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BioMed S2 > 15. Immune System > Flashcards

15. Immune System Flashcards

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1
Q

What is the immune system?

A

A versatile defence system that protects us from pathogenic microbes

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2
Q

What are the layers of the defence strategy?

A
  1. First line - innate immunity (barrier)
  2. Second line - innate immunity (response)
  3. Third line - specific/adaptive immunity
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3
Q

What is the first line of defence - innate immunity?

A

Physical barrier created by the skin and mucous membranes*

and associated secreted chemicals

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4
Q

What is the second line of defence - innate immunity?

A

Non-specific immune response that includes some immune cells, proteins, fever and inflammation

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5
Q

What is the third line of defence - specific/adaptive immunity?

A

Activated by the innate immune system, producing a response towards a specific pathogen

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6
Q

What is a pathogen?

A

An infectious agent that can cause disease in a host

Microbes
Macro-organisms (e.g parasitic worms)

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7
Q

How can pathogens enter the body?

A 
Breaks in the skin
Respiratory system
Digestive system
Reproductive system (male and female)
Eyes
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8
Q

What is an antigen*?

ANTIbody GENerator

A

A substance that can be recognised by leukocytes

Antigens can stimulate an immune response to defend the body

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9
Q

What are the two types of antigen?

A
  1. Foreign antigens
  2. Self-antigens*

The immune system is usually tolerant of self-antigens,

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10
Q

What are foreign antigens?

A

Microbes
Food
Drugs

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11
Q

What are self-antigens?

A

Found on cell membranes
Transmembrane protein, produced by the cell*

*via DNA transcription, translation

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12
Q

What do antigens usually consist of?

A

Proteins (specific 3D shape)

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13
Q

What are antibodies?

A

Proteins produced in response to a specific antigen

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14
Q

What do antibodies and the specific antigens do?

A

Combine, creating an ‘immune response’

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15
Q

What makes the skin a first line of defence against pathogens?

A

Made up of layers of tightly packed epithelial cells

Outer epidermis - consists of dead epithelial cells are constantly being shed to remove microbes

Dermis - contains accessory structures such as sebaceous glands and sweat glands

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16
Q

How does sweat perform an immune function?

A

Removes microbes from skin
Contains IgA antibodies*

Immunoglobulin A : also in salivia, tears and breastmilk

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17
Q

How does sebum perform an immune function?

A

Contains fatty acids which inhibit microbial growth

*stop mitosis in bacteria

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18
Q

Where can mucous membranes be found?

A
  • Digestive tract
  • Respiratory tract
  • Urogenital tract
  • Conjunctiva
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19
Q

What is the function of mucous membranes?

A

Prevent entry of pathogens into the membrane

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20
Q

How do the mucous membranes perform an immune function?

A

Mucous traps microbes and foreign particles
Saliva, tears and mucous secretions wash away the trapped microbes
They also contain anti-microbial substances

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21
Q

How does the immune function work in the respiratory tract?

A

Mucocillary escalator

Cilia propel any foreign substances towards the pharynx where they are swallowed or coughed up

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22
Q

How do tears and saliva perform an immune function?

A

Contain IgA and lysozymes

Lysozymes are enzymes that break down bacterial cell walls

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23
Q

How does the nose perform an immune function?

A

Hairs in the nose filter air

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24
Q

How does the vagina perform an immune function?

A

In menstruating women, vagina is acidic making it unfavourable for microbes

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25
Q

How does gastric acid perform an immune function?

A

Acidity destroys many bacteria

pH 2-3

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26
Q

How do microflora perform an immune function?

A

Outcompete pathogens for
* attachment sites on epithelial cell surfaces (esp in large intestine*)
* essential nutrients

*Proximity to GALT aids learning for lymphocytes

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27
Q

How does the excretion of urine and faeces perform an immune function?

A

Both expel microbes

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28
Q

How does vomiting and diarrhoea perform an immune function?

A

Both rapid means of expelling pathogens

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29
Q

When does the second line of defence get activated?

A

When pathogens penetrate the physical and chemical barriers of the skin and mucous membranes

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30
Q

What does the second line of defence consist of?

