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Baz: Semester 2 > Integrity: Immunology > Flashcards

Integrity: Immunology Flashcards

1
Q

Give brief definitions of each of these molecules and cells of the immune system:

Molecules
* Complement
* Cytokines
* Chemokines
* Antibodies

Cells
* Leukocytes
* Innate cells
* Adaptive cells

A

Molecules:

  • Complement - system of soluble serum proteins that interacts with pathogens to mark them for destruction by phagocytes
  • Cytokines - immune messenger hormones
    * Chemokines (cytokines which specialise in making cells move)
  • Antibodies - secreted molecules which bind pathogens

Cells

  • Leukocytes = all immune cells (innate and adaptive) Literally “white
    blood cell”
  • Innate cells (Macrophages, dendritic cells, neutrophils, eosinophils,
    basophils and mast cells)
  • Adaptive cells (T cells, B cells) (lymphocytes)
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2
Q

How are the following tissues involved in the immune system?

  • Lymphatics
  • lymph nodes
  • spleen
  • thymus
  • bone marrow.
A
  • Lymphatics - drainage system for peripheries therefore a good place to scan for problems
  • Lymph nodes - collections of immune cells at lymphatic junctions
  • Spleen - filters blood so immune cells present
  • Thymus - involved in the creation of immune cells
  • Bone marrow - where all blood cells originate hence all immune cells
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3
Q

How does the skin provide a barrier to pathogens?

A

The epidermis consists of dead cells and viruses need alive cells to infect

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4
Q

What is the anti-viral state?

A

When a cell is infected by a virus it releases IFN-alpha and IFN-beta.

These cause the surrounding cells to enter an antiviral state

  • Upregulate antiviral proteins (including more IFNs), and antigen
    presentation
  • Downregulate everything else by degrading mRNA and
    inhibiting protein translation factors (suppress viral
    proliferation)
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5
Q

What are the interferons involved in inducing an anti-viral state?

A

IFNα and IFNβ

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6
Q

What are IFNα and IFNβ

A

They are interferons released when a cell detects that it is infected by a virus and they induce an anti-viral state in surrounding cells

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7
Q

What are the two things you need in order to get an adaptive immune response?

A

Danger and non-self

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8
Q

Two types of danger molecules?

A

PAMPs = Pathogen Associated Molecular Patterns

  • types of molecules only produced by infectious agents
    and not host tissue - critical for survival/virulence
  • Example = bacterial cell wall constituents
    (lipopolysaccharide - LPS)

DAMPs = Damage Associated Molecular Patterns

  • Molecules released from injured cells
  • Examples = DNA, RNA, ATP, breakdown products of
    extracellular matrix
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9
Q

What are PAMPs and why do pathogen make them?

A

PAMPs = Pathogen Associated Molecular Patterns

  • types of molecules only produced by infectious agents
    and not host tissue - critical for survival/virulence
  • Example = bacterial cell wall constituents
    (lipopolysaccharide - LPS)

They are usually critical for pathogen survival otherwise the pathogens would evolve not to make them and therefore not get recognised

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10
Q

What are DAMPs

A

DAMPs = Damage Associated Molecular Patterns

  • Molecules released from injured cells
  • Examples = DNA, RNA, ATP, breakdown products of
    extracellular matrix
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11
Q

What is a pattern recognition receptor (PRR)

A

These are the things that recognise PAMPs and DAMPs

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12
Q

Toll like receptors are an example of PRRs.

What do each of the toll like receptors recognise?

  • TLR3
  • TLR4
  • TLR5
A
  • TLR3 binds double-stranded RNA (viruses)
  • TLR4 binds LPS (bacterial cell wall)
  • TLR5 binds flagellin (flagellated bacteria)
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13
Q

Three pathways of complement activation

A
  • Classical pathway
  • Mannose-binding
    lectin pathway
  • Alternative pathway
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14
Q

Describe the classical pathway of complement activation

A
  • This occurs in the presence of antibodies specific to foreign antigens
  • The antibodies bind to compliment C1q
  • C1q then activates the rest
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15
Q

Which complement is first activated in the classical pathway?

