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Sandra Phase 2a > Immunology- Introduction to Clinical Sciences > Flashcards

Immunology- Introduction to Clinical Sciences Flashcards

1
Q

What is immunology

A

Study of the immune system
and how it has evolved to protect us from pathogens/non-self

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2
Q

What is innate immunity

A

Instinctive, non-specific, does not depend on lymphocytes, present from birth

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3
Q

What is adaptive immunity?

A

Specific ‘Acquired/learned’ immunity, requires lymphocytes, antibodies

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4
Q

What are adaptive and innate immunity made up of

A

cells and soluble factors (humoral)

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5
Q

What is serum

A

plasma without fibrinogen and other clotting factors

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6
Q

What makes up blood?

A
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7
Q

Where are leukocytes made

A

Made in the bone marrow - Haematopioesis

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8
Q

Components of the immune system

A
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9
Q

Cells of the Immune system

A

Also:

Mast cell
Natural Killer Cell
Dendritic cells:
Kupffer- liver
Langerhans-skin

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10
Q

Soluble Factors called?

A

3 types:

Complement
Antibodies
Cytokines, Chemokines

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11
Q

Modes of action for complement (C’) factors

A
  1. Direct lysis
    2.Attract more Leukocytes to the site of infection
  2. Coat invading organism
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12
Q

How are complement factors only activated by?

A

They are activated only as part of the immune response – 3 activation pathways

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13
Q

What are complement factors?

A

Group of ~20 serum proteins secreted by the liver that need to be activated to be functional

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14
Q

What do antibodies bind to?

A

specifically to Antigens (Ag)

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15
Q

Are immunoglobulin soluble?

A

Yes

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16
Q

Where can you find immunoglobulins?

A

Cell Surface (on B cells)

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17
Q

5 distinct classes of immunoglobulins?

A

IgG
IgA
IgM
IgD
IgE

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18
Q

What do antibodies act as?

A

Adapter that links microbe to a phagocyte

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19
Q

What cells secrete cytokines?

A

Immune and non-immune cells

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20
Q

Types of cytokines?

A

Interferons (IFN)
Interleukins (IL)
Colony Stimulating Factors
Tumour Necrosis Factors (TNFa & b)
Chemokines

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21
Q

What do Interferons (IFN) do?

A

induce a state of antiviral resistance in uninfected cells IFNa & b - produced by virus-infected cells
IFNg - released by activated T cells

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22
Q

Role of interleukins (IL)

A

produced by many cells, over 30 types

It can be pro-inflammatory (e.g. IL1) or anti-inflammatory (e.g. IL-10)

Can cause cells to divide, differentiate and secrete factors

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23
Q

Role of Colony-Stimulating Factors

A

Involved in directing the division and differentiation of bone marrow stem cells – precursors of leukocytes

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24
Q

What are Colony-Stimulating Factors precursors of ?

A

Leukocytes

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25
Q

Role of Tumour Necrosis Factors (TNFa & b)

A

Mediate inflammation and cytotoxic reactions

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26
Q

What are Chemokines

A

Leukocyte chemoattractants

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27
Q

Defensive mechanisms?

A

Innate (non-specific)
Adaptive (specific)

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28
Q

Innate vs Adaptive Immunity

A
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29
Q

What does innate immunity integrate with

A

adaptive response

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30
Q

Innate Immunity is composed of …

A

Physical and chemical barriers
Phagocytic cells (neutrophils and macrophages)
Blood proteins (complement, acute phase)

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31
Q

Physical barriers (exterior defences)

A
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32
Q

Interior defences (Inflammatory Response)

A

Stop bleeding (coagulation)
Acute inflammation (leukocyte recruitment)
Kill pathogens, neutralise toxins, limit pathogen spread
Clear pathogens/dead cells (phagocytosis)
The proliferation of cells to repair damage
Remove blood clot – remodel the extracellular matrix
Re-establish normal structure/function of tissue

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33
Q

How are defence mechanisms/barriers breached?

A

Tissue damage (trauma) or infection

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34
Q

Define inflammation.

A

A series of reactions that brings cells and molecules of the immune system to sites of infection or damage

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35
Q

Hallmarks of inflammation

A

Increased blood supply
Increased vascular permeability
Increased leukocyte transendothelial migration ‘extravasation

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36
Q

Types of Inflammation

A

Acute Inflammation
Chronic Inflammation

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37
Q

What is an acute inflammation

A

Complete elimination of a pathogen followed by resolution of damage, the disappearance of leukocytes and full regeneration of tissue

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38
Q

What is chronic inflammation

A

Persistent, un-resolved inflammation

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39
Q

Sensing microbes in blood consist of?

A

Monocytes
Neutrophils

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40
Q

Sensing microbes in tissue consist of?

A

Macrophages
Dendritic cells

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41
Q

What is PRR, and where are they found

A

Pattern Recognition Receptors
on cells

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42
Q

What is PRR, and where are they found

A

Pathogen-Associated Molecular Patterns
Found on microbe

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43
Q

The function of complement factors?

