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Phase 2a > Immunology > Flashcards

Immunology Flashcards

1
Q

What do all blood cells derive from?

A

Multipotential haematopoietic stem cells

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2
Q

What do common myeloid progenitors specialise into?

A

Megakaryocytes
Erythrocytes
Mast cells
Myeloblasts

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3
Q

What do megakaryocytes specialise into?

A

Platelets

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4
Q

What do myeloblasts specialise into?

A

Basophils
Neutrophils
Eosinophils
Monocytes

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5
Q

What do monocytes specialise into?

A

Macrophages and dendritic cells

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6
Q

What do common lymphoid progenitors specialise into?

A

NK cells and small lymphocytes

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7
Q

What do small lymphocytes specialise into?

A

T and B lymphocytes

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8
Q

What is the innate immune system?

A

The initial rapid and non-specific response to antigenic material with no immunological memory

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9
Q

What do haematopoietic stem cells specialise into?

A

Lymphoid and myeloid progenitors

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10
Q

What causes acute lymphocytic leukaemia (ALL)?

A

Lymphoid progenitors causing increased amounts of immature lymphocytes

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11
Q

What cells does chronic lymphocytic leukaemia affect (CLL)?

A

Naïve (not exposed to antigen) mature B cells

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12
Q

What cells do lymphomas affect?

A

Mature naïve T cells and B cells in germinal centres

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13
Q

What is multiple myeloma?

A

Cancer of plasma cells

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14
Q

What is acute myeloid leukaemia (AML)?

A

Cancer of myeloid progenitors causing a decrease in their downstream cells

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15
Q

Give some examples of myeloproliferative disorders

A

Chronic myeloid leukaemia

Proliferation of granulocytes

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16
Q

What are the primary lymphoid organs?

A

Bone marrow and thymus

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17
Q

Where do all immune cells originate from?

A

Bone marrow

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18
Q

Where do B cells mature?

A

Bone marrow

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19
Q

Where do T cells mature?

A

Thymus

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20
Q

What are the secondary lymphoid organs?

A

Lymph nodes and spleen

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21
Q

What happens within the lymph nodes?

A

Site of B and T cell interaction. They also interact with dendritic cells that are delivering the antigen

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22
Q

What happens within the spleen?

A

Site of removal of RBCs and Ab-coated bacteria

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23
Q

What are the tertiary lymphoid organs?

A

Transient formation of germinal centres, usually pathology related

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24
Q

What is the role of secondary lymphoid tissues?

A

(Lymph nodes) provide the stage to allow foreign antigen to interact with lymphocytes

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25
Q

What are tertiary lymphoid organs?

A

Lymph node like ectopic structures that form during chronic inflammation such as in chronic infection, transplant graft rejection and autoimmunity

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26
Q

Give an example of a condition where tertiary lymphoid organs are involved.

A

In multiple sclerosis focal TLOs form in the brain which produces anti-myelin antibody leading to the demyelinating pathology

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27
Q

What happens to dendritic cells once they enter the lymph nodes?

A

DC enter with Ag in afferent lymphatics and interact with naïve CD4+ cells to activate them in the paracortex. T cell either become effector cells or memory cells.

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28
Q

What are lymphoid follicles?

A

Germinal centres which are the site of somatic hypermutation (this achieves a higher affinity Fab and class switching)

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29
Q

What is the role of the red pulp of the spleen?

A

Mechanical filtration of RBCs

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30
Q

What is the role of the white pulp in the spleen?

A

Active immune responses through humoral and cell-mediated immunity

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31
Q

What makes up the white pulp of the spleen?

A

Primary follicles
Marginal zone
Periarteriolar lymphoid sheath (PALS)

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32
Q

What is found within the periarteriolar lymphoid sheath (PALS) of the spleen?

A

Rich in T cells

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33
Q

What is found within the lymphoid follicles of the spleen?

A

Rich in B cells

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34
Q

What is the role of the spleen only in the foetus?

A

Production of RBCs up to the 5th month of gestation

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35
Q

What is the role of the spleen in people with thalassaemia?

A

Results in haemolytic anaemia so the spleen produces RBCs once more

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36
Q

What is thalassaemia?

A

Decreased Hb

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37
Q

What does the spleen store?

A

RBCs, lymphocytes, platelets and other elements

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38
Q

What percentage of lymphocytes are stored in the spleen?

A

~25%

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39
Q

What percentage of RBCs are stored in the spleen?

A

~30%

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40
Q

When are the RBCs stored in the spleen released?

A

In hypovolaemia and hypoxia

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41
Q

What does the spleen clear from circulation?

A

Old platelets

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42
Q

Describe the receptors of the innate immune system.

A

Primitive and broad

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43
Q

Describe the receptors of the adaptive immune system.

A

Highly specific (T and B cell receptors)

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44
Q

Describe the kinetics of the innate immune system.

A

Fast (hours-days)

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45
Q

Describe the kinetics of the adaptive immune system.

A

Slow (days-weeks)

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46
Q

What type of immunity is highly regulated?

A

Adaptive immunity

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47
Q

What type of immunity can be amplified?

A

Adaptive immunity

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48
Q

What type of immunity can self-discriminate?

A

Adaptive immunity

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49
Q

Describe the duration of the innate immune response.

A

Short (days)

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50
Q

Describe the duration of the adaptive immune response.

A

Long (months/years)

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51
Q

What type of immunity has an aspect of memory?

A

Adaptive immunity

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52
Q

Which WBC is most abundant in the blood?

A

Neutrophils

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53
Q

What percentage of WBC in the blood is neutrophils?

A

70%

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54
Q

Describe the lifespan of neutrophils.

A

Short lived

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55
Q

Where do neutrophils travel to?

A

Rapidly egress into tissues during acute infection

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56
Q

What type of cell is a neutrophil (other than being a WBC)

A

Phagocytic and bactericidal

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57
Q

Describe the nucleus of a neutrophil.

A

Polymorphonuclear cells (multilobed)

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58
Q

What are pathogens detected by in phagocytosis?

A

Pattern recognition receptors of innate phagocytic cells

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59
Q

What is the principal cell of acute inflammation?

A

Neutrophils

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60
Q

How do neutrophils carry out phagocytosis?

A

They kill by internalising bacteria and degranulating their contents into a phagolysosome

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61
Q

What are the major components found within a phagolysosome?

A

Alpha-defensins and lactoferrin

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62
Q

Other than phagocytosis, how else can neutrophils kill bacteria?

A

Respiratory burst

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63
Q

What is the first stage of the respiratory burst carried out by neutrophils?

