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Immunology Flashcards

1
Q

What are the 2 ways the immune system can identify harmful microorganisms/toxins?

A
  1. by distinguishing self from non-self proteins

2. by identifying danger signals (eg from inflamamtion)

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2
Q

What 5 things can occur when the immune system goes wrong?

A 
allergy
recurrent infections
autoimmune disease
cancer
transplant rejection
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3
Q

What is variolation?

A

immunisation where the same organism is administered as the disease-causing organism but the route of administration is different
(eg small pox variolation through scratch on arm)

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4
Q

How can immunisation with one disease protect against another?

A

cross reactive antibodies that neutralise the other infection too

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5
Q

Why is ‘global village’ a factor in the emergence of new infectious disease?

A

increased mobilty- local infection can rapidly become a global epidemic

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6
Q

Why is population growth a factor in the emergence of new infectious disease?

A

proximity
sanitation
loss of natural habitat

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7
Q

Whats an example of a change in human behaviour that has become a factor in the emergence of new infectious diseases?

A

increased sexual partners

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8
Q

Give an example of how increasing prevalence of HIV has led to the re-emergence of other diseases.

A

eg TB

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9
Q

Why is there an unequal battle in the ‘arms race’ between pathogen and host?

A

pathogen replicates- and therefore can evolve- millions of times faster than the host

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10
Q

What does the host rely on in the ‘arms race’ between pathogen and host? bearing in mind that the pathogen can evolve millions of times faster

A

host relies on a flexible and rapid immune response, with a degree of non-specificity

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11
Q

what 5 organs/structures protect against infection?

A
  1. skin (physical barrier)
  2. stomach (stomach acid)
  3. respiratory system (mucociliary escalator)
  4. lymph nodes (lymphocytes)
  5. spleen
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12
Q

What 4 factors of the skin limit colonisation by micro-organisms?

A
  1. skin is composed of tightly packed, highly keritinised, multilayered cells
  2. cells constantly undergo renewal and replacement
  3. pH 5.5 (most pathogens are sensitive to acidic environment)
  4. low oxygen tension
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13
Q

What 4 substances do sebaceous glands produce that further limit skin colonisation by microorganisms?

A
  1. hydrophobic oils (which repel water and microorganisms)
  2. lysozyme (destroys the structural integrity of bacterial cell walls)
  3. ammonia (anti-bacterial properties)
  4. antimicrobial peptides (eg defensins)
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14
Q

What are the 4 ways mucous prevent infection?

A
  1. physical barrier (traps invading pathogens)
  2. secretory IgA (prevents bacteria and viruses attaching to and penetrating epithelial cells)
  3. enzymes
  4. cilia (mucociliary escalator)
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15
Q

What enzymes in the mucous prevent infection? (and function)

A

lysozyme, defensins, antimicrobieal peptides: directly kill invading pathogens
lactoferrin: acts to starve invading bacteria of iron

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16
Q

how do commensal bacteria prevent pathogenic colonisation?

A
  1. compete with pathogenic microorganism for scarce resources
  2. produce fatty acids and bactericidins that inhibit the growth of many pathogens
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17
Q

What is the first line of defence?

A

physical barriers

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18
Q

what is the second line of defence?

A

immune system

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19
Q

What are the 4 classes of pathogen that the immune system protects against?

A
  1. extracellular bacteria. parasites, fungi
  2. intracellular bacteria, parasites
  3. viruses (intracellular)
  4. parasitic worms (extracellular
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20
Q

Describe the innate immune response.

A 
rapid response (mins - hours)
same general response to many different pathogens
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21
Q

Describe the adaptive immune system.

A

slow response (days)
unique response to each individual pathogen
responsible for generating immunological memory

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22
Q

what 4 leukocytes are classed as phagocytes?

A

neutrophils
monocytes
macrophages
dendritic cells

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23
Q

what 3 leukocytes are classed as lymphocytes?

A

T cells
B cells
Natural Killer cells

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24
Q

apart from phagocytes and lymphocytes, what are the other cells important in the immune system?

A

eosinophils, mast cells, basophils

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25
Q

What are the soluble (humoral) components of the immune system?

A

antibodies

complement proteins

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26
Q

What are the proteins that are produced in response to an antigen and bind specifically to that antigen?

A

immunglobulins, antibodies

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27
Q

What are antibodies effective in providing defence against?

