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ODDR Immunology > Immunology > Flashcards

Immunology Flashcards

1
Q

what are the 3 layers of defence our immune system has?

A
  • physical barrier
  • innate arm of immune response
  • adaptive arm of immune response.
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2
Q

what are some physical barriers of the immune system?

A

skin, nails, epithelial, mucosal layers.

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3
Q

what are lysozymes in saliva most effective against?

A

most effective against gram +ve bacteria

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4
Q

how do lysozymes preform their function in the oral cavity?

A

they cleave the chemical bonds between sugars on the peptidoglycan layer of bacteria, enabling other microbial agents to destroy the lipid bilayer around bacteria.

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5
Q

how do antimicrobial peptides preform their function in the oral cavity?

A

attack the exposed lipid bilayer around bacteria.

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6
Q

what are some antimicrobial peptides found in the oral cavity?

A
  • Defensins
  • Cathelicidins
  • Histatins
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7
Q

what is the purpose of defensins in the oral cavity?

A

several can insert into the lipid bilayer of bacteria, creating a pore - allowing the content to leak out.

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8
Q

what is the purpose of cathelicidins in the oral cavity?

A

cause membrane disruption.

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9
Q

what type of cathelicidins are found in humans?

A

LL-37

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10
Q

what is the purpose of histatins in the oral cavity?

A

fight fungal pathogens

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11
Q

what produces histatins?

A

salivary glands.

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12
Q

what kind of receptors are found on innate arm response cells?

A

genome encoded receptors.

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13
Q

which arm of the immune system has lasting protection?

A

adaptive responce.

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14
Q

what is the purpose of the innate arm?

A

provide initial defence, limiting pathogen proliferation and spread.

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15
Q

How long does it take the adaptive arm to start?

A

up to 4 days.

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16
Q

why do the cells of the adaptive arm have a vast range of receptors? and what does this mean?

A
  • as the receptors are not genome encoded so receptor recognition improves.
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17
Q

why does the adaptive arm need to be more potent?

A

to control more virulent pathogens,

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18
Q

why does the adaptive arm take longer?

A

because it has to be started by the innate response. And it takes time to raise population of cell specific for pathogen.

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19
Q

what is the complement system?

A

plasma that ‘complemented’ the killing of bacteria by phagocytes.

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20
Q

what are the functions of complement?

A
  • facilitate recognition of bacteria by phagocytes.

- directly lyse bacteria.

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21
Q

what is the classic pathways that the complement system can be activated?

A 
when C1 interacts with a pathogen surface or binds to antibodies bound to the surface. 
has C1q (recognition component) and C1r+C1s (proteases) - these 3 form C1 complex.
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22
Q

what is the alternative pathways that the complement system can be activated?

A

C3 undergoes spontaneous hydrolysis - forming a complex with factor D,P,B producing C3bBb complex (C3 convertase)

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23
Q

what is the lectin pathways that the complement system can be activated?

A

lectin like molecules do the recognition and ficoline bind carbs on pathogen surface leading to C3 convertase.

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24
Q

what do all compliment pathways generate?

A

C3 convertase.

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25
Q

what is the purpose of C3 convertase?

A

cleaves C3 - leaving C3b bound to microbial surface and releasing C3a.
The C3b then starts the release of C5a.

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26
Q

How do C3a and C5a aid in the immune response?

A

they recruit phagocytic cells to the site of infection and promote inflammation,

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27
Q

what is the purpose of compliment leaving C3b on the surface of the pathogen?

A

phagocytes with receptors for C3b with come and engolf + then destroy the pathogen.

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28
Q

what does completion of the complement cascade lead to?

A

formation of a membrane-attack complex (MAC) - which disrupts cell membrane and causes cell lysis.

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29
Q

what is a zymogen?

A

an inactive form of an enzyme, usually protease, that must be modified in some way (eg cleaved in a particular site) to become active.

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30
Q

where are immune effector cells derived from?

A

common pluripoten progenitor cell types in bone marrow

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31
Q

after a stem cell divides in the bone marrow, the daughter cells can either differentiate or divide - what happens if they differentiate?

A

they mature. This then restricts their potential and they lose the ability to self renew.