A

Electrons are pumped into the phagolysosome by NADPH oxidase

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64
Q

What happens after electrons have been pumped into the phagolysosome during the respiratory burst carried out by neutrophils?

A

The electrons combine with molecular oxygen to produce superoxide ions

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65
Q

What happens after the formation of superoxide ions during the respiratory burst carried out by neutrophils?

A

These ions combine with protons present in the granules to produce peroxide which is bactericidal in itself

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66
Q

What happens after the formation of peroxide during the respiratory burst carried out by neutrophils?

A

Myeloperoxidase can then chlorinate the peroxide to produce a hypohalous acid which is also bactericidal

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67
Q

What is the first stage in the movement of neutrophils out of capillaries in acute inflammation?

A

E-selectin is activated by IL-1 and TNF-α from damaged cells, and binds to the glycoprotein CD15 on neutrophils in blood

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68
Q

What is E-selectin?

A

An adhesion molecule on the capillary endothelium

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69
Q

What happens in the movement of neutrophils out of capillaries in acute inflammation after the neutrophils have bound to E-selectin?

A

This causes neutrophils in the blood to slow down and roll along the endothelium lining

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70
Q

What happens in the movement of neutrophils out of capillaries in acute inflammation after neutrophils have rolled along the endothelium lining?

A

ICAM-1 on endothelium (induced by LPS, IL-1, TNF-α) binds to integrin on neutrophil; the neutrophil stops

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71
Q

What happens in the movement of neutrophils out of capillaries in acute inflammation after neutrophils have stopped rolling?

A

Diapedesis: neutrophil squeezes through endothelium (holes caused by C3a, C5a, chemokines, histamines, prostaglandins, leukotrienes (causing smooth muscle contractions in the bronchioles))

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72
Q

What is the role of macrophages?

A

Phagocytosis, antigen presentation and cytokine secretion

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73
Q

What cytokines do macrophages secrete?

A

TNFα, IL-1, IL-6, IL-8, and IL-12

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74
Q

Describe the nuclei of macrophages.

A

Round single nuclei often with a small indentation

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75
Q

What do macrophages derive from?

A

Blood monocytes or as tissue resident macrophages

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76
Q

How do macrophages detect pathogens?

A

Detect pathogens and damage markers by pattern recognition receptors

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77
Q

In what type of inflammation are macrophages one of the principal cells?

A

Chronic

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78
Q

Where do tissue resident macrophages derive from?

A

Tissue resident macrophages are derived from the yolk sac and foetal liver during development

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79
Q

Where are tissue resident macrophages found?

A

Persist in tissues via self renewal

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80
Q

What are M1 macrophages?

A

M1 is considered pro-inflammatory due to its ability to metabolise arginine to nitric oxide

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81
Q

What are M2 macrophages?

A

M2 are considered anti-inflammatory due to their ability to metabolise arginine to the repair molecule ornithine

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82
Q

What do pattern recognition receptors (PRRs) on macrophages detect?

A

Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs)

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83
Q

What is the role of TLR4?

A

Found on macrophages and detects LPS on g-ve bacteria

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84
Q

Where do antibodies bind to pathogens?

A

By their Fab regions

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85
Q

How do macrophages use receptors and antibodies to phagocytose bacteria?

A

Macrophages have Fc receptors that bind antibody and in turn phagocytoses the bacteria the antibody has bound

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86
Q

What do macrophages do when antibodies bind to pathogens?

A

Complement then binds antibody Fc regions forming a complex. Macrophages have complement receptors that recognise this complex

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87
Q

When do basophils release histamine?

A

Upon IgE crosslinking Fcε receptors

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88
Q

What do basophils release?

A

Histamine, serotonin and heparin

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89
Q

In what conditions are basophils important?

A

Asthma, anaphylaxis, atopic dermatitis, and hay fever

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90
Q

What cells can basophils be compared to?

A

Circulating mast cells - they do not egress into tissues and become mast cells

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91
Q

What type of infection are eosinophils important in?

A

Parasitic infections

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92
Q

What do eosinophils release?

A

Release cationic granules such as major basic protein, ROS, eicosanoids, leukotrienes, elastase etc.

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93
Q

What cells are classed as granulocytes?

A

BEN: basophils, eosinophils and neutrophils

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94
Q

What is the role of mast cells?

A

Important in parasitic infection and allergic reactions

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95
Q

Where are mast cells found?

A

At mucosal surfaces

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96
Q

What is important for the development of mast cells?

A

Stem cell factor

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97
Q

What cell is the main source of histamine?

A

Mast cells

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98
Q

How are mast cells activated?

A

By immune complex IgE cross-linking FcεR1

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99
Q

What do mast cells secrete?

A

Histamine, cytokines (IL-4, IL-13 and TNFα) and lipid mediators (leukotrienes and prostaglandins)

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100
Q

What does histamine do?

A

Increases vascular permeability and causes smooth muscle contraction

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101
Q

What does IL-4 do?

A

Promotes Th2 differentiation

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102
Q

What does IL-13 do?

A

Promotes IgE production

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103
Q

What does TNFα do?

A

Promotes tissue inflammation

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104
Q

What do lipid mediators such as leukotrienes and prostaglandins do?

A

Increase vascular permeability
Cause smooth muscle contraction
Stimulate mucus secretion
Chemoattractants for T cells, eosinophils, mast cells and basophils

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105
Q

What happens when IgE binds to an allergen?

A

Activates mast cells via Fc receptor

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106
Q

Where are NK cells found?

A

In blood and tissues

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107
Q

What receptors do macrophages have?

A

CD14+ and CD40+

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108
Q

What receptors do NK cells have?

A

CD16+

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109
Q

What process do NK cells use to kill pathogens?

A

Antibody-dependent cellular cytotoxicity (ADCC) - not phagocytic

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110
Q

How do NK cells kill pathogens?

A

Release lytic granules that kill virus infected cells

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111
Q

How do NK cells recognise self and non-self?

A

NK cell’s inhibitory receptors detect levels of MHC-I on cell surfaces

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112
Q

What molecule does ADCC not require?

A

Complement

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113
Q

How many cell types does ADCC use?

A

1

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114
Q

What is the first stage of ADCC?

A

IgG will bind surface antigens on the pathogen-infected cell

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115
Q

What happens during ADCC once IgG is bound to antigens?

A

NK cells have Fc receptors (CD16) that recognise the antibody Fc region

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116
Q

What happens during ADCC once NK cells have bound to the antibody?

A

This cross-linking triggers degranulation and cell apoptosis

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117
Q

How do viruses become antibody targets?

A

Viral proteins are expressed on the surface of cells during viral replication

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118
Q

What do the lytic granules of NK cells contain?