A

C1q

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16
Q

Describe the mannose-binding lectin pathway of complement activation

A

Mannose is present on the surface of bacteria and not on any host cells.

Mannose binding lectin then bind to mannose triggering complement activation

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17
Q

Describe the alternative pathway of complement activation

A

Complement componant C3 spontaineously binds to surrounding cells

Host cells contain control proteins which prevent further complement activation

Bacteria do not

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18
Q

Complement involved in the alternative complement activation pathway?

A

C3

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19
Q

Describe the process of complement membrane lysis

A
  • Membrane Attack Complex (MAC) forms in membrane of bacteria, this is a barrel-like structure formed from multiple late complement components (C5b,C6-C9)
  • Water rushes in, ions rush out, bacteria swells and
    bursts
  • Can also happen to host/foreign cells marked for killing
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20
Q

What is the barrel like structure in complement membrane lysis called?

A

Membrane attack complex
MAC

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21
Q

Which complement componants are involved in forming the membrane attack complex?

A

C5b,C6-C9

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22
Q

What are anaphylatoxins?

A

They are complement componants that cause vessels to become leaky

This allows the flodding of immune cells in the blood to the site of infection

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23
Q

What complement are anaphylatoxins?

A

C3a,C5a

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24
Q

What is opsonisation

A

This is where compliment C3b and C4b bind to pathogens and mark them for phagocytosis

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25
Q

Complement factors involved in oponisation?

A

C3b and C4b

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26
Q

Describe the complement cascade using all the complement componants

C1
C2 a/b
C3 convertase
C4 a/b
C3 a/b
C5 a/b
C6-C9

A

We need to get to the formation of C3 convertase which will cleave C3 into C3a and C3b

Classical: C1 cleaves C2 and C4. C3 convertase is then formed from C2b and C4b fragments. C4b oponiser

Mannose-binding lectin: Binding firectly cleaves C2 and C4. C3 convertase is then formed from C2b and C4b fragments. C4b oponiser

Alternative: C3 cleaved spontainously in C3b and C3a. C3b binds to pathogen surface and is activated by factor B to form another C3 convertase

C3 convertase cleave C3 into C3a and C3b.

C3a is an anaphylatoxin.

C3b is an oponiser and goes on to combine with C3 convertase to form C5 convertase which cleaves C5.

C5 cleaved by C3a into C5a and C5b.

C5a is an anaphylatoxin

C5b goes on to trigger and partake in complement membrane lysis with C6-9

In general “a” are anaphylotoxins while “b” are oponisers and cleavers of further complemments

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27
Q

List all the innate immune cells

A

Phagocytes:

Neutrophils
Macrophages
Dendritic

Allergic/parasites:

Eosinophil
Basophil
Mast cell

Virally infected:

NK Cell

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28
Q

Which of the innate immune cells are phagocytes?

A

Phagocytes:

Neutrophils
Macrophages
Dendritic

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29
Q

Which innate immune cells are involved in allergic reactions and parasite response?

A

Eosinophil
Basophil
Mast cell

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30
Q

Which innate immune cells are involved in killing virally infected cells?

A

Natural killer “NK” cells

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31
Q

Comparing the phagocytes

A
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32
Q

What is Extravasation?

A

Neutrophils need to get from the circulation to the site of inflammation - process of
extravasation

  • Endothelium of blood vessel altered by inflammatory cytokines
  • Neutrophil starts to roll along endothelium, then firmly adheres, and exits between
    endothelial cells (diapedesis)
  • Follows chemokine gradient to site of inflammation.
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33
Q

Describe the process of phagocytosis

A
  • Phagocyte detects pathogen and
    engulfs it - forms phagosome
  • Lysosome fuses with phagosome
  • lysosome contains toxic products
    to kill/degrade pathogen
  • Now called phagolysosome
  • Phagolysosome “matures” as
    more lysosomes fuse with it and
    H+ ions are pumped in - acid!
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34
Q

What is the phagosome, lysosome and phagolysosome

A

Phagosome - vesticle containing the munch

Lysosome - vesticle containing digestive chems and enzymes

Phagolysosome - fused phagosome and lysosome

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35
Q

How are macrophages activated to become phagocytes?