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32
Q

after a stem cell divides in the bone marrow, the daughter cells can either differentiate or divide - what happens if they divide?

A

they continue being a stem cell.

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33
Q

where do the adaptive effector cells come from?

A

a lymphoid and myeliod path in the bone marrow.

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34
Q

where do the innate effector cells come from?

A

a lymphoid and myeliod path in the bone marrow.

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35
Q

what are the adaptive effector cells?

A
  • B cells
  • Plasma cells
  • T cells
  • Activated T cells.
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36
Q

what are the lymphoid innate effector cells?

A

Natural Killer Cells and Activated Natural killer cells.

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37
Q

what are the myeliod innate effector cells?

A
  • Granulocytes
  • Mast cells
  • Macrophages
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38
Q

what is the function of a macrophage in the innate immune response?

A
  • 1st responders .
  • phagocytosis.
  • remove dead cells and debris.
  • draw in other immune cells
  • present antigen from phagocyte on its surface for T cells.

(killers nad whistle blowers)

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39
Q

What are granulocytes?

A

polymorphonuclear leukocytes, (neutrophils)

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40
Q

what is the function of neutrophils in the innate immune response?

A
  • Phagocytic
  • Bactericidal

(many killer soldiers)

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41
Q

what is pus?

A

dead neutrophils

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42
Q

where are neutrophils located?

A

in the blood.

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43
Q

where are macrophages located? (mature and immature)

A

mature = most tissues in submucosal layers.

immature = in blood.

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44
Q

what is the function of dendritic cells in the innate immune response?

A

phagocytosis. - to then present the antigen to the adaptive arm - activating the adaptive arm.

(transporter)

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45
Q

what is the function of Natural killer cells in the innate immune response?

A

release cytotoxic granules. These can damage host cells .

they look for cells that are infected with a virus or a tumour.

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46
Q

where are dendritic cells located? (mature and immature)

A

immature = under surface epithelial and in solid organs.

Once they phogolose a pathogen they move to the lymph nodes and mature.

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47
Q

where are natural killer cells located?

A

blood.

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48
Q

what cells can phagocytose?

A
  • macrophages
  • neutrophils
  • Dendritic cells.
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49
Q

what are the receptors that are found on phagocytic cells that start an immune response?

A
  • Fc receptors.
  • complement receptors. (recognise C3b)
  • Pattern recognition Receptors (PRR)
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50
Q

what are PAMPS?

A

Pathogen associated molecular patterns that are found on pathogens.

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51
Q

what are the 3 types of PAMPS?

A
  • Lectin Like
  • Scavenger receptors
  • Toll like receptors.
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52
Q

what are the stages of phagocytosis?

A
  • bacterial binds to receptor on cell surface
  • endocytosis (engolfing) of the bacterial into the cell
  • this created a membrane bond vesicle in the cell. (phagosome)
  • lysosomes fuse with the phagosome forming the phagolysosome - they inject toxic material breaking and killing it.
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53
Q

what is the function of toll like receptors?

A

to recognises a distinct set of PAMP not found in vertebrates.

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54
Q

why are toll like receptors important?

A

in preventing fungal infections.

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55
Q

how do phagocytes prevent bacterial growth and kill some?

A

pH is very low.

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56
Q

what are the antimicrobial mechanisms of phagocytes?

A
  • pH very low
  • Respiritory burst (cause cells stimulated to produce lots of toxic o2 species and toxic nitrogen species which damage the engulfed microbes.
  • Phagocytes stimulated to reases anti-microbial peptides (cathelicidin)
  • produce decretive enzymes (lyzsozyme)
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57
Q

what is a cytokine?

A

a small protein that affects the behaviour of other cells.

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58
Q

what is chemokine?

A

small chemoattractant protein that draws cells to where they are needed.

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59
Q

during the immune response what cells initiate inflammation?

A

macrophages and complement.

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60
Q

when macrophages engulf the bacterial what is triggered to be released?

A

cytokine (eg IL-1 and chemokine)

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61
Q

what makes the blood vessels in the infected areas more permeable and why?

A
  • cytokines.
  • they make it more permeable meaning that neutrophils can come out more easily. It also allows more plasma to leave the blood. (increasing complement proteins for clotting factors and phagocytosis)
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62
Q

what are the purposes of cytokines in the innate immune response?