A 
extracellular pathogens (therefore most types of bacteria)
viruses (intracellular)
toxins
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28
Q

Where are complement proteins produced?

A

liver

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29
Q

what type of tissues do complement proteins enter?

A

infected and inflammed tissues

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30
Q

When a specific complement protein is triggered, what occurs?

A

complement cascade

the proteins enzymatically activate other complement proteins

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31
Q

haematopoietic stem cells form what 3 progenitor cells?

A

common lymphoid progenitor
common myeloid progenitor
common erythroid megakaryocyte progenitor

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32
Q

what do common lymphoid progenitors differentiate into?

A

lymphocytes

B cells, T cells, NK cells

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33
Q

what do common myeloid progenitors differentiate into?

A

phagocytes (neutrophils, monocytes, dendritic cells, macrophages) + basophils + eosinophils + mast cells

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34
Q

what do common eythoid megakaryocyte progenitors differentiate into?

A

platelets and erythrocytes

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35
Q

Where do NK/T cell precursors (from common lymphoid progenitors) develop?

A

thymus

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36
Q

What are the 8 cell types of the innate immune system?

A
  1. platelets
  2. neutrophils
  3. monocytes
  4. macrophages
  5. dendritic cells
  6. eosinophils
  7. basophiles
  8. mast cells
    (sometimes NK cells are classified as innate immunity)
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37
Q

where do mast cells reside?

A

in tissues, protect mucosal surfaces

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38
Q

where do basophils and eosinophils reside?

A

circulate the blood and are recruited to sites of infection by inflammatory signals

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39
Q

What immune cells are highly granular?

A

mast cells, basophils and eosinophils

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40
Q

What granules do mast cells, basophils and eosinophils release?

A

things that will cause acute inflammation such as histamine, heparin and cytokines

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41
Q

what do mast cells, basophils and eosinophils have an active role against?

A

parasties

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42
Q

what adverse immune response do mast cells, basophils and eosinophils have a key role in?

A

allergic responses

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43
Q

how do phagocytes work?

A

ingest and kill bacteria and fungi
also clear debris from dead/dying tissue cells
produce cytokines that will promote an acute inflammatory response

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44
Q

where do neutrophils reside?

A

circulate freely in the blood and are rapidly recruited into inflamed and infected tissues

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45
Q

monocytes are the circulating precursors of what immune cells?

A

tissue-resident macrophages

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46
Q

What is the function of dendritic cells?

A

reside in peripheral tissues as immature cells, but when activated in response to a pathogen, mature and migrate into the secondary lymphoid tissues for antigen presentation

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47
Q

What are the 3 cell types of the adaptive immune system?

A

lymphocytes

B cell, T cell, NK cell- lymphoid lineage

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48
Q

what type of cells do NK cells kill?

A

tumour cells
virally infected cells
antibody-bound cells/pathogens

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49
Q

how do NK cells kill their target cells?

A

by releasing lytic granules

NK cells are large granular lymphocytes

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50
Q

where do mature T and B cells reside?

A

constantly circulate the blood, lymph and secondary lymphoid tissues

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51
Q

when do T and B cells become active?

A

when they meet a pathogen or antigen

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52
Q

what are very long-lived T and B cells called?

A

memory cells

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53
Q

What is the role of B cells?

A

responsible for the production of antibodies

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54
Q

What is the role of T cells?

A

defence against intracellular pathogens eg viruses and some bacteria

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55
Q

what type of pathogen is mycobacteria?

A

an atypical bacteria- intracellular

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56
Q

what are the 2 types of T cells?

A

helper T cells

cytotoxic T cells

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57
Q

what is the function of helper T cells?

A

key regulators of the entire immune system

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58
Q

what is the function of cytotoxic T cells?

A

kill virally infected body cells

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59
Q

what occurs in primary lymphoid tissue?

A

leukocyte development

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60
Q

what occurs in secondary lymphoid tissue?

A

adaptive immune responses are initiated (through antigen presentation)

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61
Q

why are lymph nodes positioned regularly along lymph vessels?

A

to remove pathogens and antigens from lymph

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62
Q

what leukocyte is the main link between the innate immune system and the adaptive immune system?

A

dendritic cells

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63
Q

What are the 2 mechanisms of communication in the immune system?

