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Immunology Flashcards

1
Q

Definition of immunity?

A

The ability of an organism to resist an infection/toxin by the action of specific antibodies or sensitised white blood cells

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2
Q

What is humoral immunity?

A

Made up of cells and soluble factors

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3
Q

Characteristics of innate immunity? (4)

A

Instinctive, non-specific, doesn’t depend on lymphocytes, present from birth

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4
Q

Characteristics of adaptive immunity? (4)

A

acquired/learned, specific, requires lymphocytes, has antibodies

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5
Q

What are the 3 layers of a blood sample once centrifuged?

A

Upper - plasma
Middle - buffy coat (leukocytes)
Lower - haematocrit

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6
Q

What does haematopoioesis mean?

A

Made in the bone marrow

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7
Q

What are some examples of leuokocytes?

A

Lymphocytes, phagocytes, and auxillary cells

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8
Q

Which cells are classed as lymphocytes?

A

B cell, T cell, granular lymphocyte

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9
Q

Which cells are characterised as phagocytes?

A

monocyte, neutrophil, eosinophil

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10
Q

What cells are classed as auxillary cells?

A

basophils, mast cells, platelets

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11
Q

Which immune cells are mononucelar?

A

B cell, T cell, monocyte

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12
Q

Which immune cells are polymorphponuclear?

A

Neutrophil, eosinophil, basophils

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13
Q

What is special about dendritic cells?

A

It is an antigen presenting cell considered a ‘professional’ at activating lymphocytes

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14
Q

What are neutrophils?

A

Role in innate immunity (phagocytosis) and have 2 main intracellular granules (primary lysosomes and secondary granules)

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15
Q

What are monocytes?

A

Role in innate and adaptive immunity (phagocytosis and Ag presenting). They remove any foregin microbes and dead material

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16
Q

What are macrophages?

A

Role in innate and adaptive immunity (phagocytosis and Ag presenting). Reside in tissues. Recognise and remove self and non-self material –> present Ag to T cells

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17
Q

What are eosinophils?

A

Role in parasitic infections and allergic reactions. Activate neutrophils –> induces histamine release from mast cells

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18
Q

What are basophils?

A

Role in immunity to parasitic infections and allergic reactions. Bind to IgE receptor and causes de-granulation which releases histamine

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19
Q

What are T lymphocytes?

A

Major role in adaptive immunity and recognise antigen presenting cells

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20
Q

Where do T lymphocytes mature?

A

Thymus - found in blood, lymph nodes, spleen

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21
Q

What are the different types of T lymphocytes?

A

T helper 1 and 2 (CD4): help immune response for intracellular/extracellular pathogens
Cytotoxic (CD8): able to kill cells directly
T regulatory: regulate immune responses

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22
Q

What are B lymphocytes?

A

Major role in adaptive immunity and recognise Ag displayed by APCs

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23
Q

Where do B lymphocytes mature? and what do they differentiate into?

A

Mature in bone marrow, found in blood, lymph nodes, and spleen. Differentiate into plasma cells that make antibodies.

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24
Q

What is the complement?

A

Group of 20 serum proteins secreted by the liver that need to be activated to be functional. Activated as part of immune response in a cascade.

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25
Q

What are the 3 modes of action of complement?

A
  1. direct lysis
  2. attractng more leukocytes to site of infection (chemotaxs)
  3. Coating invading organism (opsonisation)
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26
Q

What is an antibody?

A

Immunoglobulin that binds specifically to antigens and can be soluble or remain on cell surface. Acts as adapter that links a microbe to a phagocyte.

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27
Q

What are cytokines?

A

Proteins secreted by immune and non-immune cells that effect intracellular communication

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28
Q

What is an interferon?

A

A type of cytokine that induces a state of antiviral resistance in uninfected cells. Eg. IFNa/b produced by virus infected cells, IFNy released by T cells

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29
Q

What is an interleukin?

A

A cytokine that is pro-inflammatory (IL1) or anti-inflammatory (IL10). Causes cells to divide and secrete factors

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30
Q

What is a colony stimulating factor?

A

A cytokine that directs division and differentiation of bone marrow stem cells. Precursor of leukocytes.

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31
Q

What is a tumour necrosis facotr (TNFa/b)?