A
  • Activation can come from danger signalling or cytokines,
    especially IFNγ
  • IFNγ from other cells - NK cells, other activated macrophages, but
    in an established immune response, from helper T cells.
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36
Q

What is a Neutrophil NETs

A

Neutrophil Extracellular Traps

  • Neutrophils can extrude their DNA, acting like
    a net which traps pathogens.
  • = “Netosis” (vs apoptosis and necrosis)
  • Primarily seen in extracellular fungal infections.
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37
Q

What is a dendritic cells main purpose?

A

Antigen presentation

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38
Q

How does a dendritic cell present antigens to T cells?

A

When dendritic cells in the
periphery they are
constantly taking up antigen.
* If they sense danger they
“mature”
* Get better at antigen
presentation, and
upregulate different
chemokine receptors
* This results in their
migration to the
lymphatics, and into the
draining lymph node,
where they will present
antigen to T cells.

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39
Q

Difference between B and T cell antigen recognition

A

T cells must have their antigen chopped up in peptides and then loaded on
Major Histocompatibility Complex (MHC) molecules on another cell (dentritic cell)

T - fancy fucks

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40
Q

Three signals involved in antigen presentation?

A

Signal 1: the antigen peptides on the MHC

Signal 2: B7 receptor (only there if the dendritic cells sensed PAMPs/DAMPs) that binds to the CD28 ligand on the T cell. This is required for a presentation

Siganl 3: cytokine signal to signal the quality of the immune response. A way for the dendritic cell to convey more information about what it saw

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41
Q

Which cytokine is initially raised during exercise and muscle contraction? What are the effects?

A

IL-6

  • Reduces TNF from macrophages and therefor reduces inflammation
  • Mobilises NK cells
  • Improves T-cells
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42
Q

What are the six sentinels of the innate immune system in homeostasis.

4 are non-inflammatory

A
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43
Q

How does ageing inhibit your natural immunity?

A

Inhibitions

  • Reduced lymphocyte diversity (marrow and thymus atrophy)
  • Exausted immune system from chronic infection or scared severe historical infection

Effects

Reduced response to new antigens:
* More susceptable to infections
* Worse vaccine efficacy

Reduced survailence of self:
* re-emergence of latent viruses
* increased cancers

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44
Q

Why does an increasing age contribute to increasing inflammation?

A

There is an accumalation of danger signals of danger signal that trigger the innate immunity e.g. cell debris, cytokines etc.

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45
Q

What happens in inflammation in metabolic syndrome (meta-inflammation)

A

Obese adipose tissue is stressed and releases inflamatory cytokines

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46
Q

What cytokines are involved in healthy lean adipose tissue and what are in obese adipose tissue?

A

Lean:

IL-4
IL-10

Obese:

IL-1beta, IL-6, IL-12, IL-18

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47
Q

What is inflammaging?

A

Inappropriate persistent inflammation with ageing

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48
Q

What is immunosenesence?

A

Specific immunity declines with ageing

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49
Q

How to T-cells get around the brain?

A

They enter through the sinuses, search for immune signals then drain through the lymphatic vessels

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50
Q

How do the intestines keep microbes away

A

– Goblet cell mucus (gel of glycoprotein + water)
* Physical barrier
* Holds antimicrobial peptides (epithelium, Paneth cells) and immunoglobulin (IgA)
– IgA (intestinal plasma cells) transcytosed across epithelium
* coats microbes and toxins
* shapes the microbiome by selective targeting & supports some symbionts
– Steady state low level neutrophil emigration to luminal surface

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51
Q

What is a key antibody in mucous?