A
  1. Direct contact
    Receptor : Ligand interactions
  2. Indirect contact
    through cytokines
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64
Q

What cells produce and release cytokines?

A

injured tissue cells and activated immune cells

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65
Q

In a receptor : ligand interaction, what type of cells become in direct contact with immune cells?

A

pathogen
another immune cell
tissue cell

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66
Q

what proteins are produced in response to infection, inflammation and tissue damage and have a key role in co-ordinating the immune system?

A

cytokines

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67
Q

Describe the half-life of a cytokine?

A

short half-life

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68
Q

What are the 3 kind of signals cytokines can cause?

A 
autocrine signals (for self)
paracrine signals (for nearby cells)
signals for distant cells
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69
Q

What is the function of interferons?

a type of cytokine

A

anti-viral function

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70
Q

what is the function of TNF?

a type of cytokine

A

pro-inflammatory

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71
Q

what are the function of chemokines?

(a type of cytokine)

A

control and direct cell migration

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72
Q

what is the function of interleukin 2 (IL-2)?

a type of cytokine

A

T cell proliferation

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73
Q

what is the function of interleukin 10 (IL-10)?

a type of cytokine

A

Anti-inflammatory

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74
Q

what 2 outcomes does the innate immune system have in response to a pathogen?

A

acute inflammation

killing of pathogen

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75
Q

what is the time period of acute inflammation?

A

immediate- days

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76
Q

what are the 4 local physiological signs of acute inflammation?

A
  1. dilation of small blood vessels and increased blood flow through that region
  2. increased permeability of post-capillary venules and accumulation of fluid in the extravascular space (oedema)
  3. chemical mediators (bradykinin, histamine) stimulate nerve endings
  4. movement limited by swelling or pain
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77
Q

Dilation of small blood vessels and increased blood flow through that region is a local physiological sign of acute inflammation. What symptoms does this cause?

A

redness (rubor)

heat (calor)

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78
Q

increased permeability o post-capillary venules and accumulation of fluid in the extravascular space is a local physiological sign of acute inflammation. What symptom does this cause?

A

swelling (tumor)

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79
Q

chemical mediators (such as bradykinin and histamine) stimulating nerve endings is a local physiological sign of acute inflammation. What symptom does this cause?

A

pain (dolor)

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80
Q

limited movement caused by swelling/pain is a local physiological sign of acute inflammation. what symptom does this cause?

A

loss of function (functio laesa)

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81
Q

what symptom is caused by a systemic sign of acute inflammation?

A

fever

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82
Q

what are the 3 phases of innate immune cell function?

A

a) recognition phase
b) activation phase
c) effector phase

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83
Q

what type of receptor : ligand interaction is involved in the recognition phase of innate immunity?

A

Pattern-recognition receptors (PRRs) on/in innate immune cell : Pathogen-associated molecular patterns (PAMPs) on pathogens

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84
Q

PRRs on the innate immune cell’s surface are for recognition of PAMPs found on what kind of pathogen?

A

extracellular pathogen

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85
Q

PRRs found intracellularly in the innate immune cell are for recognition of PAMPs found on what kind of pathogen?

A

intracellular pathogen

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86
Q

The PRR ‘Toll-like receptor 4’ is found where in an innate immune cell?

A

cell surface

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87
Q

what is the PAMP that is recognised by the PRR ‘Toll-like receptor 4’?

A

Lipopolysaccharide (LPS)

[gram negative bacteria]

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88
Q

The PRR ‘Dectin 1’ is found where in an innate immune cell?

A

cell surface

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89
Q

what is the PAMP that is recognised by the PRR ‘Dectin 1’?

A

B-glucans

[fungi]

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90
Q

The PRR ‘NOD2’ is found where in an innate immune cell?

A

intracellularly

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91
Q

what is the PAMP that is recognised by the PRR ‘NOD2’?

A

muramyl dipeptide

[M. Tuberculosis]

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92
Q

The PRR ‘Toll-like receptor 7’ is found where in an innate immune cell?

A

intracellularly

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93
Q

what is the PAMP that is recognised by the PRR ‘Toll-like receptor 7’?

A

ssRNA

[viruses]

94
Q

what is the main aim of the activation phase and the effector phase?

A

inflammation and pathogen killing

95
Q

What initially occurs when physical barriers are breached by a pathogen?