A

A pro-inflammatory cytokine that mediates inflammation and cytotoxic reactions

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32
Q

What are chemokines?

A

Molecules that chemically attract leukocytes

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33
Q

Differences between innate and adaptive immunity?

A
  1. innate: 1st line of defence to provide barrier to antigens. adaptive: response to specific antigen
  2. innate: instinctive, un-learned. adaptive: learnt behaviour
  3. innate: slow. adpative: quick
  4. innate: no memory. adaptive: memory to specific antigen
  5. innate: present from birth. adaptive: acquired
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34
Q

What is innate immunity composed of?

A

physical and chemical barriers: lysosome in tears, commensals, skin, bronchi, gut, low pH of vagina, flushing of urinary tract

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35
Q

What cells compose the innate response?

A

Phagocytic cells, blood proteins (complement)

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36
Q

Can innate immunity integrate with adaptive response?

A

Yes

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37
Q

Does innate immunity depend on lymphocytes?

A

No

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38
Q

Why is adaptive immunity needed?

A

When microbes and intracellular viruses evade innate response - memory is needed

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39
Q

What is the difference between cell mediated and humoral resonses in adaptive immunity?

A

Cell mediated uses T cells for intraceullar microbes. Humoral uses B cells for extracellular microbes

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40
Q

What is the major histocompatibility complex (MHC)?

A

Displays peptide proteins on cell surfaces to alert invasion

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41
Q

What is the inerlay between APCs and T cells?

A

intimate cell to cell contact is required to control humoral response and recognise/kill infected cells

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42
Q

What additional things does APC and T cell interaction require?

A

MHC, intrinsic/endogenous antigens, extrinsic/exogenous antigens

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43
Q

What is T cell selection?

A

T cells that recognise self material are killed in the fetal thymus

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44
Q

What do T cells respond to?

A

Presented antigens - receptors recognise foreing antigens usign MHC

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45
Q

What does full activation of T cells require?

A

co-stimulatory molecules CD8 and CD4

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46
Q

How does CD8 activate T cells?

A

Uses class I MHC to form proteolytic granules and induce apoptosis

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47
Q

How does CD4 activate T cells?

A
  1. APC presents Ag with MHC to CD4 T cell
  2. High levels of IL-12 turn CD4 T –> CD4 Th1
  3. Th1 travels to lymphoid tissue and proliferates
  4. Th1 recognises Ag on infected cells and secretes INFy
  5. This stips virus spreading and activates macrophages
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48
Q

What do B cells express?

A

Membrane bound Ig

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49
Q

What happens to B cells that recognise self?

A

Killed in bone marrow

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50
Q

How do B cells induce phagocytosis?

A

Present Ag to T cells via MHC:
1. Peptides on surface allow CD4 Th to bind –> Th2
2. Th2 secretes cytokines that cause B cells to divid (clonal expansion) and differentiate into plasma cells and memory B cells

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51
Q

Definition of inflammatory response?

A

Response to breaching of barriers as a result of tissue damage or infection. Series of reactions that brings immune cells to site of infection/damage

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52
Q

What are 7 stages of inflamamtory response?

A
  1. coagulation - stop bleeding
  2. acute inflammation - recruit leukocytes
  3. kill pathogens and neutralise toxins - limit pathogen spread
  4. clear pathogens and dead cells - phagocytosis
  5. proliferation of cells - repair damage
  6. remove blood clot to remodel ECM
  7. re-establish normal structure and function
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53
Q

Which immune cells sense microbes in blood and tissues?

A

blood: monocytes and neutrophils
tissue: macrophages and dendritic cells

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54
Q

What are PRRs?

A

pattern recognition receptors

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55
Q

What are PAMPs?

A

Pathogen associated molecular patterns

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56
Q

How do neutrophils get to site of infection?

A

complement –> extravasation –> neutrophils become sticky and roll along endothelium –> travel through and along incrwasing concentration gradient of cytokines –> phagocytose

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57
Q

Why do we need innate immunity?

A

Infections arrive quickly and unpredictably due to continual relationship with pathogens

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58
Q

What is pattern recognition?

A

Recognition of microbes and viruses using conserved features of them - different families of receptors detect these

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59
Q

Where are PRRs found?

A

Can be secreted, circulating, or cell associated

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60
Q

What are lectins and collectins?

