genes will only combine of one has the 12 and the other has the 23 RSS. So it’s like complimentary pairing.
The number of base pairs corresponds to turns in the DNA helix

79
Q

What are p nucleotides

A

Nucleotides that are already in the sequence

80
Q

What are n nucleotides

A

Ew ones that are added by TDT

81
Q

What is the problem with junctions diversity

A

Lots of cutting and joining and adding of nucleotides this can cause lots of problems like frameshift if it’s not done in multiples of 3

82
Q

What are primary immunodeficiency

A

Fault in enzyme used in antibody production.

83
Q

What is allelic exclusion

A

This is the process where the regulation DNA rearrangement is controlled selecting different alleles if a non functional protein is produced

84
Q

Explain the steps in allelic exclusion

A
  1. DJ rearrangement
    2 V-DJ rearrangement on chromosome 1 if unsuccessful then in chromosome 2 if unsuccessful again cell dies. Successful heavy chain expressed in cell surface.
  2. Heavy chain on cell surface causes recombinase (RAG) enzymes expression switch off to stop heavy chain rearrangement and creates survival signal.
  3. Rearranging of the Kappa gene on first chromosome. Then second chromosome. Lander light chain on chromosome one. Then chromosome 2. If successful RAG 1&2 switched off. If not cell dies.
85
Q

In pre B cells we create self reactive molecules what happens to these?

A

If the Pre B cells bind to host cell at multiple sites in the bone marrow then the B cell kills it’s self.

86
Q

What happens if the immature B cell binds to little soluble host antigen.

A

Doesn’t die but become Anergic (unresponsive) so that it’s less dangerous

87
Q

When and where are the different types of antibody produced

A

All antibody classes are produced by the same cell with the same specificities just a different antibody type as well as secreted and transmembrane forms

88
Q

How is it decided if the antibody is hydrophilic or hydrophobic?

A

Alternative splicing if carboxy exons
Hydrophilic (secretory)
Hydrophobic (trans membrane domains)

89
Q

IgM?

A 
First made
Pentamer form increasing avidity
Present in blood but not tissues
Activated compliment strongly
Does not have hinge so less flexibility
90
Q

IgD

A

Made first with IgM we don’t know what it does

91
Q

IgG

A

Principle antibody in the blood and extra cellular fluids
It’s in our tissues
Activated compliment
It can be transported across placenta

92
Q

IgE

A

Offers defence against multicellular parasites. It causes allergy by binding to mast cells causing sneezing vomiting etc

93
Q

IgA

A

Very important in epithelial surfaces and in secretions
It’s monomeric or dimeric
It neutralises and can be secreted in breast milk

94
Q

How does IgG cross the placental barrier

A

They bind to FcRn causes endocytosis and then exocytosis into the baby

95
Q

How are B cells activated

A

T Independent antigens which activate B cells without help from T cells. it engages lots of B cell receptors.

T dependant antigens used with T cells providing 2 signals.

  1. Signal 1 antigen binding inter globulin in BCR causing antigen digestion and then the antigen is presented
  2. Then the complimentary helper T cell will bind then the T cell will release cytokines (interleukins) and CD40 to the B cell causing B cell proliferation
96
Q

What is linked recognition

A

The B cell presents and the T cell binds to different epitopes of the same antigen so they are physically associated

97
Q

What is a cognate T cell

A

A T cell that is primed for the same antigen (deferent epitope)

98
Q

Where do the B cells go (primary focus)?

A

The lymphnode via blood stream to encounter antigen in the follicle and then gets the complimentary T cell to help to male a little bit of antibody quickly in the first 5 days.

99
Q

What is the germinal centre reaction?

A

Goes on for 3-4 weeks post infection where stromal cells secrete chemokines causing B cells to stay put.
Point mutations occult in Ig V regions increasing affinity of these different B cells with variable affinity for the same antigen. They all compete to bind the antigen provided by follicular dendritic cells.