A 
Transferrins
Complement system
Phagocytes
Natural killer cells
Inflammation
Cytokines
Fever
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31
Q

What are transferrins?

A

Iron-binding proteins in blood*

In haemoglobin

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32
Q

How do transferrins work?

A

Inhibit the growth of certain bacteria by reducing the amount of available iron

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33
Q

Why are transferrins necessary?

A

Without transferrins, bacteria would use the iron available for their growth

Bacteria love iron. Supplements should be avoided during infection

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34
Q

What is the complement system?

A

Secondary defence system
Over 30 proteins*
Circulating in the blood in their inactive (full) form

* produced by the liver

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35
Q

How are complement proteins identified?

A

By a letter (mostly C) and a number e.g. C3

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36
Q

How does a complement protein start out?

A

Inactive
Become active when split by enzymes into active fragments
e.g. C3&raquo_space;> C3a and C3b

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37
Q

What happens when a complement protein is activated

A

Acts in a cascade

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38
Q

What is the most common mechanism through which complement proteins are activated?

A

Classical pathway

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39
Q

What is the ‘classical pathway’?

A

Antigens and antibodies join together
>Forming an antigen-antibody complex
»This triggers the immune response (cascade)

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40
Q

What is the role of complement proteins?

A
  1. Promoting phagocytosis
  2. Contributing to inflammation
  3. Causing cytolysis
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41
Q

How do complement proteins promote phagocytosis?

A

The fragment C3b coats a microbe in a process called opsonisation
This promotes the attachment of a phagocyte to a microbe

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42
Q

How do complement proteins contribute to inflammation?

A

C3a and C5a bind to mast cells and cause them to release histamine

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43
Q

How do complement proteins cause cytolysis?

A

The final 5 complement proteins join together and create a hole in the foreign cell
The hole fills with tissue fluid and makes the cell swell and rupture

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44
Q

What are cytokines?

A

Small protein hormones that stimulate or inhibit normal cell functions
Mediate the connection between the innate immune system and the adaptive immune system

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45
Q

What are cytokines secreted by?

A

Leukocytes

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46
Q

What are the types of cytokines?

A

Interleukins
Interferons
Tumour necrosis factor

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47
Q

cytokines

What are interleukins?

A

Mostly produced by T-helper cells
Mediators between leukocytes

e.g IL-1 released by macrophages > hypothal > inc in temp

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48
Q

cytokines

What are interferons?

A

Anti-viral proteins produced by cells that are infected by a virus

Tell surrounding cells to stop dividing (viruses do not self-replicate)

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49
Q

cytokines

What does tumour necrosis factor do?

A

Promotes the accumulation of neutrophils and macrophages to an area
Causes cell death

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50
Q

cytokines

How do interferons work?

A

They diffuse to uninfected neighbouring cells and induce synthesis of anti-viral proteins that interfere with viral replication

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51
Q

cytokines

Do interferons stop a virus attaching to it?

A

No but they prevent the virus from replicating

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52
Q

What do phagocytes do?

A

They perform phagocytosis - cell digestion - of anything they don’t recognise*

Non-selective

*Any cell with a foreign antigen

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53
Q

How do phagocytes work?

A

By engulfing and digesting cells
Using their lysozymes to break down the pathogen
It then displays a piece of the pathogen on its membrane

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54
Q

What is chemotaxis?

A

Directed migration* of a cell in response to a chemical stimulus

*to a site of inflammation

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55
Q

What are the two major types of phagocyte?

A

Neutrophils
Macrophages

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56
Q

What do neutrophils do?

A

First to migrate to a scene of inflammation
Like neighbourhood watch
Try to mop up the day to day problems

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57
Q

What do macrophages do?

A

They follow the neutrophils and eat up the remnants of whatever needs to be broken down and digested

They engulf and digest the pathogen, excrete some of the waste and display the rest on the cell membrane to present to T-lymphocytes

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58
Q

Where can macrophages be found?

A

In tissue

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59
Q

Where can monocytes be found?