A

tissue resident innate immune cells are activated (eg mast cells, macrophages)

96
Q

when a physical barrier is breached by an invading pathogen, what do the tissue resident innate immune cells do?

A 
initiate acute inflammatory response (mast calls and macrophages)
pathogen killing (marophages)
97
Q

what are the 2 things that a mast cell does to initiate acute inflammation in response to a pathogen?

A
  1. degranulation (histamine, tryptase)
  2. gene expression
    (TNF, chemokines, leuotrienes)
98
Q

what are the 4 pro-inflammatory effects of histamine from mast cell degranulation?

A
  1. increased vascular permeability
  2. vasodilation
  3. activation of endothelial cells
  4. pain
99
Q

what is the pro-inflammatory effect of tryptase from mast cell degranulation?

A

its a proteolytic enzme

100
Q

what are the 2 pro-inflammatory effects of TNF from mast cell gene expression?

A
  1. increased vascular permeability

2. activation of endothelial cells

101
Q

what are the 2 pro-inflammatory effects of leukotrienes from mast cell gene expression?

A
  1. smooth muscle contraction

2. increased vascular permeability

102
Q

what is the pro-inflammatory effect of chemokines from mast cell gene expression?

A

attract other innate immune cells

103
Q

what are the 5 functions of macrophages?

A
  1. ingest and kill extracellular pathogens
  2. clear debris from dead/dying tissue cells
  3. inflammation (release mediators)
  4. tissue repair and wound healing
  5. antigen presentation
104
Q

what must occur before phagocytosis can take place?

A

recognition ie PAMP:PRR binding

105
Q

what is the name of the vesicle that contains the phagocytosed pathogen?

106
Q

when a phagosome fuses with a lysosome what is formed?

A

phagolysosome

107
Q

what 3 things occur once a macrophage has phagocytosed a pathogen?

A
  1. pathogen killing
  2. release of inflammatory cytokines
  3. increased MHC II expression and antigen presentation
108
Q

what is the funciton of interleukin 1 (IL-1)?

a type of cytokine

A

pro-inflammatory

109
Q

what is the function of interleukin 6 (IL-6)?

a type of cytokine

A

pro-inflammatory

110
Q

what is the purpose of a fever?

A

reduces pathogen replication

111
Q

what response do pro-inflammatory cytokines (eg IL-1, IL-6, TNF) cause in the liver?

A

increased production of acute phase proteins

112
Q

what 3 responses do pro-inflammatory cytokines (eg IL-1, IL-6, TNF) cause in the bone marrow and vasculature?

A
  1. increase vascular permeability
  2. activation of endothelial cells
  3. increased neutrophil production and mobilisation (neutrophila)
    all result in increased phagocytosis
113
Q

what response do pro-inflammatory cytokines cause in the hypothalamus?

A

cause the hypothalamus to make a fever

114
Q

what 3 things cause pro-inflammatory cytokines (eg IL-1, IL-6, TNF) to be produced?

A

infection
trauma
chronic inflammation (eg autoimmune diseases, cancer)

115
Q

serum CRP is usually raised significantly in viruses or bacterial infection?

A

bacterial (40-200mg/l)

[in viruses it is about 10-40 mg/l]

116
Q

What molecules are expressed on active endothelial cells at sites of inflammation?

A

adhesion moleulces (selectins and ICAMs)

117
Q

What do selectins allow?

A

leukocytes to tether (bind weakly) to endothelial cells and roll slowly along the endothelial surface

118
Q

once tethered to the epithelium, what type of cytokine activates the leukocytes so that they bind strongly to the endothelial cells?

A

chemokines

119
Q

once activated, how does the leukocyte bind strongly to the endothelial cell?

A

integrins on the leukocyte bind to the ICAMs on the endothelium

120
Q

what is the term for leukocytes squeezing between endothelial cells?

A

transendothelial migration

121
Q

once inside the tissue, what does the leukocyte follow to get to the site of infection?

A

a chemokine gradient

122
Q

what is the name of the rare genetic disease defined by a loss in B2-integrins causing defective transendothelial migration- leukocytes cannot exit the bloodstream and infections cannot be cured.

A

leukocyte adhesion deficiency

123
Q

what method do neutrophils use for recognition and activation phases?

124
Q

what are the 3 mechanisms by which neutrophils directly attack pathogens?