A

Lyse microbes directly (MAC)
Chemotaxis (C3a and C5a)
Opsonisation
(C3b)

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44
Q

Stages of phagocytosis

A
  1. Binding
  2. Engulfment
  3. Phagosome Formation
  4. Lysosome fusion digestion
  5. Membrane disruption/fusion
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45
Q

Why do we need adaptive Immunity?

A

Microbes evade innate immunity (proteases, decoy proteins, etc)
Intracellular viruses and bacteria ‘hide’ from innate immunity
Need memory to specific antigen – ‘seen it before so faster response’

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46
Q

Types of adaptive immunity?

A

Cell-Mediated - T cells - intracellular microbes
Humoral (Ab) - B cells - extracellular microbes

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47
Q

What does cell-mediated immunity interlay between?

A

Antigen Presenting Cells
T cells

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48
Q

Name antigen-presenting cells

A

Macrophages
Dendritic Cell
B cells

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49
Q

What does cell-mediated immunity require?

A

Intimate cell-to-cell contact
Major Histocompatibility Complex (MHC)
Intrinsic/Endogenous (intracellular) antigens
Extrinsic/Exogenous (extracellular) antigens

Recognise Self or Non-Self

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50
Q

Why does cell-mediated immunity require intimate cell-to-cell contact

A

– to control Ab responses via contact with B cells
– to directly recognise and kill virally infected cells

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51
Q

What do T lymphocytes respond to?

A

presented antigens

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52
Q

What is a t-cell selection?

A

T cells that recognise self are killed in the foetal thymus as they mature

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53
Q

What does the T cell Receptor (TCR) recognise

A

foreign antigens in association with Major Histocompatibility Complex (MHC)

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54
Q

MHC & T cell table

A
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55
Q

What do antibodies do?

A

Neutralise toxin by binding to it
Increase opsonisation – phagocytosis
Activate complement

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56
Q

What do stem cells produce

A

precursors (immature leukocytes)

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57
Q

Where does T-cell precursor mature

A

Thymus

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58
Q

Where does B-cell precursor mature

A

Lymph node

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59
Q

What cells give rise to cells involved in adaptive immunity

A

Lymphoid progenitor cells

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60
Q

What cells give rise to cells involved in innate immunity

A

Myeloid progenitor cell

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61
Q

1st line of defence when a pathogen invades the body?

A

Innate immune system

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62
Q

What comprises the innate immune system

A

Physical barriers and chemical and biological barriers afterwards

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63
Q

What is the role of soluble proteins?

A

Opsonisation
Forming a membrane attack complex
Enhance inflammation

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64
Q

What is opsonisation

A

A process where the complement proteins coat the outer surface of the pathogen allowing the phagocytes (macrophage) to engulf the pathogen much more easily.

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65
Q

How can opsonisation occur?

A

This is because the macrophage contains special receptors for specific complement proteins

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66
Q

What is a membrane attack complex

A

A Group of complement proteins makes a hole in the pathogen, causing an in the flush of fluids, creating a disbalance in osmolarity causing the pathogen to lyse and be destroyed

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67
Q

What organ produces complement proteins?

A

Liver

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68
Q

How do complement proteins become activated

A

Circulate the bloodstream in an inactive form until they contact the pathogen. They then become activated

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69
Q

Name the three complement pathways

A

Classical pathway
Alternate pathway
Lectin pathway

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70
Q

What complement proteins are involved in the classical pathway

A

C1q
C1r
C1s
C4
C2

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71
Q

What complement proteins are involved in the alternate pathway

A

Factors:
D
B
C3
Properdin

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72
Q

What complement proteins are involved in the lectin pathway

A

Mol/Ficolin
C4
C2
MASP2

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73
Q

What is the purpose of the three complement factor pathways

A

In splitting C3 into C3a and C3b
Essentially C3 becomes activated via cleaving

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74
Q

What is the role of complement factor C3a

A

Enhance inflammation

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75
Q

What is the role of complement factor C3b

A

Opsonisation
Lysis of cell via membrane attack complex

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76
Q

How does the classical complement protein pathway start

A

Initiated when antibodies bind to the antigen of the pathogen

Complement proteins: C1q, C1R, C1s bind to the FC portion of the antibody-forming another complement protein complex called the C4b2a protein complex

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77
Q

What is another name for C4b2a protein complex

A

C3 convertase

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78
Q

Initiation of the lectin pathway

A

Complement proteins (Ficolin) bind to oligosaccharides of a pathogen
This makes the C4b2a protein complex

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79
Q

Similarities between lectin pathway and classical pathway

A

Both create the C4b2a protein complex

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80
Q

Purpose of C3b2a protein complex

A

The C4b2a protein complex splits the C3 into C3a and C3b

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81
Q

What does the alternate pathway do?