A

Perforin and granzymes that induce apoptosis and cell lysis

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119
Q

What is the effect of cancer on NK cells?

A

Cancers tend to downregulate MHC-I mediated antigen presentation

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120
Q

What happens if there is not enough MHC-1 on the cell surface due to cancer?

A

NK cells will activate and try to kill the cell

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121
Q

What is the purpose of MHC-!?

A

Cells that have MHC-I activate the inhibitory receptor and therefore does not elicit a response from NK cells.

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122
Q

When do cytotoxic T cells act on tumour cells?

A

In response to NK cell cytokine production

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123
Q

What are the professional antigen presenting cells?

A

Macrophages
B cells
Dendritic cells

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124
Q

What do the professional antigen presenting cells present?

A

Exogenous Ag on cell surface in the context of MHC-II

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125
Q

Which type of cell is the most potent antigen presenting cell?

A

Dendritic cells

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126
Q

Where do dendritic cells travel to?

A

Egress to secondary organs to aid the adaptive response

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127
Q

Which cells are capable of MHC-I presentation?

A

All nucleated cells (although thrombocytes are anucleate and still have MHC-I molecules but RBCs do not)

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128
Q

Which chromosome codes for MHC molecules?

A

Chromosome 6

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129
Q

Where is exogenous antigen processed in antigen presenting cells?

A

ER

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130
Q

Give some examples of endogenous proteins that might be present in the cytosol of an antigen presenting cell.

A

Viral proteins

Cancer-related proteins

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131
Q

Where are endogenous proteins processed in antigen-presenting cells?

A

Endosomes

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132
Q

How are endogenous proteins presented on antigen-presenting cells?

A

In the context of MHC-I

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133
Q

Which cells are capable of cross-presentation?

A

Dendritic cells

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134
Q

How do dendritic cells carry out cross-presentation?

A

They can present exogenous Ag in the context of MHC-I in order to activate Tc cells

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135
Q

What can dendritic cells be thought of as?

A

The bridge between the innate and adaptive immune responses in secondary lymphoid organs

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136
Q

What happens when immune cells come together?

A

They form an immune synapse

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137
Q

What must happen for a response to occur upon formation of an immune synapse?

A

Binding of primary receptors e.g. TCR to MHC-II
Binding of co-stimulatory molecules e.g. CD28/CTLA4 to CD80/CD86
A robust release of the appropriate cytokines

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138
Q

What happens if there is MHC binding without other stimulation?

A

Anergy

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139
Q

What is anergy?

A

T cell anergy is a tolerance mechanism in which the lymphocyte is intrinsically functionally inactivated following an antigen encounter

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140
Q

What happens to T cells during initial encounter with a novel antigen?

A

T cell will differentiate into either memory or effector T cells

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141
Q

What is the common T cell marker?

A

CD3 - the identifying co-stimulating molecule for all T cells

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142
Q

What are the 2 different T cells following maturation?

A

CD4 or CD8

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143
Q

What receptors do T cells have?

A

CD3
CD4/CD8
T cell receptor - TCR
CD25

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144
Q

What is the main function of the CD3 molecule?

A

Intracellular signalling that activates the T cell

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145
Q

What is the structure of the CD3 molecule?

A

It is a protein complex comprised of one gamma, one theta, and two epsilon polypeptide chains.

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146
Q

What do T cells start off as?

A

In the bone marrow as HSCs

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147
Q

What do T cells differentiate into from HSCs?

A

Differentiate through the lymphoid pathway into immature T cells

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148
Q

What are naïve T cells?

A

Not encountered the antigen yet. How immature T cells start as.

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149
Q

Do naïve T cells present CD4 or CD8?

A

Both - they are double positive cells.

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150
Q

What happens to naïve T cells during maturation?

A

They undergo thymic education to retain either CD4 or CD8, and they undergo VDJ recombination in the thymus to determine the antigen epitope that their TCR will recognise

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151
Q

How do T cells recognise antigens?

A

T-cells must recognise antigen in the context of MHC molecules using their T-cell receptors (except for superantigens)

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152
Q

What do superantigens do?

A

Superantigens bind the beta chain of TCR regardless of TCR

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153
Q

How are naïve T cells identified?

A

Naïve T cells are identified by being CD45RA+

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154
Q

How are memory T cells identified?

A

Memory T cells are identified by being CD45RO+

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155
Q

What receptors do cytotoxic T cells present?

A

CD8

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156
Q

What do cytotoxic T cells release?

A

Perforins and granzymes

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157
Q

How do cytotoxic T cells recognise Ag?

A

In the context of MHC-I

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158
Q

What do cytotoxic T cells become?

A

Effector or memory cells

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159
Q

How can cytotoxic T cells kill pathogens?

A

Perforin and granzymes

Expression of Fas ligand

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160
Q

How do cytotoxic T cells use perforin to kill pathogens?

A

Allows salt and water to enter cells and causing them to lyse

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161
Q

How do cytotoxic T cells use granzymes to kill pathogens?

A

They cleave a caspase protein (CPP-32) which will activate a nuclease (CAD) which initiations DNA degradation and apoptosis

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162
Q

What are granzymes?

A

Group of serine proteases

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163
Q

What is perforin?

A

Pore forming cytolytic protein

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164
Q

How do T cells use the Fas ligand to kill pathogens?

A

CD8 T cells also express the Fas ligand, this binds Fas on target cells which activates the caspase cascade and therefore apoptosis

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165
Q

What type of immunity are Th1 cells involved in?

A

Cell-mediated

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166
Q

What do Th1 cells do?

A

Activate/regulate macrophages, monocytes, cytotoxic T cells and NK cells
Elimination of cellular antigens (viruses, intracellular bacteria, tumour cells)

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167
Q

What type of immunity are Th2 cells involved in?

A

Humoral

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168
Q

What do Th2 cells do?

A

Stimulation of B cells
Boost in the synthesis of IgE, IgG1 and IgG3 antibodies
Regulate eosinophils, basophils and mast cells

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169
Q

What are Treg cells the principle cell in?

A

Peripheral immune tolerance

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170
Q

What is the key cytokine of Treg cells?

A

IL-10

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171
Q

What is the role of IL-10?

A

Mass anti-inflammatory action

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172
Q

Where are Th17 cells important?

A

Mucosal membranes

173
Q

What is the principle cytokine of Th17 cells?

174
Q

What does IL-17 do?

A

Affects innate immune cells to produce IL-8

175
Q

What is the relationship between Treg and Th17 cells?

A

They are antagonistic

176
Q

How are Treg and Th17 cells antagonistic?