A

carbohydrate containing protein PRRs that bind carbohydrates to lipids in microbes. This activates complement and improves phagocytosis

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61
Q

What are pentraxins?

A

PRRs that react with C protein of pneuomococci and activate complement, improves phagocytosis

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62
Q

What are cell-associated PRRs?

A

Receptors that are present on cell membrane or in cytosol, mainly TLRs

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63
Q

What are some other examples of membrane bound PRRs?

A

Mannose receptor, dectin-1, scavenger receptors

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64
Q

Pathology of PRRs?

A

If they recognise host cells in autoimmunity, failure to recognise pathogens, increased inflammatoy response, Eg. athersclerosis, COPD, IBS

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65
Q

How do PRRs play a role in homeostasis?

A

Blood neutrophil numbers may depend on TRL4 signalling

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66
Q

What are TLRs?

A

Type of PRR that recognise exogenous and endogenous damage molecules, activated by appearance of host molecules in unfamiliar context

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67
Q

What does TLR signalling by cellular damage activate?

A

immunity to initiate repair and enhance antimocrobial signalling

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68
Q

Example of exogenous and endogenous TLR?

A

TLR4 - exogenous = LPS, pneumolysin, viral proteins. endogenous = heat shock proteins, hyaluronic acid, fibrinogen

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69
Q

How are TLRs used as adjuvants in adaptive immunity?

A

drive cytokine production to increase likelihood of successful T cell activation

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70
Q

What are NLRs?

A

Nod-like receptors that detect intracellular microbial pathogens

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71
Q

Example of NLR?

A

NOD1 and NOD2 - NOD2 recognises breakdown product of peptidoglycan to activate inflammatory signalling pathways.
(Non functioning mutation is Crohn’s)

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72
Q

What are RLRs?

A

Type of PRR that activate interferon production to enable an antiviral response

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73
Q

What is the Fab region of an antibody?

A

Variable in sequence and bind to different antigens specifically

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74
Q

What is the Fc region of an antibody?

A

Common, constant in squence and bind to complement

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75
Q

How are the different regions of antibodies formed?

A

Encoded by separate exons

76
Q

What is the function of antibodies? (3)

A
  1. neutralise toxins by binding to them
  2. increase opsonisation through phagocytosis
  3. activate complement
77
Q

Function of IgG?

A

Main class in serum and tissues - important in memory responses and can cross placenta

78
Q

Function of IgM?

A

Important in primary responses, found in the blood

79
Q

Function of IgA?

A

Found in saliva and secretions (saliva, breast milk, alveolar) to protect mucosal surfaces in primary response

80
Q

Function of IgD?

A

unknown - present on mature B cells

81
Q

Function of IgE?

A

Present at low levels, respond to allergy and parasitic infections. Triggers histamine release.

82
Q

How does Fab region protect against infection?

A

neutralise, immobilise, prevent binding/infection of host cells through specific binding

83
Q

How does Fc region protect against infection?

A

enhances innate mechanisms by activating complement and binding to Fc receptors

84
Q

What is the difference between MHC I and II?

A

MHC I expressed by all cells and displays antigen to CD8 T cells. MHC II expressed by B cells, macrophages, and dendritic cells - display antigen to CD4 T cells

85
Q

Difference between Th1 and Th2 T cells?

A

Th1 produces IL2y and TNFb to activate macrophages and cause inflammation. Th2 produces cytokines IL4, 5, 6, 10, 13 to activate eosinophils and mast cells.

86
Q

Why do we need vaccines?

A

Controls and reduces frequency of formerly dangerous diseases

87
Q

What is natural immunity?

A

Transfer of maternal antibodies across the placenta to the deveoping fetus/breast milk

88
Q

What is artificial immunity?

A

Treatment with pooled human IgG or immunoserum against pathogens or toxins

89
Q

When is artificial immunity required?

A

When exposed to a disease that has complication, no time for immunisation to give protection, acute danger of infection, individuals with B cell deficiency

90
Q

Definition of passive immunity?

A

Transfer of performed antibodies when natural immunity is difficult to achieve

91
Q

Disadvantage of passive immunity?

A

Doesn’t activate immunological memory so no long-term protection

92
Q

What is passive immunity routinely used for?