A
  1. C3b binds to the surface of the pathogen forming C3bBb

or

  1. C3b along with properin forms C3bBb protein complex
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82
Q

What is the purpose of the alternate complement protein pathway

A

Enhances the classical and lectin pathway or vice versa

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83
Q

Purpose of C3bBb protein complex

A

Splits C3 into C3a and C3b

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84
Q

Most important complement proteins

A

C3a
C5a

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85
Q

What do C3a do?

A

C3a and C5a stimulate mast cells in producing histamine

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86
Q

Role of histamine

A

Attract leukocytes
Enhance inflammation
Increase vascular permeability

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87
Q

What does C3b do?

A

C3b thioester bonds react with the pathogen surface - allowing opsonization.

C3b can bind to the C4b2a protein complex forming the C4b2a3b complex. c4b2a3b complex activates C3 and C5. This enhances inflammation and lyses pathogen via the formation of membrane attack complex

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88
Q

What does a naive T cell express

A

CD4 and CD8 co-receptor

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89
Q

What cells are present in the germinal centre of the lymph node?

A

B cells

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90
Q

Summary of Innate immune response

A

In case of inflammation due to invasion of the pathogen, more leukocytes are recruited in the infiltrated area to phagocytose and destroy the pathogen

Activated dendritic cells migrate to the lymph node to activate T-cell

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91
Q

What leukocyte cell will be recruited in case of inflammation and why?

A

Neutrophil because its fast acting

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92
Q

What do complement factors alow

A

Complement proteins will make it easier for leukocytes to destroy pathogens.

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93
Q

How are leukocytes recruited

A

Via chemical signals

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94
Q

Role of innate immune response

A

Halt the pathogen and wait for the pathogen to be recognised by the adaptive immune cells (B and T cells)

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95
Q

In case of inflammation due to invasion of the pathogen, more leukocytes are recruited in the infiltrated area.
How is this achieved?

A

In case of inflammation due to the pathogen invasion, PAMP receptors on the pathogen are recognised by mast cells stimulating histamine release and tissue macrophages to secrete cytokines attracting more leukocytes in the infiltrated area. This allows for leukocytes, primarily neutrophils and enters the infiltrated area.

It begins phagocytosing pathogens.

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96
Q

What protein stimulates phagocytosis?

A

Complement proteins

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97
Q

What do antigen-presenting cells activate?

A

Adaptive Immune Cells

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98
Q

What do macrophages and dendritic cells make to enhance immune response.

A

Cytokines

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99
Q

Main cytokines involved in innate immune response

A

CXCL8
IL6
IL-1B
IL-12

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100
Q

Role of CXCL8 cytokine?

A

Attract more leukocytes

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101
Q

Role of IL6 cytokine?

A

Activates lymphocytes.
Stimulate liver to make more proteins for immunity

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102
Q

Role of IL-1B cytokine?

A

Increases vascular permeability

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103
Q

Role of IL-12 cytokine?

A

Activates natural killer and differentiation of CD4 naive T cell into T helper 1 cell

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104
Q

Role of TNF-α cytokine?

A

Stimulates Inflammatory response

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105
Q

Role of activated macrophages in innate immune response

A

Secretes cytokines which do the following

Liver: Secretes fibrinogen and C reactive protein
Hypothalamus: fat and muscle to increase body temp
Bone marrow epithelial: attract more neutrophils
Dendritic cells: TNF-α stimulate the migration of dendritic cells to lymph node to initiate adaptive immunity

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106
Q

Why is the dendritic cell an important connection between the innate and adaptive immune systems?

A

TNF-α stimulates the migration of dendritic cells to lymph nodes to initiate adaptive immunity.

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107
Q

How can dendritic cells move to the lymph node?

A

Via a process called licensing

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108
Q

What happens to an infected macrophage?

A

Natural Killer cells will kill an infected macrophage via apoptosis

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109
Q

What cell is regarded as the ‘professional’ antigen-presenting cell

A

dendritic cell

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110
Q

What are Haematopoietic pluripotent stem cells (haemocytoblast)

A

the stem cell that every blood cell in the body originates from

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111
Q

Role of Neutrophils in immune response

A

Plays an important role in innate immunity (phagocytosis)

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112
Q

What are the 2 main intracellular granules of neutrophils

A

o Primary lysosomes – can kill microbes by secreting toxic substances
o Secondary granules

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113
Q

Role of monocytes in immune response

A

Plays an essential role in innate AND adaptive immunity (phagocytosis and Ag presentation)

Main role – remove anything foreign (microbes) or dead

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114
Q

What does monocyte differentiate into in the tissues

A

Macrophages

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115
Q

Role of macrophages in immune response

A

Play an important role in innate and adaptive immunity (phagocytosis and Ag presentation)

The main role – remove foreign (microbes) and self (dead/tumour cells)
Most often the first line of non-self recognition
Present Ag to T-cells

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116
Q

Role of eosinophil in immune response

A

Mainly associated with parasitic infections and allergic reactions
Activates neutrophils, induces histamine release from mast cells and provokes bronchospasm

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117
Q

Lifespan of eosinophil

A

8-12 days

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118
Q

What dyes to granules stain for eosinophil?