A

Transcription factors and cytokines produced by Th17 cells suppressive T reg cells and vice versa

177
Q

What is the purpose of IL-8?

A

The most important cytokine in neutrophil production and recruitment

178
Q

What is the purpose of IL-23?

A

IL-23 maintains Th17 populations and is a target for biologics

179
Q

What receptors do B cells have?

A

BCR - B cell receptor
CD19
CD20
(CD15)

180
Q

What is the CD19 receptor?

A

Co-stimulatory molecule of mature B cells

181
Q

What is the CD20 receptor?

A

Mature B cell marker

182
Q

Where does B cell activation take place?

A

Secondary lymphoid organs (lymph nodes)

183
Q

What 2 processes are aided by dendritic and T cells?

A

Somatic hypermutation and affinity selection

184
Q

What can activated B cells become?

A

Short lived plasma cells (IgM+) or long-lived plasma cells (IgG, E, or A+)

185
Q

How are B cells activated in the absence of T cell help?

A

Directly by antigen

186
Q

Describe the response when B cells are activated directly by the antigen.

A

Rapid but short lived response

Less affinity and IgM releasing

187
Q

How are B cells activated?

A

When they internalise antigen and present it to T cells in the context of MHC II

188
Q

What happens to B cells after activation?

A

They migrate to newly formed germinal centres to undergo somatic hypermutation

189
Q

What is somatic hypermutation?

A

When RAG enzymes (activation-induced cysteine deaminase - AID) introduce random mutations in the variable region of the antibody gene

190
Q

What is the role of dendritic cells within the germinal centres?

A

They will present the same antigen to the B cell to test if the avidity of its antibodies has increased (affinity selection)

191
Q

What is affinity selection?

A

B cells with less avidity will be negatively selected and those with greater avidity will be positively selected and undergo class switching and clonal proliferation

192
Q

What type of cell appears in Hodgkin lymphoma?

A

Reed-Sternberg cells

193
Q

What are Reed-Sternberg cells?

A

These are B-cell derived giant cells that are distinctive of Hodgkin lymphoma

194
Q

What is the distinctive marker of Reed-Sternberg cells?

195
Q

What do Reed-Sternberg cells look like?

A

They have prominenteosinophilicinclusion-likenucleoli(thus resembling an “owl’s eye” appearance) under microscopy

196
Q

What B cell receptor is targeted by rituximab?

197
Q

Which part of the lymph node is the B cell region?

198
Q

Which part of the lymph node is the T cell region?

A

Paracortex

199
Q

Which part of the lymph node is the plasma cell region?

200
Q

What happens when memory B cells encounter their specific antigen?

A

They become activated and undergo clonal proliferation and begin secreting IgG

201
Q

What does the constant region of antibodies do?

A

Determines antibody type and therefore effector function

202
Q

What does the Fab (antigen-binding fragment) region of antibodies do?

A

Binds epitopes of antigen

203
Q

How are Fab regions determined?

A

Initially determined by a process called VDJ recombination during maturation in the bone marrow

204
Q

When does the avidity of an antibody for its antigen increase?

A

During infection through somatic hypermutation in the germinal centres of secondary organs

205
Q

What is the Fc (fragment crystallisation) region of antibodies?

A

The area that binds Fc receptors on immune cell surfaces

206
Q

What does the Fc region of antibodies do?

A

Binds complement to aid in opsonisation of pathogens for phagocytosis

207
Q

What are the functions of antibodies?

A

Neutralisation of toxins, opsonisation of pathogens, complement activation via the classical pathway

208
Q

Where is IgA found and what as?

A

The mucosal Ab as a dimer

209
Q

What fluid is IgA found in?

A

Present in colostrum and coats neonate gut

210
Q

What does IgM look like?

A

Pentameric

211
Q

What are the features of IgM?

A

Not entirely specific to antigen

Highest capacity to activate complement

212
Q

What antibody is most abundant in the blood?

213
Q

How many subclasses of IgG are there?

214
Q

Which antibody can cross the placenta?

215
Q

What are the features of IgG?

A

Highly specific

Important during secondary responses (second infection - levels spike most of all antibodies)

216
Q

What antibody is least abundant in the blood?

217
Q

What is IgE bound to?

A

Mast cells and basophils by FcεR

218
Q

What is IgE important in?

A

Allergy and helminth infection

219
Q

What are the features of IgD?

A

Not that important. Function is debated in the literature

220
Q

What does IL-5 promote?

A

IgA class switching

221
Q

What does IL-4 promote?

A

IgE class switching

222
Q

What does colostrum contain?

A

IgA, IgM, and IgG where IgA is the principle antibody

223
Q

What is type I hypersensitivity?

A

Anaphylactic

224
Q

What is type II hypersensitivity?

A

Cell bound

225
Q

What is type III hypersensitivity?

A

Immune complex

226
Q

What is type IV hypersensitivity?

A

Delayed hypersensitivity

227
Q

What is the mechanism of type I hypersensitivity?

A

Antigen reacts with IgE bound to mast cells

228
Q

Give some examples of type I hypersensitivity.

A

Anaphylaxis


Atopy (e.g.asthma, eczema andhayfever)

229
Q

What is the mechanism of type II hypersensitivity?

A

IgG or IgM binds to antigen on cell surface

230
Q

Give some examples of type II hypersensitivity.

A

Autoimmune haemolytic anaemia
Goodpasture’s syndrome
Pernicious anaemia
Rheumatic fever

231
Q

What is the mechanism of type III hypersensitivity?

A

Free antigen and antibody (IgG, IgA) combine

232
Q

Give some examples of type III hypersensitivity.

A

Systemic lupus erythematosus

Post-streptococcal glomerulonephritis

233
Q

What is the mechanism of type IV hypersensitivity?

A

T-cell mediated (Th1)

234
Q

Give some examples of type IV hypersensitivity.

A

Tuberculosis/tuberculin skin reaction
Graft versus host disease
Multiple sclerosis
Guillain-Barre syndrome

235
Q

Describe the rate of type I hypersensitivity reactions.

A

Fast reaction occurring in minutes

236
Q

What happens in a type I hypersensitivity reaction?

A

Cross-linking of antigen to IgE on mast cells and basophils causes massive degranulation and therefore massive release of histamine

237
Q

What happens in a type II hypersensitivity reaction?

A

IgM or IgG binds to self antigen leading to cell destruction by the membrane attack complex and cellular mechanisms

238
Q

What is the first stage of a type III hypersensitivity reaction?

A

IgG binds soluble antigen forming a circulating immune complex

239
Q

What happens after IgG has bound soluble antigen in a type III hypersensitivity reaction?