A
  1. phagocytosis
  2. release of anti-microbial peptide (defensins) and degradative proteases
  3. generate extracellular traps (NETs)
125
Q

The lysosomes within the neutrophils contain what 3 substances which are very efficient at killing pathogens that have been ingested by phagocytosis?

A

toxis reactive oxygen species (ROS)
hydrolytic enzymes
acidic pH

126
Q

what is the process by which the neutrophil uses toxis reactive oxygen species (ROS) to kill the ingested pathogens?

A

oxidative killing

127
Q

why do activated neutrophils also produce more TNF?

A

positive feedback promoting more inflammation

128
Q

What 2 things occur to the neutrophil itself after extensive phagocytosis?

A
  1. depletion of energy stores (glycogen)

2. tissue damage (due to residual enzymes/toxins being release intracellularly)

129
Q

what is the name for the collection of dead and dying neutrophils and tissue cells and microbial debris?

130
Q

what is the main clinical feature of phagocyte deficiency disease? (bearing in mind that phagocytes play a key role in defence against extracellular pathogens)

A

recurrent bacterial and fungal infections

Staph aureus, atypical mycobacteria, aspergillus etc

131
Q

what is the name of the phagocyte deficient disease?

A

chronic granulomatous disease

132
Q

what cytokine do NK cells release that is important in enhancing macrophage killing activities?

133
Q

what are the 3 pathways for converting C3 to C3b and C3a?

complement activation

A
  1. classical pathway
  2. lectin pathway
  3. alternative pathway
134
Q

why in chronic granulomatous disease do you get recurrent bacterial and fungal infections despite the phagocytes being present?

A

phagocytes dont work properly, specifically they cant make toxic reactive oxygen species to kill the pathogens and so granulomas form and infections aren’t cleared

135
Q

what does the alternative pathway of complement activation make use of?

A

an amplification loop which causes the spontaneous break down of C3 to C3b and C3a (positive feedback)

136
Q

which C3 (a or b) binds to bacterial surface proteins/carbohydrates?

137
Q

how does the lectin pathway for complement activation start?

A

with mannose-binding lectin (MBL) (an acute phase protein) binding to certain sugars on the pathogens surface

138
Q

how does the classical pathway for complement activation start?

A

with antigen-antibody complexes

139
Q

what are the 5 effector functions of complement?

A
  1. membrane attack complex
  2. opsonisation
  3. chemotaxis
  4. clearance of immune complexes
  5. inflammation
140
Q

what is opsonisation?

A

coating of microorganisms by immune proteins (opsonins)

141
Q

what are 3 examples of opsonins?

A
  1. C3b
  2. CRP
  3. antibodies
142
Q

what does opsonisation enhance?

A

phagocytosis (especially for encapsulated bacteria)

143
Q

why is it important that C3b dissolves antibody-antigen immune complexes? (which are then cleared by phagocytes)

A

otherwise the immune complexes would precipitate out in tissues/blood vessels and cause damage, inflammation and disease

144
Q

what complement proteins assemble to form the Membrane Attack Complex (MAC)?

A

C5b (which binds to the pathogen surface), C6, C7, C8, C9

145
Q

what do membrane attack complexes cause?

A

osmotic cell lysis of pathogen

146
Q

C3a and C5a bind to receptors on mast cells/basophils and cause what?

A

degranulation
(releasing chemokines and vasoactive susbtances ie histamine to increase vascular permeability and recruitment of leukocytes)

147
Q

what are the 4 complement inhibitors?

A

C1 inhibitor
Factor I
Factor H
C4 binding

148
Q

what do complement proteins have to be to be active?

149
Q

what are the 3 possible outcomes of acute inflammation?

A
  1. allows time for adaptive immune system to activate
  2. successful removal of stimulus (pathogens/trauma), leading to resolution
  3. persistent acute inflammation
150
Q

what are the 4 reasons persistent acute inflammation occurs?

A

non-degradable pathogens
viral infection
persistent foreign bodies
autoimmune reactions

151
Q

What 3 things can persistent acute inflammation cause?

A

chronic inflammation
tissue destruction (fibrosis, necrosis)
disease

152
Q

what type of communication does the adaptive immune system use between pathogen and leukocyte?