A

In blood

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60
Q

What do monocytes do?

A

Migrate to the site of infection and enlarge to form wandering macrophages

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61
Q

What do fixed macrophages do?

A

Stand guard in specific tissues

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62
Q

In which tissues can fixed macrophages be found?

A

Histiocytes (connective tissue macrophages)
Kupffer cells - liver
Microglia - nervous tissue
Alveolar - lungs
Langerhans cells - skin
Tissue macrophages - spleen, bone marrow, lymph nodes

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63
Q

What are the stages of phagocytosis?

A
  1. Chemotaxis - release of chemicals by leukocytes, damaged tissue and activated complement that attract phagocytes
  2. Adherence - attachment of phagocyte to target (aided by complement)*
  3. Ingestion - cell membrane extends to engulf the microbe
  4. Digestion - ingested structure merges with lysozymes to be digested
  5. Excretion - ingested material is excreted

*Some bacteria (eg TB) resistant to adherence - therefore phagocytosis

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64
Q

What are natural killer cells?

A

Non-specific lymphocytes

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65
Q

What percentage of lymphocytes do natural killer cells make up?

A

5-10%

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66
Q

Where can natural killer cells be found?

A

Blood
Lymph nodes
Spleen
Bone marrow

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67
Q

How do natural killer cells work?

A

They attack anything that they don’t recognise including abnormal body cells e.g. cancerous cells*

They bind to a target cell and release granules containing the protein perforin

Cancerous cells display abnormal surface antigens on their membranes

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68
Q

What does perforin do?

A

It inserts into the cell membrane and creates a channel for tissue fluid to flow into the cell - cytolysis

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69
Q

What is inflammation?

A

A non-specific defensive response to tissue damage

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70
Q

What can inflammation be caused by?

A
  • Pathogens (infection)
  • Abrasions
  • Chemicals
  • Cell distortion/disturbance
  • Extreme temperatures

Importantly, the response to different insults is the same

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71
Q

What response does inflammation create?

A

Non-specific, systemic response
Acts as an alarm attracting immune cells to the area

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72
Q

What are the 5 cardinal signs of inflammation?

A 
Redness
Heat
Pain
Swelling
Loss of function
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73
Q

Second line of defence: Non-specific immune reactions

What are the stages of inflammation?

A
  1. Vasodilation and increased permeability
  2. Migration of phagocytes
  3. Tissue repair
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74
Q

Second line of defence: Non-specific immune reactions

How does vasodilation help inflammation?

A

Allows additional blood, oxygen, nutrients, immune cells and repair substances to get to the area quicker

Quicker removal of toxins and dead cells

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75
Q

Second line of defence: Non-specific immune reactions

How does increased permeability help inflammation?

A

Permits the movement of immune cells, defensive proteins (antibodies) and clotting factors into the tissue

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76
Q

Second line of defence: Non-specific immune reactions

What is created by vasodilation and increased permeability ?

A

Redness, swelling and heat

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77
Q

Second line of defence: Non-specific immune reactions

What is the pain of inflammation a result of?

A

Injury to neurons and toxic chemicals released by microbes

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78
Q

Second line of defence: Non-specific immune reactions

What happens when phagocytes migrate to an area?

A
  1. Phagocytes migrate to the scene (via chemotaxis)
  2. Neutrophils stick to the endothelium during vasodilation and squeeze through the vessel wall to reach the damaged area
  3. Monocytes quickly follow and transform into wandering macrophages
  4. Dead phagocytes accumulate pus
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79
Q

Second line of defence: Non-specific immune reactions

What are the types of inflammatory mediators?

A

Histamine
Leukotrienes
Kinins
Prostaglandins

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80
Q

Second line of defence: Non-specific immune reactions

What is histamine and its function?

A

Released by mast cells and basophils
Causes vasodilation and increased permeability

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81
Q

Second line of defence: Non-specific immune reactions

What are leukotrienes and their function?

A

Released by basophils and mast cells
They attract phagocytes and increase permeability

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82
Q

Second line of defence: Non-specific immune reactions

What are kinins and their function?