A

IgA (Immunoglobulin A)

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52
Q

What happens in IBS

A

dysbiosis (=altered gut microbiota including bacteria, fungi, yeasts, viruses)
* reduced diversity with accumulation of pathobionts (symbionts which cause disease under
changed conditions, including bacteria, fungi, viruses)
– microbes accumulate near epithelium, penetrate into lamina propria promoting
inflammation
– cycles of inflammatory damage, barrier breakdown, further dysbiosis

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53
Q

What happens to your metabolic state during an immune response?

A

The immune cells switch from a metabolic state to an anabolic state as they are required to synthesise more proteins etc.

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54
Q

What is exudate?

A

This is the cells, fluid and proteins delivered to tissues by vessels during inflammation

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55
Q

What happens to capillary beds during inflammation?

A

The become leaky

Blood fills the capillary beds (redness and heat)
Interstitial matrix fills with fluid (swelling)

Perivascular mast cells degranulate & release cytokines through
projections into vessels. Incoming leucocytes take over

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56
Q

WHat are mast cells?

A

They are a type of sentinal cell that sits in tissue.

They are have IgE antigens and hence are recognised by IgE antibodies. The binding of IgE is a common method whereby mast cells are activated (the one involved in allergies)

Other activation triggers include cold and complement

Once activated they then degranulate releasing various mediators such as cytokines and histamines

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57
Q

What is the antibody involved in triggering mast cells in allergies?

A

IgE

58
Q

What things can be released by mast cells as they degranulate?

A
  • Histamines (vasodilation, vascular leak)
  • Leukotrienes from arachidonic acid (bronchoconstriction)
  • Cytokines (other leukocyte recrutment)
59
Q

Basophil vs Mast cell

A

Both can release histamines and are involved in allergies however mast cells are more important int his regard

Mast cell:
* found in tissues
* releases histamines in allergies but also leukotrienes in asthma and cytokines to attract other immune cells

Basophils:
* Found in the blood
* Releases histamines but it’s primary role is anti-parasitic

60
Q

How do neutrophils enter tissue?

Think glycocalyx, selectins, cytokines, platelets and fibrin

A
61
Q

What is Chemotaxis

A

Directed migration up a concentration gradient

62
Q

Once a neutrophil has oass the endothelium into tissue how does it continue to find the injury site?

A

It follows the rigitity of the injury site aka the fibrin scaffold

Phagocytes need a fibrin scaffold in order to crawl

63
Q

What is cloaking?

A

During minor injury resident macrophages can hide injury from neutrophils and prevent them trigger happy cunts from shooting up the place

If the neutrophil never actually makes contact with the injury it can’t create a the swarming effect

64
Q

What does a neutrophil look like in histology?

A

Kinda like a tiny clump of frogspawn

65
Q

What is the order of arrival of exudate out of neutrophils, monocytes/macrophages, fluid?

A
66
Q

What are 4 exudates you see in clinical practice and their constituents?

A
67
Q

4 outcomes of inflammation with increaseing severity?

A
  • Resolution - complete healing
  • Organisation - healing with scarring
  • Dissemination - sepsis
  • Chronic inflammation - inflammation persists
68
Q

What happens with inflammation resolution?

A

Danger signal wane:

  • Neutrophils undergo apoptosis
  • pro-inflammatory mediator are catabolised

Anti-imflammatory mediators predominate:

  • IL10
  • complement and cytokine inhibitors
  • pro resolving lipids
69
Q

What happens in Organisation?

A

Exudate is replaced with granulation tissue that remains to form a collagen scar.

Prone to disease progression as stiff tissue makes it easier for leukocyte adhesion

70
Q

Difference between regeneration and repair

A
  • Regeneration – renewal or compensatory growth to
    replace damaged tissues
  • Repair – fibrous scar production (fibrosis) to patch
    damaged tissues
71
Q

What are Labile cells

A

These are cells that are capable of regeneration in homeostasis such as a the skin and gut

72
Q

What are stable cells?

A

Cells which are non-proliferative in homeostasis but that are instead capable of regenerating after injury (liver, kidney)

73
Q

What are permanant cells?