A

These deposit in vessel walls especially in the kidneys

240
Q

What happens after the circulating immune complexes have deposited in vessel walls in a type III hypersensitivity reaction?

A

Here they kick off an inflammatory response causing complement deposition, opsonisation, phagocytosis etc

241
Q

What happens after the inflammatory response in a type III hypersensitivity reaction?

A

RBCs carrying the complement receptor 1 bind complement coated immune complexes and transport them to the liver and spleen for phagocytosis

242
Q

What is the first stage of a type IV hypersensitivity reaction?

A

Th1 are activated by antigen presenting cells

243
Q

What happens after Th1 cells are activated in a type IV hypersensitivity reaction?

A

Memory T cells are formed

244
Q

What happens after memory T cells are formed in a type IV hypersensitivity reaction?

A

When the memory T cells encounter the antigen again they will activate macrophages leading to tissue damage

245
Q

What happens in a type V hypersensitivity reaction?

A

IgM or IgG bind cell surface receptors and either stimulating or blocks endogenous ligand binding

246
Q

Give some examples of type V hypersensitivity reactions.

A

Grave’s disease and myasthenia gravis

247
Q

What happens during anaphylaxis?

A

IgE binds antigen which then cross-links FcεRI on mast cells and basophils leading to massive degranulation and histamine release

248
Q

What is the first thing to administer to an anaphylactic patient?

A

IM adrenaline is 1st line

249
Q

What is given to an anaphylactic patient after adrenaline?

A

Chlorphenamine (antihistamine) and hydrocortisone (cortisol)

250
Q

What do you check if you suspect a patient is anaphylactic?

A 
Airway
Breathing
Circulation
Disability
Exposure
251
Q

What do you look for to confirm a patient is anaphylactic?

A

Acute onset of illness
Life threatening airway and/or breathing and/or circulation problems
Skin changes

252
Q

What are some life-threatening airway problems?

A

Swelling, hoarseness, stridor

253
Q

What are some life-threatening breathing problems?

A

Rapid breathing, wheeze, fatigue, cyanosis, SpO2<92%, confusion

254
Q

What are some life-threatening circulation problems?

A

Pale, clammy, low blood pressure, faintness, drowsy/coma

255
Q

How does autoimmunity develop?

A

Thymic education
Tregs
CD4 activation against autoantigen

256
Q

What are the features of autoimmunity?

A

Often relapsing-remitting
Organ-specific vs systemic
Damage to or destruction of tissues
Altered organ growth/function

257
Q

What is central tolerance?

A

When TCRs and BCRs are tested against self antigen

258
Q

Where are B cells tested in central tolerance?

A

Bone marrow

259
Q

What happens to B cells in central tolerance?

A

BCRs that recognise self antigen either leads to clonal deletion (apoptosis), receptor editing, or anergy

260
Q

What is positive selection?

A

T-cells that recognise MHC molecules

261
Q

What happens if T cells can’t recognise MHC molecules in positive selection

A

They don’t receive survival signals

262
Q

How is CD4 or CD8 lineage determined?

A

Positive selection

263
Q

Where does positive and negative selection of T cells take place?

264
Q

What happens in negative selection?

A

This tests the T cell’s affinity to self

265
Q

What happens if the T cell binds to self antigens in negative selection?

A

They receive signals to apoptose

266
Q

What happens to T cells that pass both positive and negative selection?

A

They move to secondary organs as mature naïve T cells

267
Q

What is peripheral tolerance?

A

Low affinity self reactive T cells can escape the thymus to the periphery

268
Q

What happens in secondary lymphoid organs in peripheral tolerance?

A

T cells are presented self antigen again by dendritic cells and if they recognise they either are clonally deleted or converted to Treg

269
Q

How is autoimmunity treated?

A

Tx involve reducing inflammation and suppressing the immune system. This usually relieves symptoms but do not typically cure.

270
Q

What is the most common CNS immune mediated condition?

271
Q

What type of condition is MS?

A

Demyelinating

272
Q

What causes MS?

A

Failure of central and peripheral tolerance to eliminate self reactive T cells. These T cells are reactive to myelin proteins such myelin basic protein.

273
Q

What forms in the brain in MS patients?

A

Tertiary Lymphoid organs form in the brain of MS allowing T and B cell interactions and the generation of autoantibodies

274
Q

What are the different types of MS?

A 
Relapsing-remitting (RRMS)
Primary progressive (PPMS)
Secondary progressive (SPMS)
275
Q

What is RRMS?

A

Where there are periods of disease activity and no activity. Often incomplete recovery will occur > disability. Some will progress to secondary progressive

276
Q

What is PPMS?

A

Worsening neurological function from onset of symptoms with no early relapses or remissions

277
Q

What is SPMS?

A

Progressive worsening of neurological function over time. There will be periods of active disease with progression of the disease as well as periods of non-active disease where it still progresses

278
Q

How is MS diagnosed?

A

Spinal tap; demonstrating MS associated autoantibodies
MRI; Highlights brain lesions.
Evoked potential tests,which record the electrical signals produced by your nervous system in response to stimuli

279
Q

How are acute MS attacks managed?

A

IV methylprednisolone

280
Q

How is RRMS managed?

A

Immunomodulators > Interferon beta 1a, or 1b, or peginterferon beta 1a

281
Q

How is SPMS managed?

A

Siponimod or methylprednisolone

282
Q

How is PPMS managed?

A

Ocrelizumab and anti CD20 MAb similar to rituximab

283
Q

What is primary immunodeficiency?

A

Those born with intrinsic defects in their immune system

284
Q

How common is primary immunodeficiency?

A

Rare and mostly genetic disorders

285
Q

Give an example of primary immunodeficiency.

A

SCID - severe combined immunodeficiency

286
Q

What is SCID?

A

Severe combined immunodeficiency (bubble boy disease) = Where both B and T cells lose functionality. The most severe primary immunodeficiency with various genetic causes and subtypes

287
Q

What is the main hallmark of AIDS?

A

Profound immunodeficiency

288
Q

Give some examples of secondary immunodeficiencies.

A

Hypothyroidism, diabetes and hypoglycaemia

289
Q

What is secondary immunodeficiency?

A

These are acquired and are referred to generally as immunosuppression

290
Q

What drugs can induce secondary immunodeficiency?

A

Steroids, azathioprine, chemotherapy

291
Q

What diseases can induce secondary immunodeficiency?

A

Cancers of the bone marrow and blood cells (Leukaemia, Lymphoma, and Myeloma)
AIDS

292
Q

How do steroids cause immunodeficiency?

A

Suppress cell-mediated immunity by inhibiting NF-κB transcription factor which supresses IL-2 production which in turn reduced T cell proliferation

293
Q

How are steroids anti-inflammatory?