A

Proteins
Causes vasodilation and increased permeability
Also attract phagocytes and induce pain

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83
Q

Second line of defence: Non-specific immune reactions

What are prostaglandins and their function?

A

Lipids released by damaged cells
Enhance effects of histamine and kinins (intensifying the pain)

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84
Q

Second line of defence: Non-specific immune reactions

What are the benefits of inflammation?

A

Promotes phagocytosis through increased temperature
Promotes immune response via vasodilation/permeability
Dilutes toxins
Fibrin formation - isolates affected area and helps bind wound edges

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85
Q

Second line of defence: Non-specific immune reactions

What are the harmful effects of inflammation?

A

Swelling - dangerous if in cranium
Pain - can become chronic
Adhesions and scar tissue
Atherosclerosis

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86
Q

Second line of defence: Non-specific immune reactions

What are the outcomes of inflammation?

A

Resolution
Chronic inflammation
Granuloma
Fibrosis

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87
Q

Second line of defence: Non-specific immune reactions

What is chronic inflammation?

A

If the injury-causing agent persists
Can cause chronic pain
Prevalence of macrophages, plasma cells and lymphocytes

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88
Q

Second line of defence: Non-specific immune reactions

What is granuloma?

A

Cellular attempt to contain a foreign body through aggregation of macrophages surrounded by lymphocytes

eg TB is resistant to phagocytosis

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89
Q

Second line of defence: Non-specific immune reactions

What is fibrosis?

A

Replacement of functional tissue with non-functional scar tissue
Formed by the secretion of collagen by fibroblasts
Occurs as a result of chronic inflammation

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90
Q

Second line of defence: Non-specific immune reactions

What is a fever?

A

An abnormally high body temperature, creating unfavourable environment for pathogens

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91
Q

Second line of defence: Non-specific immune reactions

How does a fever occur?

A

Because the hypothalamus thermostat is reset to a higher temperature

Allowing body core temperature to rise

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92
Q

Second line of defence: Non-specific immune reactions

When is a fever most likely to occur?

A

In infection and inflammation

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93
Q

Second line of defence: Non-specific immune reactions

What happens pathophysiologically during a fever?

A

Bacterial toxins elevate body temperature which triggers release of fever-causing cytokines
e.g. interleukin-1from macrophages

94
Q

Second line of defence: Non-specific immune reactions

What is the key function of interleukin-1?

A

To induce fever
By signalling to the hypothalamus to raise body temperature

95
Q

Second line of defence: Non-specific immune reactions

What does an elevated body temperature do?

A
  • Makes interferons more effective
  • Inhibits growth of some microbes
  • Speeds up the reactions that aid repair
96
Q

Second line of defence: Non-specific immune reactions

What can be granular or agranular?

A

Leukocytes

97
Q

Second line of defence: Non-specific immune reactions

Which leukocytes are classed as granular?

A

Basophils (mast cells)
Eosinophils
Neutrophils

98
Q

Second line of defence: Non-specific immune reactions

Where can you find basophils?

99
Q

Second line of defence: Non-specific immune reactions

Where can you find mast cells?

100
Q

Second line of defence: Non-specific immune reactions

What do basophils and mast cells do?

A

Release histamine and heparin
Release leukotrienes
Express receptors for IgE*

Involved in allergy/hypersensitivity

101
Q

Second line of defence: Non-specific immune reactions

What does histamine do?

A

Causes vasodilation
Increases vessel permeability

102
Q

Second line of defence: Non-specific immune reactions

What does heparin do?

A

Anti-coagulant
Involved in inflammations

103
Q

Second line of defence: Non-specific immune reactions

What do eosinophils do?

A

Destroy parasitic worms via phagocytosis
Play a role in inflammation (central in asthma)

104
Q

Second line of defence: Non-specific immune reactions

What do neutrophils do?

A

Phagocytic cell
Granules release lysozymes that digest debris

105
Q

Second line of defence: Non-specific immune reactions

Which is the most abundant leukocyte?

A

Neutrophils (60%)

106
Q

Which leukocytes are classed as agranular?