A
  • make blood vessels more leaky

- tell neutrophils where they need to go.

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63
Q

what cells initiate the adaptive immune response?

A

dendritic cells.

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64
Q

what is the difference between PAMPS and specific antigen?

A

specific antigens are only for one receptors where as PAMPs are for many.

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65
Q

what happens to B and T cells once they mature?

A

have their own unique specificity for antigen.

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66
Q

where do B cells mature?

A

in the bone marrow

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67
Q

where do T cells mature?

A

in the Thymus

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68
Q

why only once a cell with a specific antigen for the infected pathogen does it undergo colonal expansion?

A

because there isn’t enough room in the blood for every single possible cell with a unique antigen for everything.

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69
Q

what are left behind when the infection is cleared and why do the other cells die?

A

Memory cells. The other die to allow for enough room for other cells to fight a different infection.

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70
Q

what mechanism allows us to fight infection within the limited space we have in the blood?

A

constant colonal expansion and retraction periods so there isn’t loads of these cells in the blood system at one time.

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71
Q

what is a problem with receptors in B/T cells being randomly generated?

A

we make some that are self reactive.

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72
Q

where are self reactive cell receptor cells removed?

A

either in the bone marrow or in the thymus.

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73
Q

what are the 2 cells that B cells can differentiate into?

A
  • effector cells that can produce the antigen

- memory cells.

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74
Q

what are the 2 cells that T cells can differentiate into?

A
  • effector cells

- memory cells.

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75
Q

what do B cells mature into?

A

Plasma cells.

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76
Q

what is the function of plasma cells?

A

can release their receptors and bind to a specific antigen alone.

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77
Q

what are Immunoglobulins?

A

B cells

78
Q

what do T cells mature into?

A

activated T cells.

79
Q

when can a T cell bind to antigen?

A

once it has been shown to it through the antigen having already have binded with MHC

80
Q

what is an epitope?

A

a site on an antigen that is recognised by specific lymphocyte receptors.

81
Q

Are B cell epitopes most likely to be continuous or discontinuous?

A

discontinuous

82
Q

Are T cell epitopes most likely to be continuous or discontinuous?

A

continuous

83
Q

what is mean by a multivalent antigen?

A

contains many epitopes.

84
Q

what is the basic structure of immunoglobulin?

A
  • Y shaped
  • 4 polypeptides bonded together
  • 2 light chains
  • 2 heavy chains.
85
Q

what bond holds together the 4 polypeptides of immunoglobulin?

A

disulphide bond,

86
Q

what are the unctions of immunoglobulin?

A
  • recognise and bind antigen
  • the elicit effector functions, recruiting additional immune molecules or cells to destroy pathogens following antigen binding.
87
Q

what is affinity?

A

the strength of binding of one molecule to another at a single site, eg the binding of a monovalent Fab fragment of antibody to a monovalent antigen.

88
Q

what is avidity?

A

the sum total of the strength of binding of 2 molecules or cells to one another at multiple sites.

89
Q

what is papain?

A

a protiase

90
Q

what are the effects of papain on an antibody (immunoglobulin)?

A
  • cleaves the antibody molecule. leaving 2x Fab fragments and FC fragment.
91
Q

Once a immunoglobulin have been cleaved by papain what does the Fc fragment bind to?

A

cell receptors.

92
Q

what does Fab stand for?

A

Fragment antigen binding.

93
Q

what is pepsin?

A

a protiase

94
Q

what are the effects of pepsin on an antibody (immunoglobulin)?

A
  • cleaves at a different site when compaired to papain. this results in a F(ab’)2 fragment and many peptide frgaments.
95
Q

how many binding sites will a F(ab’)2 fragment have?

A

2 - as pepsin doesn’t cleave them away from each other.

96
Q

regarding affinity and avidity: what is the same and what is different for Fab and F(ab)2 fragments?

A

affinity is the same (they both still bond to the antigen the same)
avidity is different. (they dont have the same number of binding sites, Fab only has one now, F(ab)2 has 2 binding sites.)

97
Q

What bond is stronger to an antigen, Fab or F(ab)2?