A

tetanus/diphtheria (anti-toxins), hepatitis/measles/rabies (prophylactics), snake/insect bites (anti-venins)

93
Q

Definition of active immunity?

A

Manipulation of immune system to generate a persistant protective response against pathogens by safely mimicking natural infection

94
Q

How does active immunity generate persistant protective response?

A

Mobilises arms of immune system and generates immunological memory

95
Q

What are the 4 steps of active immunisation?

A
  1. engage innate immune system
  2. elicit danger signals such as PAMPs and TLRs
  3. activate specialist APCs
  4. Engage adaptive immune system by generating memory B and helper T cells
96
Q

Difference between primary and secondary response?

A

Secondary response is quicker and stronger due to memory B cells created in primary response

97
Q

What is an example of difference in immunological memory in vaccinations?

A

influenza has rapid onset and new variants so infection can establish before memory is activated - therefore repeated immunisations maintain high levels of antibodies. Whereas polio takes longer to establish infection so opportunity for memory to be activated

98
Q

What are the different types of antigens used in vaccinations?

A
  • whole organism: live and attenuated (weakened version of disease)
  • whole organism: inactivated pathogen
  • subunit: killed inactivated pathogen
  • DNA vaccines and engineered viruses
99
Q

Examples of whole live vaccines?

A

TB, polio, MMR

100
Q

Advantages of whole live vaccines?

A

sets up transient infection, activates full natural response, comprehensive protection, memory response, single dose

101
Q

Disadvantages of whole live vaccine?

A

immunocompromised patients, complications, revert to virulent form, outbreak in areas of poor sanitation

102
Q

Examples of whole inactivated pathogen?

A

Cholera, pertussis, hepatitis A, rabies, influenza

103
Q

Advantages of whole inactivated pathogen?

A

no risk of infection, easier storage, wide range of antigenic components

104
Q

Disadvantages of whole inactivated pathogen?

A

only activate humoral responses (lack of T cells), weak without transient infection, repeated boosters required

105
Q

Examples of subunit vaccines?

A

toxoids, MenC, bezsero

106
Q

Advantages of subunit vaccines?

A

safe as only some of pathogen is used, no risk of infection, easy storage

107
Q

Disadvantages of subunit vaccines?

A

less powerful, repeated vaccination, genetic heterogeneity

108
Q

What parts of the pathogen do subunit vaccines use?

A

purified proteins, recombinant proteins, carrier proteins

109
Q

What do DNA vaccines do?

A

Transiently express genes from pathogens in host cells and generate immune responses similar to natural –> leads to T and B cell memory responses

110
Q

Advantages of DNA vaccines?

A

Safe, easily stored, adaptable to widespread vaccination programmes

111
Q

Disadvantages of DNA vaccines?

A

mild response so requires boostes, no transient infection

112
Q

What are engineered viruses?

A

imitate effects of transient infection using non-pathogenic organism

113
Q

How do engineered vaccines work?

A

genes for major pathogen antigens introduced to non-pathogenic organism and then into host

114
Q

Advantages of engineered virus vaccines?

A

ideal stimulus, produces memory, flexible, safe

115
Q

Disadvantages of engineered viruses?

A

Immunocompromised, immune response can negate effectiveness, requires refrigeration

116
Q

Definition of an allergy?

A

Abnormal response to harmless foreign material (allergens)

117
Q

Definition of atopy?

A

hereditary disposition to development of hypersensitivity against common environmental antigens

118
Q

Forms of allergens?

A

Food, venoms, drugs, environment

119
Q

Types of allergic/hypersensitive diseases?

A

anaphylaxis, asthma, rhinitis, dermatitis, conjunctivitis, oral allergy angioedema

120
Q

Clinical skin manifestations of allergies?

A

swelling, redness, itching

121
Q

Clinical airway manifestations of allergies?

A

excessive mucus, bronchoconstriction

122
Q

Clincial GI manifestations of allergies?

A

abdominal bloating, vomiting, diarrhoea

123
Q

Clinical cardiovascular manifestations of allergy?

A

vasodilation, increased vascular permeability, lowered BP

124
Q

What is anaphylaxis?

A

An acute allergic reaction to an antigen, to which the body has become hypersensitive. Life-threatening, generalised, or systemic

125
Q

What is the criteria for anaphylaxis?