A

Monocytes/macrophages
Natural killer cells
B and T lymphocytes

107
Q

Second line of defence: Non-specific immune reactions

Where can you find monocytes?

108
Q

Second line of defence: Non-specific immune reactions

Where can you find macrophages?

A

In tissue
Can be wandering or fixed

109
Q

Second line of defence: Non-specific immune reactions

What do monocytes/macrophages do?

A

Phagocytic
Secrete cytokines e.g. IL-1 and TNF

110
Q

Second line of defence: Non-specific immune reactions

What do natural killer cells do?

A

Target foreign cells
Secrete perforin to induce cytolysis

111
Q

Third line of defense: Specific immunity

What are B and T lymphocytes?

Lymphocytes live in the lymph (formed in the red blood marrow)

A

Effector cells of the adaptive (specific) immunity

112
Q

Second line of defence: Non-specific immune reactions

Which leukocytes are phagocytic?

A

Neutrophils
Monocytes/macrophages

113
Q

Third line of defense: Specific immunity

Name the different types of T-lymphocytes*

T-lymphocytes mature in the Thymus

A

Cytotoxic T-cells (CD8)
Helper T-cells (CD4)
Memory T-cells (only created after active exposure)
Regulatory T-cells (to stop excessive reactions)

114
Q

Third line of defense: Specific immunity

What do helper T-cells do?

A

Mediates the immune response

115
Q

Third line of defense: Specific immunity

What do cytotoxic T-cells do?

A

Immune cells out in the field

116
Q

Third line of defense: Specific immunity

What do memory T-cells do?

A

Create a memory of a pathogen after they’ve been exposed to it

117
Q

Third line of defense: Specific immunity

What do regulatory T-cells do?

A

Turn off the immune response when it’s finished to avoid excessive reactions

118
Q

Third line of defense: Specific immunity

Where are T-cells produced/mature?

A

Produced in bone marrow
Mature in the thymus

119
Q

Third line of defense: Specific immunity

Name the different types of B-lymphocytes

A

Plasma cells
Memory B-cells

120
Q

Third line of defense: Specific immunity

Where are B-cells produced/mature?

A

In red bone marrow

121
Q

Third line of defense: Specific immunity

Where do T-cells and B-cells function?

A

In the 3rd line of defence
Adaptive (specific) immunity

122
Q

Third line of defense: Specific immunity

How do T-cells and B-cells know how to respond to foreign antigens?

A

Through learning
They usually can tell the difference between self and non-self antigens

123
Q

Third line of defense: Specific immunity

Which sort of pathogens do T-cells and B-cells go after?

A

Specific ones

124
Q

Third line of defense: Specific immunity

How do T-cells and B-cells know which antigens they’ve met before?

A

Through immune memory

125
Q

Third line of defense: Specific immunity

What does immune memory allow T-cells and B-cells to do?

A

Produce a quicker and more effective attack next time they encounter the pathogen

126
Q

Third line of defense: Specific immunity

When is the 3rd line of defence activated?

A

When the 1st and 2nd lines fail to destroy the pathogen

Otherwise they are resting

127
Q

Major Histocompatibility Complexes

What are major histocompatibility complexes (MHC)?

A

Group of proteins on cell surface that are used by the immune system to recognise cells that are self cells vs non-self

128
Q

Major Histocompatibility Complexes

What are MHCs formed from?

A

4 polypeptide chains

129
Q

Major Histocompatibility Complexes

How do MHCs work?

A

They display a protein (a self-antigen) produced by the cell on its binding groove

130
Q

Major Histocompatibility Complexes

How do MHCs help T-cells?

A

By presenting foreign antigens to T-cells

131
Q

Major Histocompatibility Complexes

Name the two types of MHC

A
  1. Class I Major Histocompatibility Complex (MHC-I)
  2. Class II Major Histocompatibility Complex (MHC-II)
132
Q

Major Histocompatibility Complexes

Where can you find MHC-I?

A

On all body cells except erythrocytes

133
Q

Major Histocompatibility Complexes

How do MHC-I work?

A

Essentially our self-antigen.