100
Q

What is somatic hypermututation

A

Triggered by AID enzymes (activation induced cytosine deaminaze) when DNA is transcribed AID swaps C for u (base) causing DNA repair to correct this alteration and this is less accurate because not always the correct base is put back. This increases affinity so the best most effective B cells become memory cells. Hence why secondary response is better.

101
Q

What is class switching?

A

This is the same antibody is produced in different classes. The HC VDJ region is combined wit any HC C region. Transcription or C exams opens DNA allowing AID to repair recombination machinery

102
Q

What’s a hybridoma

A

Immortal cell line

103
Q

How are monoclonal antibodies produced?

A

Immortal cell and B cell fused to produce immortal B cell, best B cell made to produce loads of antibody

104
Q

What is the ELISA test

A

Identifies specific protein and it’s concentration

105
Q

SDS/PAGE/western blotting/immunoblotting

A

Identifies specific protein estimates it’s molecular size and quantity

106
Q

Immunohistochemistry/immunocytochemistry

A

Research and diagnostic technique

107
Q

Flow cytometry and FACS

A

Detects expression of molecules by cells in suspension allowing identification of different cell types in different samples

108
Q

Where do T cells mature

A

Thymus

109
Q

Where do T cells circulate

A

Thymus blood lymph node then blood agaiN

T cell primes if it finds it’s antigen

110
Q

What is a T cell receptor

A

Like and antibody but not an antibody similar to a Fab fragment with only one binding site
That can only bind to antigen when it is processed and combined with an MHC complex

111
Q

What is CD3

A

This complexes with the T cell receptor and senses when a T cell receptor has bound to antigen and tells this to the rest of the cell

112
Q

What is CD8

A

Found in cytotoxic T cells

Goes MHC1

113
Q

What is CD4

A 
Found in helper T cells ramp up macrophage activity and kill resistant bacteria 
Pairs MHC class 2
114
Q

How are TCR genes rearranged

A

Rag proteins perform V(D)J somatic recombination guided by 12/23 rule and have hypervariable regions

115
Q

What is the structure of a T cell receptor

A 
Antigen binding site 
Constant region
Variable region 
Cytoplasmic tail 
Carbohydrate
116
Q

What is the MHC complex majour histocompatibility complex

A

Transmembrane glycoproteins
Variation in MHC lead to transplant graft rejection
I travel Lylas and extracellular antigen is presented with tissue type matching

117
Q

What’s a the similarities and differences between MHC 1 and 2

A

Class 1
Binds and presents Intracellular antigen
Carried out by all cells but not red blood cells
Healthy host proteins won’t cause a response
Viruses within cell are non self am will cause response
Mutated tumour antigens won’t be recognised as self
Class 2
Binds extracellular antigen
Carried out by professional antigen presenting cells
Bacteria or products infested elicit response

118
Q

What is the difference in structure of the MHC classes

A

Class 1 has microglobulin and has only 8-10 binding residues
Class 2 has 13 residues

119
Q

How is class 1 antigen processed

A

1 viral protein cooped to peptides by enzymes
2 TAP transporter transport fragments across membrane
3class 1 MHC is being produced at the same time that large and small chains of the MHC molecule come together
4 the antigen binding groove binds to the small peptides viral or self
5 the Golgi apparatus then exports this to be presented for inspection of T cells

If the protein is host then it will be ignored this is the internal antigen thus it can only be viral presented

120
Q

What is the MHC 2 activation pathway

A

Bacteria destroyed via phagocytosis
Endsomes chop antigen Into 10 amino acid length fragments
MHC 2 being created
To stop MHC 2 binding intracellular antigen the invariant chain is carriages with very high affinity for the MHC2 thus outcompete gets any other molecule
The class 2 MHC is in vesicle which fuses with another vesicle containing endosomes to destroy inveriant chain to clip molecules
This vesicle then fuses again with a extracellular peptide contain vesicle and a DM protein containing vesicle the DM binds CLIp and the MHC2 binds the extracellular protein
This is presented in macrophage membrane
Helper cell recognised this and created lymphokines causing good immuglobin supply