A

Acidic dyes

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119
Q

Role of basophil

A

Mainly involved in immunity to parasitic infections and allergic reactions
Binding of IgE to receptor causes de-granulation releasing histamine – main cause of allergic reactions

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120
Q

Lifespan of basophil?

A

2 days

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121
Q

What dyes to basophilic granules stain for?

A

Basic dyes

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122
Q

What cells are basophils very similar to?

A

Mast cells

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123
Q

Where are mast cells found

A

Only in tissues (precursor in blood)

124
Q

Role of mast cells in immune response

A

Binding to IgE to receptor causes de-granulation releasing histamine – main cause of allergic reactions

125
Q

Role of T cells

A

Play a major role in adaptive immunity
Recognise peptide Ag displayed presenting cells (APC)

126
Q

Lifespan of T cells

A

hours-years

127
Q

Where are T cells found?

A

blood, lymph nodes and spleen

128
Q

4 main types of T cells

A

T helper 1 (CD4 – help immune response intracellular pathogens)
T helper 2 (CD4 – help produce antibodies extracellular pathogens)
Cytotoxic T cell (CD8 – can kill cells directly)
T regulator – regulate immune responses

129
Q

What do B cells do?

A

Play a major role in adaptive immunity
Recognise Ag displayed by antigen-presenting cells (APC)

130
Q

The lifespan of B cells

A

hours-years

131
Q

Where do B cells mature

A

Bone marrow

132
Q

What do B cells differentiate into?

A

plasma cells that make antibodies

133
Q

Where are B cells found?

A

blood, lymph nodes and spleen

134
Q

Where are natural killer cells found?

A

Spleen
Tissues

135
Q

Role of Natural Killer Cells

A

They recognise and kill by apoptosis;
o Virus-infected cells
o Tumours cells

Account for 15% of lymphocytes

136
Q

Role of IgG

A

Predominant in human serum, 70-75% of total Ig in serum
Crosses placenta

137
Q

Role of IgA

A

Accounts for 15% of Ig in serum
Predominant Ig in mucous secretions such as saliva, milk and bronchiolar secretions

138
Q

Role of IgM

A

Accounts for 10% of Ig in serum
Mainly found in blood (they’re big so they can’t cross the endothelium)
Mainly primary response, initial contact with Ag

139
Q

Role of IgD

A

Accounts for 1% of Ig in serum
A transmembrane monomeric form is present on mature B cells

140
Q

Role of IgE

A

Accounts for ~0.05% of Ig in serum
Basophils and mast cells express an IgE-specific receptor that has a high affinity for IgE – binding triggers the release of histamine
Associated with allergic response and defence against parasitic infections

141
Q

Define epitope

A

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

142
Q

Define affinity

A

measure of binding strength between an epitope and an antibody binding site. The higher the affinity the better

143
Q

Define Antigen (Ag)

A

a molecule that reacts with preformed antibody and specific receptors on T and B cells.

144
Q

Define Antibody.

A

the protein produced in response to an antigen. It can only bind with the antigen that induced its formation – i.e. specificity.

145
Q

Define Cytokines?

A

proteins secreted by immune and non-immune cells. Substances produced by one cell influence the behaviour of another, thus effecting intercellular communication.

146
Q

What are chemokines

A

Group of approx. 40 proteins that direct the movement of leukocytes from the bloodstream into the tissues or lymph organs by binding to specific receptors on cells.
They attract leukocytes to sites of infection/inflammation – like magnets.

147
Q

Anatomical barriers

A

Skin – dermis and epidermis
Sebum (skin secretions)
Intact skin – prevents penetration, prevents growth

148
Q

Mucous membranes – a physical barrier

A

Saliva
Tears – lysozyme in tears and other secretions
Low pH and commensals of the vagina
Mucous secretions
Mucous–entrapment
Cilia – beating removes microbes
Commensal colonies – attachment, nutrients

149
Q

Physiological barrier

A

Temperature – chickens have high body temperatures and are Anthrax resistant
Fever response inhibits micro-organism growth
pH
Gastric acidity – neonate stomach is less acidic than an adult, so susceptible to infection

150
Q

What happens when a naive t cell recognises a self-antigen

A

The naive T cell will be destroyed before it matures because we don’t want a T cell attacking our own body

151
Q

How does a CD8 T cell become activated

A

When an infected antigen-presenting cell, such as a phagocyte, presents a foreign antigen on MHC class 1 to the naive CD8 T cell.
The activated CD8 T cell then becomes a cytotoxic T cell.

152
Q

What do cytotoxic cells do?