A

F(ab)2 as it has 2 binding sites so the avidity is twice as strong.

98
Q

what are the 2 types of light chains found in humans?

A

kappa and lambda

99
Q

How many light chain immunoglobulin folds are in IgG?

A

2

100
Q

How many heavy chain immunoglobulin folds are in IgG?

A

4

101
Q

what causes changes in antigen binding specificity of immunoglobulin?

A

changes in amino acid sequence at the hypervariable regions which alter the CDRs.

102
Q

how are antigen and antibodies binded non-covalently?

A
  • electrostatic forces
  • hydrogen bonds
  • hydrophobic forces
  • van der waals forces.
103
Q

what can disrupted antigen and antibody binding?

A
  • high salt concentration
  • extreme pH
  • detergents
  • high concentration of purified epitope
104
Q

what is the function of different Ig classes determined by?

A

the heavy chain Fc region.

105
Q

what are the functions of the different Ig classes?

A
  • neutralisation
  • opsonisation
  • activation of the complement
  • TRIM 21 activation.
106
Q

what is meant by Ig neutralisation?

A

antibodies bind to pathogen and toxins, preventing binding to the cellular receptors that pathogens use to gain entry to the cell.

107
Q

what is meant by Ig opsonisation?

A

coating of pathogen with antibody phagocytes recognise the Fc region and triggers phagocytosis.

108
Q

what is TRIM 21 ?

A

a receptor within a cell that detect the invaded antibody and recruits proteasome to degrade it.

109
Q

what are the primary/ central lymphoid organs?

A

inside the Thymus or bone marrow.

110
Q

what are the secondary/ peripheral lymphoid organs?

A
  • adenoids
  • tonsils
  • lymph nodes
  • spleen
  • appendix
  • peyers patches.
111
Q

what is mean by some T and B cells are nieve?

A

they havent come across any antigen yet.

112
Q

how are the variable regions of Ig gene encoded?

A

gene segments.

113
Q

How is there diversity in Ig?

A
  • Germline diversity (multiple choice for each gene segment)

- Combinatorial diversity (segments randomly selected and together in different combinations)

114
Q

what are the 2 types of segments that encode for the light chain variable regions?

A
  • variable

- joining.

115
Q

what are the 3 types of segments that encode for the heavy chain variable regions?

A
  • variable
  • joining
  • diversity
116
Q

What does the control of recombination always ensure (within the Ig chains) is joined together?

A

that variable segment is always joined to a joining segment (or in heavy chains that variable is always connected to diveristy)

so always a 23 space joins a 12 space.

117
Q

why is you more likely to find pseudogenes (mutations that cannot produce functional proteins) in Ig?

A

because there is less pressure on them to get it correct evolutionary

118
Q

what proteins cleave DNA?

A

RAG proteins.

119
Q

what are the 3 ways in which Ig can get diversity?

A
  • Germline (different gene segments available)
  • Combinatorial (different combo of gene segments and different heavy/light chains)
  • Junctional (adding /removing nucleotides)
120
Q

what are some genetic disorder that affect the immune system?

A
  • severe combined immunodeficencies
  • deficiencies in antibody production
  • phagocytic disorders
  • complement deficiencies
121
Q

what does allelic exclusion regulate?

A
  • rearrangement of Ig.

- make sure B cells have only 1 specific antigen receptor.

122
Q

what is a problem with the way in which we generate Ig diversity?

A

it generates some self reactive B cells.

123
Q

How do we prevent B cells that are self reactive to leave the primary lymphoid organ?

A

cause cell death though B cell receptor clustering.

124
Q

what is B cell receptor clustering?

A

where many receptors on the B cell attach to the self cell receptors - the self cells send a strong message to B cell and it undergoes colonial deletion.

125
Q

what is IgM good for?

A
  • Strong activator of the complement system

- good at controlling infection in blood stream

126
Q

what is a limitation of IgM?

A

not as flexible as other Ig due to having no hinge.

127
Q

what is IgG good at?

A
  • diffuses into tissues well
  • good activator of complement
  • preform neutralisation and optimisation.
  • transported across placenta to protect the baby.
128
Q

where is IgG the principle antibody?

A

in the blood/ extracellular fluid.

129
Q

what is IgE good at?