A

Steroids, specifically glucocorticoids, are anti-inflammatory by blocking eicosanoid production

294
Q

How does azathioprine cause immunodeficiency?

A

Azathioprine is an immunosuppressive drug that is a purine analogue that inhibits fast proliferating cells such as T cells

295
Q

How does HIV cause immunodeficiency?

A

HIV has a cell tropism for CD4+ T cells. In uncontrolled infection there is increasing destruction of CD4 cells

296
Q

What must the CD4 T cell count be to diagnose AIDS?

A

Once it drops below 200 cells/uL there is profound immunodeficiency and is defining aspect of the development of AIDS

297
Q

What is the negative phase?

A

A period after initial antigen exposure where ones immunity is actually lower than before encountering the antigen.

298
Q

How many doses are most vaccines?

A

A lot of vaccines have an initial “prime” dose followed by a “boost dose”

299
Q

What will an ideal vaccine do?

A

Induce both T and B memory cells

300
Q

What do adjuvants do?

A

Help boost the immune response

301
Q

What is often used to boost the immune response?

A

Viral vectors

302
Q

Where are monocytes found?

A

Bone marrow/blood

303
Q

Where are Kupffer cells found?

304
Q

Where are sinus histocytes found?

A

Lymph nodes

305
Q

Where are alveolar macrophages found?

306
Q

Where are tissue macrophages leading to giant cells found

A

Connective tissue

307
Q

Where are microglia found?

308
Q

Where are Hofbauer cells found?

309
Q

Where are intraglomerular mesangial cells found?

310
Q

Where are osteoclasts found?

311
Q

Where are epithelioid cells found?

A

Granulomas

312
Q

Where are sinusoidal lining cells found?

A

Red pulp of the spleen

313
Q

Where are Langerhans cells found?

314
Q

What is the main source of IL-1?

A

Macrophages

315
Q

What is the main source of IL-2?

316
Q

What is the main source of IL-3?

A

Activated T helper cells

317
Q

What is the main source of IL-4?

318
Q

What is the main source of IL-5?

319
Q

What is the main source of IL-6?

A

Macrophages, Th2 cells

320
Q

What is the main source of IL-8?

A

Macrophages (can be released from any TLR bearing cell)

321
Q

What is the main source of IL-10?

322
Q

What is the main source of IL-12?

A

Dendritic cells, macrophages and B cells

323
Q

What is the main source of tumour necrosis factor-α (TNF-α)

A

Macrophages

324
Q

What is the main source of interferon-γ?

325
Q

What is the function of IL-1?

Pro/anti-inflammatory?

A

Acute inflammation
Induces fever
Pro-inflammatory

326
Q

What is the function of IL-2?

Pro/anti-inflammatory?

A

Stimulates growth and differentiation of T cell response

Pro-inflammatory

327
Q

What is the function of IL-3?

Pro/anti-inflammatory?

A

Stimulates differentiation and proliferation of myeloid progenitor cells
Pro-inflammatory

328
Q

What is the function of IL-4?

Pro/anti-inflammatory?

A

Stimulates proliferation and differentiation of B cells
Promotes class switching to IgE in B cells
Anti-inflammatory

329
Q

What is the function of IL-5?

Pro/anti-inflammatory?

A

Stimulate production of eosinophils

Pro-inflammatory

330
Q

What is the function of IL-6?

Pro/anti-inflammatory?

A

Stimulates differentiation of B cells
Induces fever
Pro-inflammatory

331
Q

What is the function of IL-8?

Pro/anti-inflammatory?

A

Neutrophil chemotaxis (can attract all granulocytes but neutrophils most)
Promotes phagocytosis
Pro-inflammatory

332
Q

What is the function of IL-10?

Pro/anti-inflammatory?

A

Inhibits Th1 cytokine production

Anti-inflammatory

333
Q

What is the function of IL-12?

Pro/anti-inflammatory?

A

Activates NK cellsandstimulates differentiation of naive T cells into Th1 cells
Pro-inflammatory

334
Q

What is the function of tumour necrosis factor-α (TNF-α)?

Pro/anti-inflammatory?

A

Induces fever
Neutrophil chemotaxis
Pro-inflammatory

335
Q

What is the function of interferon-γ?

Pro/anti-inflammatory?

A

Activates macrophages + NK cells

Pro-inflammatory

336
Q

What phenotype of macrophage does IL-4 promote?

A

Promotes M2 phenotype macrophages and therefore aids in wound healing

337
Q

What happens when IL-4 is released from T cells?

A

Positive feedback loop when released from T cells so Th2 is favoured and Th1 is suppressed

338
Q

What is IL-8 also known as?

A

CXCL9 and an angiogenesis promoter

339
Q

What are interferons?

A

Cytokines released by the body in response to viral infections and neoplasia

340
Q

What interferons bind to type 1 receptors?

A

IFN-alpha (all WBC) and IFN-beta (fibroblasts)

341
Q

What interferons bind to type 2 receptors?

A

IFN-gamma (NK and Th)

342
Q

Give some examples of immune based therapies.

A

Monoclonal antibodies
Immunosuppressive drugs
Cytokines and anticytokines
Intravenous immunoglobulin

343
Q

What is the mechanism of monoclonal antibodies as a therapy?

A

Very targeted. Do not carry antigenic segments. Designed to either deplete certain cell populations or functionally downregulate a population

344
Q

Give some examples of immunosuppressive drugs.

A

Glucocorticoids
Ciclosporin, tacrolimus and rapamycin
Purine analogues (most important is azathioprine)
Alkylating agents e.g. cyclophosphamide

345
Q

What is the mechanism of cytokines and anticytokines as therapies?

A

Either activate or block cytokine receptors to achieve immunomodulatory effects e.g. pegylated interferon

346
Q

What is the mechanism of intravenous immunoglobulin?

A

Replacing IgG in patients with immunodeficiencies. Can also be used in certain inflammatory conditions

347
Q

Give an example of monoclonal antibody therapy.

A

Anti-TNF therapy

348
Q

What is anti-TNF therapy used to treat?

A

Autoinflammatory conditions e.g. Crohn’s disease - Infliximab is a chimeric mAb used in CD often in acute infusions. Adalimumab is a humanised mAb that is a subcut injection that is patient administered and can be preferred when encouraging patient autonomy.

349
Q

Give some examples of glucocorticoids.

A

Hydrocortisone, prednisone

350
Q

What do glucocorticoids do when given as an immune based therapy?