A

antigens : antigen receptors

153
Q

what is the T cell antigen receptor? (TCR)

A

membrane-bound protein heterodimer

154
Q

what is the B cell antigen receptor?

A

membrane bound antibody (IgM or IgD)

155
Q

describe a protein heterodimer.

A

has an alpha chain and a beta chain

156
Q

describe an antibody.

A

2 heavy chains linked to 2 light chains by dulsulphide bridges. Each chain contains a variable region as well as a constant domain

157
Q

what are the 2 forms of antibodies?

A
  1. membrane bound (on the surface of B cells)

2. soluble proteins (secreted into extracellular fluids)

158
Q

on the antibody, what forms the antigen-binding site?

A

the variable regions

159
Q

what is the structural difference between the subtypes of antibodies? (eg IgM, IgG, IgA etc)

A

same basic structure but different heavy chain constant regions

160
Q

what parts of genes are the non-coding parts?

161
Q

when are introns removed from the 1st mRNA produced from transcription?

162
Q

what process occurs in individual B cells and T cells as they develop?

A

random rearrangement of gene segments (to make highly varied light and heavy chains or alpha and beta chains)

163
Q

what is the potential downside of this random gene rearrangement?

A

the potential for generation of auto-reactive cells

164
Q

what type of tissues do mature-antigen specific T cells and B cells circulate between?

A

secondary lymphoid tissues

165
Q

What 3 things are trapped in secondary lymphoid tissues?

A

pathogenic antigens
debris
intact pathogens

166
Q

what are the main secondary lymphoid tissues of the lymphatic system?

A

lymph node

167
Q

what is the main secondary lymphoid tissue of the blood circulatory system?

168
Q

how do antigens from sites of infection reach lymph nodes?

169
Q

what process do T cells and B cells enter the lymph nodes through?

A

transendothelial migration from the blood system

170
Q

what happens if B cells and T cells don’t encounter specific antigens after several days?

A

they return to the blood via the efferent lymphatics

171
Q

inflammatory TNF stimulates expression of what molecule in immature tissue-resident dedritic cells?

172
Q

what do dendritic cells phagocytose?

A

pathogen-derived particles and antigens released from phagocytes (macrophages)

173
Q

for antigen presentation, how do dendritic cells present the pathogenic antigens?

A

on the dendritic surface, in complex with MHC proteins

then travel to local lymph nodes

174
Q

where are stromal cells found and what do they do?

A

found in B cell zones

trap opsonised antigens

175
Q

how many signals do B cells need to become activated?

176
Q

what are the 3 ways 2 signals can be provided for B cell activation?

A
  1. signal 1: BCR + antigen, signal 2: T cell help
  2. signal 1: BCR + antigen, signal 2: PRR + PAMP
  3. signal 1 + 2: multiple BCRs + antigens engaged
177
Q

what are the only cells that can recognise peptide antigens presented by MHC?

178
Q

what type of cells are MHC I proteins expressed on?

A

ALL nucteated cells

179
Q

what do MHC I proteins do?

A

present peptide antigens to cytotoxic T cells

180
Q

what type of cells are MHC II proteins expressed on?

A

expressed only on professional antigen presentating cells (dendritic cells, macrophages, B cells)

181
Q

what do MHC II proteins do?

A

present peptide antigens to helper T cells

182
Q

after clonal expansion of activated B cells what two types of cell are the B cells differentiated into?

A
  1. plasma cells (effector B cells that produce antibodies)

2. memory B cells

183
Q

how long does the process from infection to antibody production take?

184
Q

which is the most abundant Ig in plasma?

185
Q

which Ig is the first type produced during an immune response?

186
Q

when in the soluble protein form, what is the structure of IgM?

187
Q

What Ig is normally produced in response to parasitic infection and allergic responses?

188
Q

What Ig is the 2nd most abundant type?

189
Q

in blood, structural shape does IgA take?

A

monomeric form

190
Q

in breast milk, saliva, tears and mucosal secretions what structural shape foes IgA take?

A

dimeric form

191
Q

Where is IgM present?

A

only in plasma/secretions

192
Q

how is passive transfer of pre-formed IgG passed from mother to baby?

A

actively transported across the placenta

193
Q

how is passive transfer of pre-formed IgA passed from mother to baby?

A

through breast milk

dimeric form

194
Q

What type of immunoglobulins can be found B cell membranes as B cell antigen receptors?