A

Destroy infected cells with the same specific antigen as was presented by the infected phagocyte

153
Q

How does a CD4 T cell become activated

A

When a non-infected antigen-presenting cell, such as a phagocyte presents a foreign antigen on an MHC class 2 to the naive CD4 T cell

The activated CD4 T cell becomes a T-helper cell

154
Q

What is the purpose of a T helper cell

A

Enhance the immune response by activating B cells, macrophages, natural killer cells and other phagocytes

155
Q

How does a naive B cell become activated

A

Naive B cells can recognise a specific antigen of a pathogen, causing the naive B cell to engulf the pathogen, process and present foreign antigen on MHC class 2 to the activated T helper cell

156
Q

Relationship between T-helper cell and B cell

A

The activated T-helper cell can activate B cell to proliferate, and differentiate into either a memory B cell or a plasma cell

157
Q

What do plasma cells secrete

A

specific antibodies towards that antigen memory B cells for the memory of that specific antigen, so the next infection can be resolved quickly

158
Q

Role of antibodies

A

Neutralise a pathogen: antibodies prevent bacterial adhesion
Opsonisation: antibodies promote phagocytosis
Complement activation: antibodies activate complement -> opsonisation causes lysis of pathogen

159
Q

How do B and T cells recognise specific antigens

A

B -cells have specific antibodies on the surface of their cell membrane that only binds to a specific antigen

160
Q

What gives antibodies diversity to bind to different antigens

A

Antibody consists of:
Variable region on the N terminal
Constant agent on the C terminal

The constant agent determines what class of antibody this is
The variable region can be composed of diff types of amino acid sequences giving it its uniqueness

161
Q

When does adaptive immunity take place?

A

Microbes evade innate immunity
Intracellular viruses and bacteria hide from innate immunity

162
Q

Types of adaptive immunity

A

Cell-mediated – T cells – intracellular microbes
Humoral (Ab) – B cells – extracellular microbes

163
Q

What does the Major histocompatibility complex (MHC) display

A

Peptide from self OR non-self proteins (e.g. degraded microbial proteins) on the cell surface – invasion alert

164
Q

Different types of MHC

A

MHC I – glycoproteins on all nucleated cells
MHC II – glycoproteins only on APC
MHC III – code for secreted proteins

165
Q

Intrinsic (intracellular) & MHC

A

class I (all cells) – Tc (CD8) – kill infected cell with intracellular pathogen

166
Q

Extrinsic (extracellular) & MHC

A

class II (APC only) – Th (CD4) – help B cell make Ab to extracellular pathogen

167
Q

What does cell-mediated immunity interlay between

A

-Antigen-presenting cells (APC)
Macrophages
Dendritic cells
B cells

-T cells

168
Q

What is required for cell-mediated immunity

A
  • Requires intimate cell-to-cell contact
    Control Ab responses via contact with B cells
    Directly recognise and kill virally infected cells.
  • Major histocompatibility complex (MHC)
  • Intrinsic (endogenous) antigens
  • Extrinsic (exogenous) antigens
  • Recognise self or non-self
169
Q

What do T cells only respond to?

A

to intracellular presented antigens

170
Q

When do B cells become activated

A

upon binding with an antigen

171
Q

Where does the clonal expansion of B cells take place

A

go to the lymph nodes where clonal expansion takes place with the cells differentiating into plasma cells

172
Q

What do plasma cells secrete

A

Ab (usually IgM), which later turns into IgG

173
Q

What happens with clonal expansion with B cells

A

B cells divide – clonal expansion and differentiate into plasma cells and memory B cells.

174
Q

What leads to a secondary response?

A

Re-stimulation of memory B cells

175
Q

What does a T cell receptor contain, and what does this allow?

A

Can bind to a specific epitope of an antigen as it has both a variable and constant region

176
Q

How does a T cell become activated

A

Infected phagocyte presents epitope of antigen to naive T cell on either MHC I or MHC II.

177
Q

What does hypersensitivity refer to?

A

abnormal reactions of the immune system against certain antigens

178
Q

Causative factors for hypersensitivity

A

Self-reactivity of immune cells
Effectors/Regulators’ Imbalance

179
Q

What occurs in Type 1 hypersensitivity

A

Previous exposure to the antigen results in the production of antibody IgE
IgE molecules bind to the receptors on the surface of mast cells and basophils
Upon re-exposure to the same antigen, it causes mast cell degranulation and the release of pharmacologically active substances such as histamine

180
Q

What is required for a type 1 hypersensitivity allergic reaction to take place?

A

Prior exposure to the antigen

181
Q

Signs of type 1 hypersensitivity allergic reaction?

A

Immediate response:

Smooth muscle spasms and inflammation

182
Q

Examples of type 1 hypersensitivity allergic reaction

A

Anaphylaxis
Allergies:
-food
-drugs
-pollen
Allergic bronchial asthma

183
Q

How does a Type II hypersensitivity allergic reaction take place?

A

Previously formed IgG or IgM antibodies bind to the surface of a particular cell type.
Antibody marking marks the cell for destruction, with cytotoxic cells killing cells by complement system or phagocytosis

184
Q

Examples of Type II hypersensitivity allergic reaction?

A

Autoimmune diseases (immune thrombocytopenia, autoimmune neutropenia, myasthenia gravis)

185
Q

How does a Type III hypersensitivity allergic reaction take place?