A
  • sudden onset and rapid progression of symptoms
  • life threatening airway/breathing/circulation problems associated with skin and mucosal changes
126
Q

What type of hypersensitivity reaction is anaphylaxis?

127
Q

How does a type 1 hypersensitivity reaction work?

A

IgE binds to receptors on mast cells/basophils and primes them. Cross-linking causes degranulation and liberation of mediators - histamine is released and uses H1 and H2 receptors

128
Q

What is recommended treatment for anaphylaxis?

A
  1. rapid assessment ABCDE
  2. call for help
  3. administer adrenaline into anterolateral thigh
  4. establish airway and high flow O2, IV fluids, chlorphenamine, hydrocortisone
  5. monitor pulse, ECG, blood pressure
129
Q

Recommended dose of adrenaline?

A
  • 500ug in adults and children > 12
  • 300ug in children 6-12
  • 150ug in children < 6
130
Q

How does adrenaline relieve anaphylaxis?

A
  • stimulates beta 1 receptors so heart rate and contraction increase
  • stimulates beta 2 receptors so more bronchodilation
  • reduces inflammatory mediators by increasing cAMP
131
Q

What is mast cell tryptase?

A

Enzyme elevated for up to 6 hours after anaphylaxis - marker for showing degranulation of mast cells

132
Q

What are the cells involved in anaphylaxis?

A
  • mast cells, eosinophils, basophils
  • lymphocytes (Th2) and dendritic cells (antigen presentation)
  • epithelial cells, smooth muscle, fibroblasts
133
Q

What is a type II hypersensitivity reaction?

A

cytotoxicity, primarily IgG –> drug allergies

134
Q

What is a type III hypersensitivity reaction?

A

immune complex formation (IgG and IgM) –> serum sickness

135
Q

What is a type IV hypersensitivity reaction?

A

delayed hypersensitivity, cell dependent (on Th1, cytotoxic T cells, macrophages) –> dermatitis, chronic asthma, chronic allergic rhinitis

136
Q

What is the high affinity receptor for IgE?

A

FcεRI expression through mast cells and basophils

137
Q

How is response amplified in IgE reaction?

A

clustering and cross-linking causes assembly of signalling complexes

138
Q

What is the low affinity receptor of IgE?

A

FcεRII expression through B cells, T cells, monocytes, eosinophils, neutrophils, platelets

139
Q

Function of low affinity IgE receptors?

A

regulate IgE synthesis, trigger cytokine release by monocytes, antigen presentation

140
Q

What are mast cells?

A

Major cell types that express high affinity IgE receptor so involved in host defence against parasites. Primary role in innate and acquired immunity

141
Q

What are mast cells produced and characterised by?

A

Produced by specific cell lineage in marrow, characterised by requirement for c-kit protein

142
Q

Where do mast cells exist?

A

In tissues

143
Q

What do mast cells release immediately, after a few minutes, and after hours?

A

immediately: histamine, chemotactic factors, proteases, prosteoglycans
after minutes: lipid derived mediators (leukotrines, prostagaglandins, PAF)
after hours: cytokines

144
Q

What are indirect activators of mast cells?

A

Most allergens - requires prior sensitisation

145
Q

What are direct activators of mast cells?

A

cold/mechanical deformation, aspirin, preservatives, latex

146
Q

What makes an allergen?

A

particulate delivery of antigens, presence of weak PAMPs, nasal/skin delivery, low doses, stimulation of IL-4 from mast cells in absence of IgE

147
Q

Definition of asthma?

A

Inflammatoty disease of bronchi commonly triggered by allergens - can involve IgE and eosinophil influx into lungs

148
Q

What type of T cell does chronic asthma use?

A

CD8 T cells to control eosinophil responses

149
Q

What are some treatment options for asthma?

A
  • desensitisation (increasing doses of allergen)
  • preventing IgE production (delivery of suppressive cytokines/blockade)
  • preventing mast cell activation
  • inhibit mast cell products
150
Q

What are host-pathogen interactions?

A

Describes how pathogens sustain themselves within host organisms

151
Q

What is infectivity?

A

Ability to become established in a host, can invilve adherence and immune escape

152
Q

What is virulence?

A

A pathogen’s ability to cause disease once established

153
Q

What is invasiveness?