A
  • defence against multicellular parasites
  • functions in allergy
  • binds mast cells which have induce pathogen expulsion by coughing, sneezingm vomiting.
130
Q

where is IgA a principal antibody?

A

in secretions. (saliva)

131
Q

what is IgA good at?

A
  • good at neutralisation

- transports across epithelium.

132
Q

how does IgG trigger engulfment of a phagocyte?

A

binds to the phagocyte FcRs.

133
Q

How does IgG cross the placental?

A

binds to neonatal FCR and gives passive maternal derived protection to newborns.

134
Q

what Ig can be found in breast milk?

A

IgA and IgG.

135
Q

where does B cell activation occur?

A

in the secondary lymphoid organs.

136
Q

what is different about a T-independent antigen?

A

can activate B cells alone 0 without T cell help.

137
Q

How do the T-dependant antigens activate the B cells?

A
  • B cell receptor binds to antigen, B cell engulfs the antibody/antigen complex. Digest it via MHC molecule. Which is them placed on the surface of the B cell- showing it to T cells.
  • T helper cell activates the 2nd signal by putting cytokines into the B cell and connects the T and B cell via a CD40/CD40L to the MHC molecule.
138
Q

what is linked recognition?

A

where T cells must respond to the same antigen as the b Cell.

139
Q

what do B cells after they have been activated differentiate into?

A

memory cells and plasma cells.

140
Q

what do plasma cells produce?

A

antibodies. (Immunoglobulin)

141
Q

how long can a germinal centre reaction last post infection?

A

3-4 weeks after

142
Q

where do activated B cells go to proliferate?

A

germinal centre.

143
Q

what is somatic hypermutation? and why does it occur when B cells proliferate?

A

where the cells reproducing have a high rate of mutation.

This is because B cells express an enzyme (AID) which attacks the DNA of our Ig genes.

144
Q

what does AID do to your Ig genes?

A

AID swaps some of the bases as Ig is being transcribed. This causes mutations .

145
Q

what are the effects of bases swaps in Ig due to AID?

A
  • can improve the function of B cells

- Can reduce the function of B cells.

146
Q

How is the secondary response better that the primary response in the adaptive immune response?

A

due to mulations with Ig due to AID in B cell cell activation and proliferation making B cells better at phagocytosis. So this means that ‘un-mutated’ B cells are less competitive and die. Leaving behind highly efficient B cells.

147
Q

what is Affinity maturation?

A

Improving of the B cells via mutations during the Ig production by AID

148
Q

Where can Ig switch class?

A

in the germinal centre

149
Q

what does Ig need in order to switch class?

A

AID

150
Q

what are the results of mAb?

A

cells combining the characteristics of producing antigen specific antibody with ability to grow in culture with unlimited lifespan.

151
Q

what are some immunological techniques for research etc?

A
  • ELISA
  • SDS/ western blotting / immunoblotting
  • Immunohistochemistry / Immunocytochemistry
  • Flow cytometry and FACs
152
Q

where do T cells develop their specific antigen receptors?

A

Thymus.

153
Q

once a T cell has found an antigen and undergoes proliferation, what does it differentiate into?

A

effector cells (memory T cells)

154
Q

what type of family is the T cell receptor part of?

A

Ig family - but it isnt an Ig

155
Q

what is the structure of a T cell receptor?

A

2 polypeptide chains - alpha and beta.

156
Q

what is the bond between the chains on a T cell receptor ?

A

disulphide bond

157
Q

How many binding sites does a T cell receptor have?

A

1.

158
Q

what do T cell receptors bind to?

A

antigen presented within a complex with MHC ll

159
Q

what are the other receptors on a T cell?

A
  • CD3
  • CD8
  • CD4
160
Q

what is the purpose of a CD3 on a T cell?

A

informs the inside of the cell that the receptor has bound to an antigen

161
Q

what is the purpose of a CD4 on a T cell?

A

found on T helper cells - helps B cells join (how the B cells are activated)

162
Q

what is the purpose of a CD8 on a T cell?

A

only found on cytotoxic T cells. Kills host cells that they detect are effective by a virus or will become a cancer cell.

163
Q

How are T cell receptors generated?