A

Mediated by IgG or IgM
The antibodies bind to free-floating antigens forming antibody-antigen complexes.
The complement system is activated, and inflammation causes damage to the affected tissue

186
Q

Examples of Type III hypersensitivity allergic reaction

A

Serum sickness
Arthus reaction

187
Q

What is a Type IV hypersensitivity allergic reaction

A

Delayed (after a day) reaction mediated by T cells

188
Q

How does a Type IV hypersensitivity allergic reaction happen

A

Pre-sensitised T cells are produced during the previous contact with the antigen.
Upon exposure to the same antigen, T helper cells release inflammatory cytokines while T killers induce cytotoxic reactions

189
Q

Examples of Type IV hypersensitivity allergic reaction

A

Contact dermatitis
TB skin test

190
Q

Name the three different vaccines used.

A

whole killed
toxoids
live attenuated

191
Q

Define Passive immunity

A

Passive immunity is short-term immunity which results from the introduction of antibodies from another person or animal

192
Q

Advantages of Passive Immunity

A
  • Gives immediate protection
  • Effective in immunocompromised patients
193
Q

Disadvantages of Passive Immunity

A
  • Short-lived
  • Possible transfer of pathogens
194
Q

Define vaccines

A

antigenic substance prepared from the causative agent of a disease

195
Q

What is active immunisation

A
  • Non-living vaccines (whole killed and toxoids)
  • Live attenuated vaccines
196
Q

What are non-living vaccines, and how does it work?

A

Whole killed vaccines
These vaccines do not cause infection, but the antigens contained in them induce an immune response which protects against infection.

197
Q

Limitations to non-living vaccines

A
  • The organisms must be grown to high titre in vitro
  • Whole pathogens often cause excessive reactogenicity
  • usually need at least two vaccinations
198
Q

What are toxoids vaccines?

A

Non-living vaccines can also be cell-free toxoids (inactivated toxins).

199
Q

What are Live attenuated vaccines

A

The organisms replicate within the host, and induce an immune response which is protective against the wild-type organism

200
Q

Advantages of Live attenuated vaccines

A
  • Lower doses are required, so the scale of in vitro growth needed is lower
  • Immune response more closely mimics that following real infection
  • Route of administration may be more favourable
  • Fewer doses may be required
201
Q

Limitations to live attenuated vaccines

A
  • Often impossible to balance attenuation and immunogenicity
  • Reversion to virulence
  • Transmissibility
  • Live vaccines may not be so attenuated in immunocompromised
202
Q

Which pathogens lack vaccines?

A
  • HIV
  • Malaria
  • Herpes simplex virus
203
Q

Why do some pathogens lack vaccines

A
  • Pathogen is too hard to grow
  • Killed pathogen not protective
  • Impossible to obtain attenuated and suitably immunogenic strain
204
Q

Novel approaches to vaccines?

A
  • Recombinant proteins
  • Synthetic peptides
  • Live attenuated vectors
  • DNA vaccines
205
Q

Stages of vaccination

A
  1. Engage the innate immune system
  2. Danger signals that activate the immune system triggers such as molecular fingerprints of infection – PAMPs (pathogen-associated molecular patterns)
  3. Engage TLR receptors
  4. Activate specialist APC
  5. Engage the adaptive immune system
    a. Generate memory T and B cells
    b. Activate T cell help
206
Q

What does PAMP stand for?

A

Pathogen Associated Molecular Pattern

207
Q

Where is PAMP found?

A

On pathogens such as viruses and bacteria.
Not normally found inside the body

208
Q

Examples of PAMP

A

Lipopolysaccharides (LPS)
Lipoproteins
Peptidoglycans

209
Q

What organisms can you find PAMP?

A

Pathogenic and non-pathogenic organisms

210
Q

What are PAMP essential for?

A

The survival of all pathogens

211
Q

What is the receptor for PAMP referred to as?

A

PRR (Pattern Recognition Receptor)

212
Q

Where can PRRs be found?

A
  1. Secreted and circulating PRRs
  2. Cell-associated PRRs (more traditional receptors)
213
Q

What do PRRs trigger?

A

Innate Immune Response and inflammatory response

214
Q

What is the role of PRRs

A

Optimise the pathogen
Activate the complement protein
Phagocytise the pathogen
Activate the inflammatory mediators
Secrete: Interferons, cytokines, pro-inflammatory cytokines
Induce apoptosis

215
Q

What is Secreted and circulating PRRs

A
  • Antimicrobial peptides secreted in lining fluids from epithelia
  • Lectins and collectins (carbohydrate-containing proteins that bind carbohydrates or lipids in microbe walls
216
Q

What does secreted and circulating PRRs do?