A

Capacity to penetrate mucosal surfaces to reach normally sterile states

154
Q

What are the 4 stages of pathogenesis?

A
  1. exposure (contact)
  2. adhesion (colonisation)
  3. invasion
  4. infection
155
Q

When is a pathogen cycle completed?

A

When the pathogen exits the host and is transmitted to a new host

156
Q

What are commensals?

A

Microorganisms of resident flora, usually nonpathogenic

157
Q

When might commensals cause disease?

A

In a particular context (prosthetics), if they overgrow, if they translocate

158
Q

Commensals are normally asymptomatic, when can they become opportunistic?

A

When the immune status is altered

159
Q

What type of mechanism does immune response to stimulus produce?

A

specific and non-specific

160
Q

Why do viruses need rapid cell entry?

A

Free viruses are easily neutralised and destroyed

161
Q

What type of immune response do viral infections produce?

A

Humoral (antibodies) and cell-mediated (cytotoxic T lymphocytes)

162
Q

Are most viruses directly or indirectly cytotoxic?

A

indirectly

163
Q

What is viral evasion?

A

Process by which viruses evade the immune system and interfere with specific or non-specific defence

164
Q

How does influenza cause viral evasion? (2)

A
  1. changes coat antigen - spherical particles surrounded by lipid bilayer acquired from infected host cell
  2. glycoprotein projections facilitate attachment and viral budding
165
Q

How do HIV and MMR cause viral evasion?

A

HIV: antigenic variation
MMR: immune suppression

166
Q

What is the difference between antigenic shift, and antigenic drift?

A

antigenic shift: spontaneous mutations that occur gradually, minor changes –> epidemics
antigenic drift: sudden emergence of new subtype –> pandemic

167
Q

How does the number of virulence effect the humoral response during bacterial infection?

A

low number = phagocytes activated
high number = immune response generated

168
Q

How do bacterial pathogens colonise flora?

A
  1. sequestering nutrients
  2. novel metabolic pathways
  3. out-compete other microorganisms
169
Q

How does the snesor-kinase system of bacteria alter gene transcription regulation?

A

detects sensing changes in competing bacteria

170
Q

What forms can bacterial toxins take?

A

chromosomal or on plasmids

171
Q

What are adhesins?

A

help bacteria to bind to mucosal surfaces, eg. fimbriae, glycosaminoglycans, lipids, pili filamentous proteins

172
Q

What are biofilms?

A

extracellular polymeric substance secreted by bacteria in order to stick on surfaces. Made up of protein, polysaccharides, and DNA.

173
Q

How do biofilms protect against microbials?

A

distinct genes expressed in response to environmental cues. Eg. dental plaque

174
Q

What specific immunoglobulins and antibodies are included in the host response to bacteria?

A

IgA - blocks attachment to host cells
AbC3b - opsonisation, prevents proliferation, neutralises toxins

175
Q

What is delayed-type hypersensitivity?

A

Immune response that occurs through direct action of sensitised T cells when stimulated by an antigen

176
Q

Examples of protozoan infection?

A

Malaria, sleeping sickness, amoebiasis

177
Q

Which type of immunity involved in blood and tissue stages of protozoan infection?

A

blood = humoral
tissue = cell mediated

178
Q

What immunoglobulins do protozoa activate?

A

IgE - binds to mast cells - degranulation - cytokine release

179
Q

Why are helminths (worms) not intracellular?

A

Lay eggs but do not multiply in humans

180
Q

Why is immune response poor to helminths?

A

few parasites carried so IgE response triggered but not sufficient to kill

181
Q

What happens when helminth infections establish hyporesponsiveness?

A

decrease antigen expresion and create glycolipid/protein coat

182
Q

What are tumour-infiltrating lymphocytes

A

contribute to cancer growth and cause immunosuppression

183
Q

What are tumour-associated macrophages?

A

major component of infiltrate of most cancers

184
Q

What PAMP is associated with TLR2 and what is this present on?

A
  1. peptidoglycans
  2. gram +ve bacteria
185
Q

What PAMP is associated with TLR4 and what is this present on?

A
  1. lipopolysaccharide (LPS)
  2. gram -ve bacteria
186
Q

What PAMP is associated with TLR5 and what is this present on?

A
  1. Flagellin
  2. Flagellated bacteria

ICS/GP/ILA (9 decks)

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