A

Permanent cells – unable to regenerate (neurons,
cardiac myocytes)

74
Q

With regard to regeneration skin cells and GI tract cells are examples of what?

A

Labile cells

75
Q

With regards to regeneration, liver and kidney cells are examples of what?

A

Stable cells

76
Q

With regards to regeneration, neurons and cardiac myocyte are examples of what?

A

Permanent cells

77
Q

What kind of healing is associated with TGF-alpha (transofrming growth factor) and which TGF-beta

A

TGF-alpha - signal which promotes regeneration of cell capable of regeneration

TGF-beta - signal which promotes repair, it produces fibroblast
migration & proliferation

78
Q

What collagen is involved in scar formation

A

fibrillar type I
/III

79
Q

Three stages to scar formation

A
  • Fibroblast migration and proliferation
  • Extracellular matrix deposition - collagen
  • Tissue remodelling
80
Q

What breaks down the ECM in order for remodelling to occur?

A

Matrix metalloproteinases
(MMPs)

81
Q

What is liver cirrhosis?

A

Even though the liver can regenerate there is still some scarring, repeated injury leads to irreverible scarring known as liver cirrhosis

82
Q

Definition of sepsis

A

Life-threatening organ dysfunction caused by a dysregulated host response to infection

83
Q

What is the first stage in sepsis?

A

Cytokine storm

84
Q

Main cytokines involved in the cytokine storm relating to sepsis?

A

TNF + IL-18
Ifn-γ
IL1-β

85
Q

Main effects of sepsis

A

Extreme vasodilation leaky vessels leading to fluid build up and bleeding

Glycocalyx degradation leads to coagulation & platelet deposition which cause wide spread thrombosis

Hyperclotting then depletes clotting
factors/platelets leading to haemorrhage

86
Q

What is endothelial glycocalyx

A

Is is a protective layer on the endothelium

87
Q

What kicks of the hyper thrombitic activity in sepsis?

A

Glycocalyx degradation

88
Q

Why does sepsis keep exaggerating itself?

A

Tissue necrosis (such as the loss of glycocalyx) and inflammation perpetuates danger signals leading to sequential organ failure (lung, cardiovascular, CNS, renal, marrow, liver)

89
Q

Blood test result for septic shock

A

High blood serum lactate.

This is due to a build up of lactic acid as a result of anaerobic respiration due to widespread hypoxia

90
Q

Ongoing problems after sepsis recovery

A
  • Fatigue
  • Mental health issues
  • Immediate immonosuppression due to immune rebound (immune system exhausted)
  • Sepsis survivors have lingering immune suppression
91
Q

What is granulation tissue?

A

Granulation tissue is a type of new connective tissue made up of fibroblasts, vessels, lymphatics.

It willl eventually become a collagen scar

Surrounds dead tissue, pus or irritants

92
Q

What is an inflammatory sinus

A

Abnormal tract in an epithelial surface lined by granulation tissue.

A sinus ends whereas a fistula link two epithelial surfaces

93
Q

What is an inflammatory fistula

A

Abnormal tract in an epithelial surface lined by granulation tissue.

A sinus ends whereas a fistula link two epithelial surfaces

94
Q

What is an ulcer

A

A localised defect in epithelial tissue caused by the shedding of inflammatory nectrotic tissue

95
Q

What is an abscess

A

Pus in a newly formed cavity surrounded by granulation tissue

96
Q

What is a granuloma

A

Organised cluster of mature activated macrophages, in response to persistent stimuli

97
Q

Low turn over granuloma vs high turnover granuloma

A

Low turnover:

Foreign body present, inert and indigestable leads to a persistant long lived macrophage population

High turnover:

Due to infection or toxic agents. Short-lived macrophages with continual replenishment. T cells & other immune cells also present

98
Q

How does TB take advantage of macrophages?

A

It encourages it’s own phagocytosis avoiding lysosomes, once inside a macrophage the infected marophage undergoes apoptosis.