A

Activate complement
Improve phagocytosis

217
Q

What are the main family of Cell associated PRRs

A

Toll-Like Receptors (TLR)

218
Q

What do Cell-associated PRRs recognise

A

broad range of molecular patterns

219
Q

What does the recognition of microbes and viruses depend on

A

seeing ancient, conserved features of them

220
Q

Role of pattern recognition

A

pathogen responses
homeostasis
damage recognition

221
Q

Why do families of receptors in pattern recognition exist?

A

to detect these in fluids, cell surfaces and compartments, and intracellularly

222
Q

Pattern recognition and homeostasis

A
  • Blood neutrophil numbers may be dependent upon TLR4 signalling, independent of LPS (lipopolysaccharide) in homeostasis
  • Induction of endotoxin tolerance in the new born gut
  • Maturation of the normal immune system
223
Q

What are TLRs adapted to recognise

A

range of endogenous damage molecules, which may share characteristics of hydrophobicity

224
Q

What does TLR signalling by cellular damage products activate

A

immunity to initiate tissue repair and perhaps enhance local antimicrobial signalling

225
Q

What is PRRs involvement with disease

A
  • Recognition of host molecules in autoimmune disease
  • Failure to recognise pathogens or increased inflammatory responses
226
Q

What is the recognition of molecular patterns key to

A

survival and successful establishment of commensal microbiome

227
Q

Pattern recognition receptors are highly conserved systems of …

A

immunity, evolved to recognise unchanging patterns

228
Q

What TLR form dimer when peptidoglycan, lipoproteins, zymosan e.t.c are detected

A

TLR 1 & TLR 2
TLR 2 & TLR 6

229
Q

What does TLR 4 recognise

A

Lipopolysaccharides of Gram +

230
Q

What does TLR 5 recognise

A

Flagella

231
Q

What TLRs are found within endosomes?

A

TLR 3,6,7,9

232
Q

How is TLR 3 activated

A

Once it comes into contact with double-stranded RNA (virus)

233
Q

How are TLR 7 & 8 activated?

A

Once it comes into contact with single-stranded RNA viruses

234
Q

How is TLR 9 activated

A

Once it comes into contact with the CPG DNA of bacteria or fungi

235
Q

What happens once TLRs become activated?

A

Initiate a cascade of events -> leading to the activation of certain transcription factors. These transcription factors then become translated to do the following:

-Make proteins for cell signalling
-Make interferons
-Make proinflammatory cytokines

236
Q

The immune system is non-specific, meaning it doesn’t differentiate between pathogens

A

Innate

237
Q

The innate immune system responds (faster/slower) ________ than the adaptive immune system.

A

Faster

238
Q

Immunologic memory is a feature of the (adaptive/innate) immune system.

A

Adaptive

239
Q

Clonal deletion is when most of the clonally expanded cells of the immune system die off after the infection is over.

A

Adaptive

240
Q

The ________ develop into cells of the innate immune system like neutrophils, eosinophils, basophils, mast cells, dendritic cells, macrophages, and monocytes.

A

myeloid progenitor cells

241
Q

of the innate immune system destroy pathogens using cytoplasmic granules or oxidative burst.

A

Neutrophils

242
Q

Monocytes migrate into tissues and differentiate into
____ which remain in tissues and aren’t found in the blood

A

Macrophages

243
Q

cells destroy pathogens and break up its proteins into short amino acid chains to present to T-helper cells.

A

Dendritic cells

244
Q

cells are large lymphocytes that target cells infected with viruses and cancer cells.

A

Natural Killer

245
Q

Antibodies are produced by lymphocytes.

A

B

246
Q

CD8 T cells only kill the body’s own cells that present antigens on ____- molecule on the cells surface.

A

MHC type I

247
Q

Cytokines promote (3 processes) of immune cells.

A

activation, proliferation, and differentiation

248
Q

___ is a cytokine secreted by CD4+ T helper cells that promotes the proliferation of all lymphocytes.

A

IL-2

249
Q

IL-1beta, IL-6, and TNF-alpha are cytokines that travel to the liver and promote the production of proteins like C-reactive protein and complement proteins.

A

Acute phase

250
Q

______ are cytokines numbered in the order they were identified.

A

Interleukins

251
Q

are cytokines in charge of activating endothelial cells, increasing vascular permeability, and helping to induce fever

A

Interferons

252
Q

______- is an inhibitory cytokine that helps CD4+ T cells develop into a regulatory cell that can slow down or stop the overall immune response.

A

TGF-beta

253
Q

What are the major cell type of the immune system

A

Phagocytes

254
Q

How does opsonisation occur

A

via the binding of soluble proteins to microbial surfaces so that they can be recognized later by phagocytes.

255
Q

What is damage-associated molecular patterns.

A

The components of dying cells that are recognized by pattern recognition receptors on phagocytes

256
Q

What prtoein is expressed on cell types that transmit the signal to inhibit phagocytosis.

A

CD47

257
Q

What are TLR

A

family of pattern recognition receptors that have dimers of chains with extracellular leucine-rich domains that bind to microbes.

they interact with extracellular ligands on the microbes’ plasma membrane.

258
Q

Type I interferons are typically produced by (virus/bacteria) ____-infected cells.