A

They downregulate the monocyte production of IL-1 and TNF-alpha. They block the T-cell production of IL-2 and IFN-gamma and therefore humoral immunity. They also reduce the activation and migration of innate and adaptive cells in general

351
Q

What do ciclosporin, tacrolimus and rapamycin do when given as immune based therapies?

A

Are all calcineurin inhibits and inhibit Ca2+ dependent second messenger signals in T cells following TCR activation. This makes them potent T cell inhibitors

352
Q

What are purine analogues used for?

A

IBD and organ rejection

353
Q

What do purine analogues do when given as immune based therapies?

A

They incorporate into DNA resulting in chain termination. They are a potent antiproliferative in dividing adaptive immune cells

354
Q

What do alkylating agents do when given as immune based therapies?

A

Interfere with DNA synthesis and induce immunosuppression

355
Q

What do cytokines and anticytokines do when given as immune based therapies?

A

Cytokines are pleotropic and regulate the immune system so are attractive targets for therapy e.g. anakinra and pegylated interferon

356
Q

What does anakinra do?

A

IL-1 receptor antagonist which is beneficial in type 2 DM

357
Q

What does pegylated interferon do?

A

Used in chronic hepatitis C infection

358
Q

What is IV immunoglobulin?

A

A preparation of poly specific IgG pooled from a large number of healthy donors (>20k)

359
Q

What is IV immunoglobulin used for?

A

Patients with primary or secondary immunodeficiencies e.g. selective IgA deficiency
Recommended for a small number of other diseases such as immune-mediated thrombocytopenia, and Kawasaki’s

360
Q

What are the possible mechanisms of IV immunoglobulins?

A

Fc receptor blockade to prevent phagocytosis, inhibition of autoantibody synthesis, inhibition of complement activation, induction of T cell regulation

361
Q

What is complement?

A

An acute phase protein that are synthesised by the liver and circulate in an inactive form

362
Q

How is complement activated?

A

Complement proteins are cleaved by convertases into two components e.g. C3 becomes C3a and C3b

363
Q

What are complement components ending in ‘a’ involved in?

A

Inflammation and chemotaxis

364
Q

What are complement components ending in ‘b’ involved in?

A

Opsonisation of pathogens - the membrane attack complex inserts itself into pathogen membranes and causes lysis

365
Q

What do all complement pathways converge to?

A

Activate C3 convertase

366
Q

What is the complement classical pathway?

A

Initiated by antigen-antibody complexes (IgM/IgG) which bind complement and activate the cascade

367
Q

What is the complement alternative pathway?

A

The alternative pathway is activated when C3b (which is free and abundant in plasma) binds pathogens surfaces directly e.g. in G-ve bacteria

368
Q

What does the complement protein C3 do?

A

C3 has the ability to auto hydrolyse into C3a and C3b where C3b then goes on to activate the cascade

369
Q

What is the mannose binding lectin (MBL) pathway?

A

MBL binds mannose on pathogens’ surface. Mannose is not present on human cells. This activates MASP proteins (serine proteases) and cleave C2 and C4

370
Q

What markers are found on haematopoietic stem cells?

371
Q

What markers are found on helper T cells?

A

CD4, TCR, CD3, CD28

372
Q

What markers are found on cytotoxic T cells?

A

CD8, TCR, CD3, CD28

373
Q

What markers are found on regulatory T cells?

A

CD4, CD25, TCR, CD3, CD28

374
Q

What markers are found on B cells?

A

CD19, CD20, CD40, MHC II, B7

375
Q

What markers are found on macrophages?

A

CD14, CD40, MHC II, B7

376
Q

What markers are found on NK cells?

A

CD16, CD56

377
Q

What are CD1 molecules?

A

MHC molecule that presents lipid molecules

378
Q

What are CD2 molecules?

A

CD2Found on thymocytes, T cells, and some natural killer cells that acts as a ligand for CD58 and CD59 and is involved in signal transduction and cell adhesion

379
Q

What are CD3 molecules?

A

The signalling component of the T cell receptor (TCR) complex

380
Q

What are CD4 molecules?

A

Found on helper T cells. Co-receptor for MHC class II Used by HIV to enter T cells

381
Q

What are CD5 molecules?

A

Found in the majority of mantle cell lymphomas

382
Q

What are CD8 molecules?

A

Found on cytotoxic T cells. Co-receptor for MHC class I Found on a subset of myeloid dendritic cells

383
Q

What are CD14 molecules?

A

Cell surface marker for macrophages

384
Q

What are CD15 molecules?

A

Expressed on Reed-Sternberg cells (along with CD30)

385
Q

What are CD16 molecules?

A

Bind to the Fc portion of IgG antibodies

386
Q

What are CD21 molecules?

A

Receptor for Epstein-Barr virus

387
Q

What are CD28 molecules?

A

Interacts with B7 on antigen presenting cell as costimulation signal

388
Q

What are CD45 molecules?

A

Protein tyrosine phosphatase present on all leucocytes

389
Q

What are CD56 molecules?

A

Unique marker for natural killer cells

390
Q

What are CD95 molecules?

A

Acts as the FAS receptor, involved in apoptosis

391
Q

What is passive immunisation?

A

Transfer of performed antibodies to the circulation can be natural or artificial

392
Q

When does natural passive immunity occur?

A

This occurs naturally by the transfer of maternal antibodies across the placenta to the developing foetus

393
Q

What does natural passive immunity provide protection against?

A
  • Diptheria
  • Tetanus
  • Streptococcus
  • Rubella
  • Mumps
  • Polio virus
394
Q

When is artificial passive immunity used?

A
  • Those with agammaglobulinaemias - essentially B cell defects, these are
    treated with pooled normal human IgG
  • Exposure to a disease that could cause complications - like an
    immunocompromised patient who is exposed to measles for example
  • When there is no time for active immunisation to give protection i.e. a
    pathogen with a short incubation time e.g. rabies
395
Q

For what diseases is passive immunisation used?

A

Botulism, tetanus, diphtheria - given anti-toxin

Hepatitis, measles, rabies - used prophylactically to reduce the chance of establishing infection after exposure

396
Q

What are the drawbacks of passive immunisation?

A
  • Does not activate immunological memory
  • No long term protection
  • Possibility of reaction to antisera (due to the fact its non-self so if used second time will be immune to it itself and could result in anaphylaxis)
397
Q

What is active immunisation?

A
  • The production of high affinity protective antibodies against the immunogen
  • Protection that is produced by an individuals own immune system and is usually long- lasting
398
Q

What is the goal of active immunisation?

A

The goal of immunisation is to achieve initial exposure without the risks of an actual infection

399
Q

What are the aims of a perfect vaccine?