A

IgM and IgD

195
Q

what function do the variable regions of antibodies have?

A

recognition function

196
Q

what function does the constant regions of antibodies have?

A

effector function

197
Q

What is recognition function of antibodies?

A

ability to bind to antigen, this is mediated by vairbale region sites

198
Q

what is effector function of antibodies?

A

clearance mechanisms

199
Q

What is the constant region of an antibody called?

200
Q

how is clearance mechanisms of antibodies mediated?

A

by Fc region interacting with either complement proteins or Fc receptors

201
Q

how do antibodies prevent the infection of adjacent cells? (ie by a virus)

A

bind to virus when it leaves the infected cell and causes agglutination, virus cant enter next cell

202
Q

what is the process of agglutination?

A

immune complex formation

203
Q

how do antibodies prevent microbial toxins from disrupting normal cell dunction?

A

bind to the toxin and causes agglutination, toxin cant bind to next cellular receptor

204
Q

how do antibodies work as opsonins?

A

phagocytes have Fc receptors and therefore bind to the constant region of immunoglobulins which are circling the pathogen, enhancing phagocytotic clearance.

205
Q

how do antibodies help stimulate natural killer cells?

A

NK cells have Fc receptors and so bind to antibodies bound to the pathogen
the NK cell kills the cell by apoptosis

206
Q

how do antibodies trigger allergic response?

A

mast cells have Fc receptors. when these receptors bind to antibodies bound to allergens, the mast cell degranulates

207
Q

what is the predominant antibody class of a primary response to an antigen?

208
Q

what antibody classes have the neutralisation effector function?

A

mainly IgG, dimeric IgA

209
Q

what antibody classes have the agglutination (immune complex formation) effector function?

210
Q

what antibody class has the opsonisation effectorfunction?

211
Q

what antibody class has the complement activation effector function?

A

IgM and IgG

212
Q

what antibody class has the effector function of NK cell activation?

213
Q

what antibody class has the effector function of mast cell activation?

214
Q

what antibody class has the effector dunction of B cell activation?

A

IgM, IgD (surface monomer)

215
Q

after clonal expansion of activated T cells, what do they differentiate into?

A

effector T cells and memory T cells

216
Q

what cytokine do helper T cells produce to increase proliferation of both helper T cells themselves and cytotoxic T cells?

217
Q

once helper T cells have migrated to sites of infection and inflammation, how are they reactivated by macrophages?
(this time in an antigen specific manner)

A

2 interactions
MHC II antigen complex :TCR
and
CD40 (on macrophage) : CD40L (on Th cell)

218
Q

once activated in an antigen specific manner, what do cytokine does the Th cell produce to enhance the macrophages kiling and pro-inflammatory activites?

219
Q

how do effector Th cells provide a stimulatory signal for B cells?

A

receptor ligand interaction:

CD40L (Th cell): CD40 (B cell)

220
Q

what cytokines do T cells also secrete to further activate the B cell?

A

IL-5, IL-4, IL-13

221
Q

what 4 stages happen during adaptive B cell development in the germinal centre?

A
  1. B cell proliferation
  2. antibody heavy chain switching (class switching)
  3. generation of high affinity antibodies (somatic hypermutation)
  4. differentiation into plasma cells and memory cells
222
Q

what is the aim of somatic hypermutation?

A

to produce antibodies that recognise the same antigen but with increased affinity

223
Q

how is somatic hypermutation achieved?

A

point mutations made in the heavy/light chain gene sements

224
Q

what 3 proteins are present in lytic granules of cytotoxic T cells?

A

perforin
granzymes
granulysin

225
Q

what is the function of perforin?

A

polymerizes o form a pore in target membrane

226
Q

what is the function of granuzymes?

A

granuzymes are serine proteases which activate apoptosis once inside cytoplasm of target cell

227
Q

what is the function of granulysin?

A

induced apoptosis

228
Q

what ligand : receptor mechanism do cytotoxic T cells use to kill infected cells?

A

Fas ligand mediated killing

229
Q

what are the 3 factors of memory cells that ensure a good secondary response?

A
  1. high numbers
  2. lower threshold for activation
  3. memory B cells have already undergone class switching and somatic hypermutation
230
Q

what Ig is predominant in the secondary response to an antigen?

Principles (8 decks)

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