A

virus

259
Q

Three of the major proinflammatory cytokines released in response to pattern recognition receptor activation are

A

interleukin-1, interleukin-6, and tumor necrosis factor-α.

260
Q

What chemokine serves as a chemoattractant for neutrophils in the early stages of infection.

A

IL-8

261
Q

What does complement refer to?

A

collection of serum proteins that connects the innate and adaptive immune systems.

262
Q

What enzyme component cleaves the complement components C3 and C5 respectively.

A

C3 and C5 convertases

263
Q

What is a T cell ?

A

type of lymphocyte involved in paracortex hyperplasia of a lymph node.

264
Q

What is the most abundant lymphocyte in a normal person.

A

T cell

265
Q

What is the T cell that MHC 1 binds to?

A

CD8+ T cell

266
Q

What is the T cell that MHC 2 binds to?

A

CD4+ T cell

267
Q

What is a CD4+ T cell?

A

type of T cell that functions to produce cytokines that activate other cells of the immune system.

268
Q

What is a CD8+ T cell?

A

type of T cell that functions to kill virus-infected cells directly

269
Q

What are TH1 cells?

A

class of lymphocytes that proliferate during a type IV hypersensitivity reaction.

270
Q

What is a regulatory T cell?

A

type of T cell that functions to maintain specific immune tolerance through the suppression of CD4+ and CD8+ T cell effector function.

271
Q

How to Regulatory T cells differentiate from other T cells

A

Through cytokine activity TGF beta are involved in the down-regulation of effector T cells.

272
Q

What induces the differentiation of T cells to TH1 cells

A

Interleukin-12, released from macrophages

273
Q

two immunoglobulin isotypes expressed on the surface of mature, naive B cells

A

IgM and IgD

We B naive MD’s

274
Q

Which type of inflammation is characterized by the presence of lymphocytes and plasma cells in tissue?

A

Chronic

Remember, acute = neutrophils

275
Q

Which immune cell is associated with a clock-face distribution of chromatin?

A

Plasma cells

276
Q

What cell surface marker is associated with helper T cell

A

CD4

277
Q

The first immunoglobulin made in response to an infection is

A

IgM

278
Q

There are 5 major types of heavy chains which encode the classes of immunoglobulins.

A

IgM, IgD, IgG, IgA, and IgE

GAMED

279
Q

Whihc antibody is the most numerous antibodies in the serum and their main role is to serve as opsonins

A

IgG

280
Q

___ antibodies can be found in large quantities in breast milk.

A

IgA

281
Q

What do IgD antibodies do?

A

found on mature B-cells and serve as a signal that they are ready to leave the bone marrow.

282
Q

The only class of antibody that does not need T-cells to be produced is

A

IgM

283
Q

___ antibodies form the antigen receptors on B-cells

A

IgM

284
Q

What do vaccines induce?

A

active long-term immunity

285
Q

What are adjuvants

A

The substances that are added to vaccines to enhance the response

286
Q

What vaccines have the advantage of inducing both humoral and cell-mediated immunity

A

Live

287
Q

What is immunisation?

A

The process of evoking a long-lived immune response against a particular pathogen

288
Q

Vaccination (does/does not) ____ ensure immunity

A

does not

289
Q

What is a vaccine

A

form of a pathogen that is intentionally introduced to an individual without causing disease.

290
Q

Maternal IgG crossing the placenta is known as (passive/active) _______ immunity.

A

passive

291
Q

What is antiserum

A

substance consisting of preformed antibodies that is injected into a patient to confer passive immunity.

292
Q

Toxin or venom exposure warrants the use of (active/passive) ______ immunization.

A

passive

293
Q

Does passive immunisation activate the host’s own immune system

A

No

294
Q

What are two ways that confer active immunity

A

vaccine and natural infection

295
Q

Define herd immunity

A

The phenomenon known as herd immunity protects individuals who were not adequately protected from a vaccine in the past.

296
Q

What is the prime target location for vaccines

A

Mucosal surface

297
Q

Are Inactivated vaccines are more/less safe than live attenuated vaccines.

A

More

298
Q

What vaccine means that there is a lack of pathogenicity

A

attenuated vaccine

299
Q

How can Attenuated live vaccines be generated

A

by growing a pathogenic bacterium or virus in abnormal culture conditions for a long period.

300
Q

Inactivated vaccines elicit a (weaker/stronger) immune response than live attenuated vaccines.

A

weaker

301
Q

Attenuated live vaccines typically require

A

one immunization(s)

302
Q

Adjuvants have improved

A

humoral immunity

303
Q

What is alum

A

adjuvant used in human vaccines that enhances the TH2 responses more than TH1.

304
Q

What do DNA vaccines utilise

A

plasmid DNA that encode for particular antigenic proteins

305
Q

Inactivated vaccines are (more/less) effective at inducing cell-mediated immunity because they do not replicate in the host.

A

Less

Sandra Phase 2a (17 decks)

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