A
  • To achieve long term protection (ideally from a small number of
    immunisations)
  • To stimulate both B cells and T cells
  • To induce MEMORY B cells and T cells
  • To stimulate protective high affinity IgG production (IgA too if possible (can migrate through mucosal barriers useful some pathogens infect primarily through mucous membranes))
  • The importance the memory B cell response depends on the nature of the pathogen
400
Q

What happens in active immunisation?

A

The first stage of any immunisation is to engage the INNATE IMMUNE SYSTEM:
• Elicit ‘danger’ signals that activate the immune system - triggers such as pathogen-associated molecular patterns (PAMPs) to engage the toll- like receptors on T cells
• Activate specialist antigen presenting cells - e.g follicular dendritic cells
• Lastly engage the ADAPTIVE IMMUNE SYSTEM - generate memory T and B cells and active T helper cells

401
Q

Which diseases use a live attenuated (not harmful) pathogen as a vaccine?

A

Tuberculosis:

  • Bacilus Calmette-Guerin (BCG)
  • Polio Sabin:
  • Polio virus grown on monkey kidney epithelial cells
  • Typhoid
  • Mumps
402
Q

What are the advantages of live attenuated vaccines?

A
  • Attenuated pathogens sets up a transient infection
  • Activation of full natural immune response
  • Prolonged contact with the immune system
  • Stimulation of a memory response in the T and B cell compartments
  • Often only a single immunisation is required - advantages in the third world
403
Q

What are the disadvantages of live attenuated vaccines?

A
  • Immunocompromised patients may become infected as a result of immunisation
  • Complications:
  • In live measles vaccine occasionally the attenuated
    organism can revert to its virulent form
  • Refrigeration and transport:
  • Typically live organisms need to be refrigerated for stable storage
  • Can be a issue in remote areas of the world
404
Q

Which diseases use a killed, inactivated pathogen as a vaccine?

A
  • Anthrax
  • Cholera
  • Hepatits A
405
Q

What are the advantages of killed, inactivated pathogens as vaccines?

A
  • No risk of infection

- Storage is less critical

406
Q

What are the disadvantages of killed, inactivated pathogens as vaccines?

A
  • Tend to just activate the humoral response
  • Lack of T cell involvement
  • Without transient infection the immune response can be quite weak
  • Repeated booster vaccines required - patient compliance can be an issue
407
Q

Which diseases use toxoids (inactivated exotoxins) as a vaccine?

A

Diptheria:
- This toxin is an inhibitor of translation resulting in necrosis of the heart and liver
Tetanus:
- Neurotoxin resulting in uncontrolled contraction of
voluntary muscles

408
Q

What are the advantages of toxoid vaccines?

A
  • Theoretically safer than handling live or inactivated pathogens
  • No risk of infection
  • Easier to store and preserve
409
Q

What are the disadvantages of toxoid vaccines?

A
  • Immune response is less powerful than to live attenuated vaccines
  • Repeat vaccinations required and adjuvants
410
Q

What are adjuvants?

A
  • Any substance that is added to a vaccine to stimulate the immune system
  • Ensures a powerful immune response
411
Q

What can be used as an adjuvant?

A
  • Whole killed organisms - trigger the immune system and send out ‘danger signals’
  • Toxoids - trigger the immune system and send out ‘danger signals’
  • Proteins
  • Chemicals:
  • Aluminium salts (extend the half life of immunogen in the site of the injection, resulting in a depot effect - the slow release of vaccine)
  • Paraffin oil
412
Q

What do DNA vaccines do?

A
  • Aim to transiently express genes from pathogens in host cells
  • Generates immune response similar to natural infection leading to T and B cell memory responses
413
Q

What are the advantages of DNA vaccines?

A
  • DNA vaccines do not require complex storage

- Delivery can be simple and adaptable to widespread programs - no refrigeration is necessary

414
Q

What are the disadvantages of DNA vaccines?

A
  • As with ‘killed’ vaccines and subunit vaccines there is no transient infection
  • DNA vaccination is likely to produce a mild immune response and will require subsequent boosting
415
Q

What is the aim of recombinant vector vaccines?

A

Aim is to imitate the effect of transient infection with pathogen but using a non-pathogenic organism

416
Q

How are recombinant vector vaccines used?

A

Genes for major pathogen antigens are introduced into a non- pathogenic or attenuated microorganism and introduced into the host

417
Q

What microbes do recombinant vector vaccines use?

A

Can be viral (e.g. attenuate poliovirus) or bacterial (e.g. attenuated strains of salmonella)

418
Q

What are the advantages of recombinant vector vaccines?

A
  • Produce immunological memory

- Safe - relative to live attenuated pathogen

419
Q

What are the disadvantages of recombinant vector vaccines?

A
  • Requires refrigeration for transport

- Immune response to virus in subject can negate effectiveness

420
Q

What does complement do when activated?

A
  • Lyse microbes directly (Membrane Attack Complex - when a group of complement proteins make a hole in a pathogen which causes an inrushing of fluids that results in lysis and thus the destruction of the pathogen)
  • Increase chemotaxis (C3a & C5a)
  • Enhance inflammation
  • Induce opsonisation (C3b) - process by which an antigen becomes coated with substances (i.e. complement) that make it more easily engulfed by phagocytic cells since macrophages have special receptors for specific complement proteins
421
Q

What is the purpose of the complement pathway?

A

The major purpose of the complement pathway is to remove or destroy antigen, either by direct lysis or by opsonisation

422
Q

What is an epitope?

A

The part of the antigen that binds to the antibody/receptor binding site

423
Q

What is affinity in terms of antibodies?

A

A measure of binding strength between an epitope and an antibody binding site - the higher the affinity the better

424
Q

What are cytokines?

A

Soluble proteins secreted by lymphocytes or macrophages/monocytes that act as stimulatory or inhibitory signals between cells

425
Q

What is MHC I glycoprotein?

A
  • Intracellular i.e virus
  • Found on the surface of virtually all cells of the body except erythrocytes
  • Cytotoxic T cells (CD8) require an antigen to be associated with class I MHC proteins before they kill the cell containing the intracellular pathogen
426
Q

What is MHC II glycoprotein?

A
  • Extracellular i.e. phagocytosis
  • Found mainly on the surface of macrophages, B cells & dendritic cells (i.e antigen presenting cells)
  • Helper T cells (CD4) require class II MHC proteins before they help B cells to make antibodies to the extracellular pathogen
427
Q

What is atopy?

A

Inherited tendency for overproduction of IgE antibodies to common environmental antigens

428
Q

What is immunodeficiency?

A

Deficiency in the immune response, can either be acquired (HIV) or inherited (defects in T cell function)

Phase 2a (25 decks)

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