New macophages come and consume the aopoptitic infected macrophages and get infected themselves

This eventually forms a granuloma

99
Q

What are unactivated T/B cells called?

A

naive T/B cells

100
Q

What are activated T/B cells called?

A

effector T/B cells and some become memory T/B cells.

101
Q

Where are the majority of T/B cells found?

A

Spend most of their time in the secondary lymphoid organs (eg
spleen and lymph nodes)
* Recirculate via the lymph and blood, then back to secondary
lymphoid organs

102
Q

What is the function of a B cell

A

Once activated they become plasma cells where they make antibodies for specific antigens

103
Q

What is a B cell called once activated?

A

Plasma cell
or
Effector B cell

104
Q

What are the two main types of T cell

A

CD8+ Cytotoxic T Lymphocyte (CTL)
* kills infected/mutated ‘self’ cells

CD4+ T helper cell (Th cell)
* Organise immune responses - produce different cytokines
* can differentiate into different types - Th1, Th2, Th17, Treg

105
Q

What is the job of a Cytotoxic T Lymphocyte (CTL)

A

kills infected/mutated ‘self’ cells

106
Q

What is the job of a T helper cell (Th cell)

A

Organises immune responses by producing produce different cytokines

107
Q

What are the 4 different types of T helper cell?

A

Th1, Th2, Th17, Treg

108
Q

How are T/B cells trained?

A

Each T/B cell in the pool of naive T/B cells has a randomly generated anti-gen receptor

If this binds to antigen it then proliferates

Some remain after in the pool of naive as memory cells for a faster response in the future

109
Q

What is the difference between a B cell antigen receptor and a T cell antigen receptor

A

B cells are just an embedded antibody with light chain and heavy chain

T cells are straight

110
Q

What is the difference between the variable region of an antigen receptor and the constant region?

A

Variable region - different on every naive cell

Constant - the same on every type of that cell

111
Q

How is BcR and TcR diversity acheived?

A

The variable regions are made up of one of each of the VDJ gene segments (variable, diversity and joining).

By randomly selecting one of each you get considerable variation

Each receptor is made up of two creating further diversity e.g. alpha/beta in TcR and light/heavy in BcR

Lastly when joining the genes joining nucleotides can be added or removed

112
Q

Two types of diversity creating BcR and TcR diversity

A

Combinational: varying VDJ combinations

Junctional diversity: random error in joining the genes

113
Q

Class 1 and class 2 MHC

A

MHC (Major
Histocompatibility Complex) is the things that presents antigens to T cells.

CD8+ CTLs only bind antigen on class I MHC which are found on all nucleated cells except for neurons> They will kill tumors and virally infected cells

CD4+ T helper cells only bind antigen on class II MHC which are only found on dendritic cells

114
Q

What is MHC polymorphism?

A

Variations of the gene amoungst the whole population (most polymorphic of all human genes)

This is a common cause of transplant rejection (1 in100,000 chance of matching an unrelated donor)

115
Q

What is tolerance?

A

The process of training T and B cells to not recognise self

Self reacting T cells are deleted in the thymus

Self reacting B cells are deleted in the bone marrow

There is also some peripheral tolerance, once lymphocytes have passed the self/non-self test and are in the lymph nodes, if they recognise an antigen without danger they get deleted (stop allergies)

116
Q

Regarding T cell selection in the thymus what is positive and negitive selection?

A

To test cells they have to pass two criteria, do they work and are they harmful

They have to be able to bind MHC to some degree (positive selection)

If they bind the testing MHC too well then they are considering self reacting and are deleted (negative selection)

117
Q

Peripheral tolerence

A

T cells are killed in the lymph nodes if a dendritic cell presents an anti-gen with out the danger signal

118
Q

Overall picture of T and B cell map (just for looking at)

A
119
Q

Five forms of antibody

A

Antibody = immunoglobulin = Ig

5 forms of antibody: IgM, IgG, IgA, IgE, IgD

Hint: GAMED

120
Q

5 Different purposes of antibodies

A
  1. Neutralisation (binds to viruses and prevents them from infecting IgA)
  2. Oponisation (marks fro phagocytosis IgA and IgG)
  3. Pro inflammatory (IgE when bound to mast cells triggering allergic response)
  4. Complement activation (IgM and IgG)
  5. ADCC (Antibody-dependent cell cytotoxicity) (marks cells for kill by NK cells and neutrophils
121
Q

What is B cell class switching?