121
Q

How are T cells primed

A

Naive T cells are make way to lymph node to T cell area. If there is no interaction it will exit and move to another lymph node
If it does then it will proliferate and undergo more maturation
T cells express interleukin 2 receptors (autochrine stimulatuon)

122
Q

What are the 3 types of antigen presenting cells

A

Dendritic cells taking antigen from anywhere
Macrophages engulf and kill harbour pathogen and present
B cells

123
Q

What do cytotoxic T lymphocytes do

A

Respond to MHC1
Forms immunoglobulin synapse sends cytotoxic granules toward cell
Forms a pore within membrane and granzyme B and others cause apoptosis
Same way NK cells kill

124
Q

What’s positive selection and negative selection

A

Positive is survive signal

Negative is suicide signal

125
Q

What is a hypersensitivity reaction

A

Exaggerated reaction (not normal)

126
Q

What’s a type 1 hypersensitivity reaction

A

Mediated by IgE
Soluble antigen picked up by dendritic cells priming an immune response
IgE bonds to mast cells via Fc region
Re exposure causes mast cell to degranulate releasing antihistamine
It’s immediate

127
Q

What’s type 2 hypersensitivity reaction

A

Mediated by IgG cell specific can result in the activation of compliment phagocytic of NK cells
If the antigen is a cell surface receptor IgG will interrupt this by blocking it

128
Q

What is type 3 hypersensitivity reaction

A

This is also mediated by IgG
It binds to soluble antigen to form complexes
Serum sickness is a type 2 hypersensitivity reaction this forms rash driver 7-10 days after antigen exposure

129
Q

What’s a type 4 hypersensitivity reaction

A

This is a delayed type reaction
Mediated by effector T cells and cytotoxic T cells
Allergens are highly reactive molecules that bind to and alter host proteins
2 stages sensitisation and elicitation

130
Q

What is an autoimmune disease

A

A disease in which the pathology is caused by and adaptive response to self antigens
It can occur when tissue damage exceeds repair
They can be systemic or organ specific

131
Q

What factors lead to an autoimmune diseases

A

Genetic susceptibility
Tolerance breakdown
Infection/ environmental exposures

132
Q

Give an example of a site specific autoimmune disease

Systemic autoimmune disease

A

Type 1 diabetics

Arthritis

133
Q

What type is diabetes
What type is arthritis
What type is heart valve scarring

A

4
3
2

134
Q

What is he difference between HIV 1&2

A

1 causes most AIDS

2 is and endemic in west Africa

135
Q

What is the structure of HIV

A

2 copies of RNA
Gp120 surface protein I fects cells with CD4
numerous copies of viral enzymes required for initial infection
The genome can be read in 3 reading frames
Long polypeptides cleaved to make multiple functional proteins

136
Q

How is the virus replicated

A 
Gp120 binds CD4
RNA converted to cDNA by viral enzymes 
cDNA interstates into human genome by integrase 
Viral genes made by host 
Multiple viruses made
137
Q

How does HIV kill CD4 positive cells

A

Direct killing by overwhelming
Apoptosis chance increased
Cytotoxic T cells will kill the jnfected cells

138
Q

How does HIV escape elimination by the immune system

A

CD4 T cells are the ones that fight the infection
The antibodies produce do not bind well to intact virus particles of infected cells
HIV rapidly mutates

139
Q

How do HIV drugs work/not work

A

The only work in combination because soon HIV mutates to resist one drug hence a combination needs to be taken

Post exposure prophylaxis reverse transcriptase inhibitors viral protease inhibitors
Fusion and entry inhibitors

140
Q

What is the HIV and saliva problem

A

There is some in saline probably from GCF
HIV is rarely transmissible by saliva
Saliva contain anti HIV factors as well
Mucins and leukocyte protiase inhibitor produces by saliva stops HIV access

ODDR (5 decks)

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