A
  • similaer process to Ig

- uses RAG proteins to perform V(d)J somatic recombination.

164
Q

where is the hypervariable regions on a T cell receptor?

A

where the antigen binding site is.

165
Q

what is it that can lead to a transplant graft/organ rejection?

A

polymorphisms (many different genetic variations exist within a species) in MHC

166
Q

how are their 2 type of MHCs?

A

intra and extra cellular antigen. MHC 1 is intracellualr.

MHC ll is extracellular.

167
Q

what does MHC l bind and present?

A

intracellular derived antigen

168
Q

where can MHC l be found?

A

on the majority of cells (just not RBC)

169
Q

what does MHC ll bind and present?

A

extracellular derived antigen.

170
Q

what type of cells carry out MHC ll?

A

professional antigen presenting cells (APC)

171
Q

on what cells is MCH l found?

A

all cells

172
Q

on what cells is MHC ll found?

A

dendritic cells
B cells
Macrophages.

173
Q

what receptor on a T cell does MHC l bind to?

A

CD8

174
Q

what is the pathway of MHC l antigen?

A
  • virus in cells, takes over protein making machinery, produces viral proteins
  • infected cells creates viral+own proteins down to small peptides
  • peptides taken to endoplasmic reticulum through TAP
  • MHC (at the same time) is being synthesised on the ribosomes of the Rough Endoplasmic reticulum
  • large+small chanins of MHC 1 come together to form MHC 1
  • antigen binding grooves of MHC 1 bind to the incoming small peptides.normal cell transport mechanisms take place. (MHC 1 is inserted through the cell onto the membrane)
175
Q

what is TAP and what is its purpose inside a cell?

A

TAP= specialised transporter channel

It transports peptides into the endoplasmic reticulum.

176
Q

What cells will recognise MHC 1 with viral proteins?

A

cytotoxic T cells

177
Q

what receptor on a T cell does MHC ll bind to?

A

CD4

178
Q

How does the formation of MHC ll onto the surface of the membrane differ from MHC l?

A
  • once the MHC is being synthesised, the invariant chain (a small peptide) is produced to prevent MHC binding to intracellular antigens. This binds to the MHC ll.
  • this complex passes through the golgi, where endosome containing enzymes degrade the invariant chain down into CLIP (a small residue).
  • Vesicles containing peptides and MHC ll (with CLIP) fuse together
  • another vesicle containing DM joins.
  • DM out competes MHC ll for CLIP
  • MHC now binds to extracellular antigens.
  • MHC ll is then inserted through the cell onto the membrane.
179
Q

what drives the proliferation of T cells?

A

IL- 2

180
Q

what dells takes an antigen to the lymph nodes?

A

dendritic cells.

181
Q

what cells produce IL-2? and why?

A

T cells - because it drives the proliferation of the T cells.

182
Q

what cells are professional antigen presenting cells?

A

Dendritic cells.
Macrophages
B cells.

183
Q

what are CTLs?

A

Cytoxoxic T lymphocytes

184
Q

what is the purpose of Cytotoxic T Lymphocytes?

A

bind with complimentary antigen+MHC l on a cell surface and to polarises cytotoxic granules towards the target cell.
granules fuse with the membrane and create a pore in it. inducing apoptosis (self suicide)

185
Q

How many cells can CTLs kill?

A

many. they have along life span.

186
Q

what is the function of T helper 1 cells?

A

increase macrophage activity against intracellular bacteria.

187
Q

what is the function of T helper 2 cells?

A

promote responses to parasite, helping B cells class switch to IgE.

188
Q

what receptor on T cells does HIV bind to?

A

CD4.

189
Q

why does HIV binding to CD4 receptors lead to immune collapse?

A

means that viruses can not be detected due to CD4 receptors not being able to bind to T helper cells.

190
Q

where do immature T cells gain receptors?

A

immature T cells produced in the bone marrow relocate to the thymus where there is a re-arrangement of T cell receptors gene seguence and they then express TCRs.

191
Q

what happens to immature T cells that fail to recognise MHC? what is this process called?

A

they die so never become mature.

Positive selection

192
Q

what % of precursor T cells are screened out and die before they mature>

A

98%

ODDR Immunology (31 decks)

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