A

Naive B cells express IgM (& IgD): early response dominated by IgM

Activated B cells can class switch to make IgG, IgA and IgE

122
Q

Which different types of Fc receptor bind to whic antigens

A
  • Fcɣ receptor for IgG,
  • Fcε receptor for IgE
  • Fcɑ receptor for IgA
  • Fcμ receptor for IgM

Where these receptors are determines the function of antibodies e.g. mast cells have Fcε receptors therefore IgE is the allergy one

Simple as it’s alphabetical

123
Q

Best antibody for activating complement?

A

IgM

124
Q

Best antibody at neutralising intestinal pathogen

A

AgA

125
Q

Best antibody at opsonising, neutralising & ADCC ( a wee bit of compliment activation)

A

IgG

126
Q

somatic hypermutation

A

This is where the variable region of a B-cell antibody receptor can mutate upon activation creating strong or weaker binding to antigens

127
Q

What determines the type of T helper cell that a naive T cell becomes

A

Signal 3 (cytokines)

128
Q
A
129
Q
A
130
Q

What are the different functions of T1,T2,T17 and Treg T helper cells

A
131
Q

4 jobs of T helper cells

A
132
Q

How do T helper cells help B cells to activate?

A

If a B cell presents a T helper cell with a peptide/MCII that they recognise then in return the T helper cell provides signal 2 which activates the B cell.

Thus, CD4+ T cells effectively only provide help to B cells that
recognise the same antigen as they do - called ‘linked
recognition’

As activated T helper cells have already made sure there is danger associated with the peptide this insures that B cells don’t recognise self/ benign antigens

133
Q

How do T helper cells drive affinity maturation of B cells?

A

Following somatic hypermutation, linked recognition by
CD4+ T cells allows selection of those B cells expressing
receptors/antibodies that bind antigen most strongly

Hence, the requirement for help from CD4+ T cells is
essential to drive affinity maturation of B cells

134
Q

How do CD4+ T cells select the appropriate class
of antibody during class-switching

A

Cytokines from CD4+ T cells select class of antibody

135
Q

How do Th1 cells do their job?

A

They signal to macrophages who have engulfed a pathogen to digest the pathogen if the Th1 recognises it

136
Q

How to Th2 cells do their hob?

A

They activate mast cells and plasma cells

137
Q

How to Th17 cells do their job?

A

They make signals to attract neutrophils

138
Q

How do Treg cells do their job?

A

They inhibit dendritic cells preventing further T cell activation

139
Q

How do CD8+ Cytotoxic T
Lymphocytes (CTLs) kill a cell

A

They are presented with peptides on MHC1 which the infected cell gave to the dendritic cell. The CTL then uses these to recognise the infected cell.

CD8+ CTL kill through FAS
ligation and perforin and
granzyme release.
* FAS ligation directly signals
to induce apoptosis
* Perforin forms pore
allowing granzyme to
enter.
* Granzyme activates
caspases, DNAase
activation and
mitochondrial break down.

140
Q

What cells make IF-gamma (interferon gamma)

A

NK cells and ILC1 (innate lymphoid cells type 1) cells make it to activate and polarise the immune response to a virus

141
Q

What do innate lymphoid cells type 3 do?

A

ILC3 are are responsible activation of the immune system in response to extracellular bacteria and fungi. This response is antigen non-specific. They secrete interleukin-17 and 22.

142
Q

Shapes of the 5 antibodies?

A

All Y shaped

IgE,IgG,IgD -> single Y
IgA -> double Y
IgM -> pentamer

Baz: Semester 2 (42 decks)

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