When body cell is cancerous or invaded by pathogen, the cell starts to produce abnormal proteins

These proteins are combined with MHC-I and displayed on the cell membrane

Flags up to (mostly) cytotoxic T-cells (CD8) as a non-self antigen

134
Q

Major Histocompatibility Complexes

Where can you find MHC-II?

A

Only on the cell membrane of ‘antigen presenting cells’:
* macrophages
* B-lymphocyte

135
Q

Major Histocompatibility Complexes

How do MHC-II work?

A

The MHC-II displays the foreign antigen on its binding groove, having ingested the foreign cell

136
Q

Major Histocompatibility Complexes

What are MHC-II specifically used for?

A

Communication between themselves and T-helper cells
They present the antigen to the T-helper cells as part of antigen presentation

137
Q

Major Histocompatibility Complexes

How does an antigen become associated with MHC-I or II

A

By the route it’s trafficked through the cell

138
Q

Which type of immunity do T-cells play a central part in?

A

Cell-mediated immunity

139
Q

What is unique about T-cells?

A

Each has a unique T-cell receptor (TCR) that only recognises a specific antigen

140
Q

What are T-helper cells also known as?

A

CD4 cells

because they express the CD4 protein on their surface

141
Q

What are cytotoxic T-cells also known as?

142
Q

To function properly, which traits should T-cells have?

A

Self-recognition - to recognise self antigens
Self-tolerance - must lack reactivity to fragments of self antigens

143
Q

What does a lack of self-tolerance lead to?

A

Autoimmunity

144
Q

How are T-cells tested?

A

Against epithelial cells in thymus
Should be able to recognise self antigens

145
Q

What happens to T-cells if they don’t recognise self antigens?

A

They undergo apoptosis

146
Q

What percentage of T-cells make it through the maturing process?

147
Q

What is adaptive immunity?

A

Ability of the body to defend itself against specific foreign cells

148
Q

What is adaptive immunity characterised by?

A

Specificity for particular foreign antigens
Production of immune memory

~~~

```

149
Q

What are the two types of adaptive immunity?

A
  1. Cell-mediated
  2. Antibody-mediated
150
Q

What is cell-mediated immunity?

A

Driven by T-cells
Cytotoxic T-cells directly attack specific invading antigens
Mostly against intracellular pathogens

151
Q

What is antibody-mediated immunity?

A

Driven by B-cells
B-cells transform into plasma cells, which synthesise and secrete specific antibodies (Igs)
Mostly against extracellular pathogens

152
Q

What happens during antigen presentation?

A
  1. Antigen presenting cells break down the antigen into fragments (using lysozymes)
  2. Some fragments are combined with MHC-II molecules on their cell membrane
  3. They migrate into lymphatic tissue where they present the antigen to T-helper cells
  4. Antigen fragment binds with the T-helper cell
  5. T-helper cell secretes a cytokine called interleukin-2 (IL-2)
  6. Interleukin-2 causes the T-helper cell to undergo clonal selection
153
Q

What happens during clonal selection of T-cells?

A

Division and proliferation of activated T-cells

154
Q

What does the process of T-cell clonal selection produce?

A
  1. Cytotoxic T-cells that bind to target cell and destroy it using granzymes and perforin
  2. Memory T-cells - these are inactive but will recognise the antigen in the future if it appears again
  3. Helper T-cells that release cytokines which increase the activity of immune cells such as T, B and NK cells
155
Q

What do granzymes do during T-cell clonal selection?

A

Break down the foreign cell

156
Q

What does perforin do during T-cell clonal selection?

A

Burst the foreign cell

157
Q

Why are regulatory T-cells important?

A

Without them the body would continue to fight off a disease that no longer exists and could end up fighting its own cells
Maintain immunity homeostasis
Implicated in autoimmune diseases

158
Q

Antibody mediated immunity

What happens during antibody mediated immunity?

A
  1. Antigen binds to specific B-cell receptors
  2. It’s taken into the cell and broken down into fragments
  3. Fragments are expressed on the MHC-II
  4. Helper T-cells recognise the antigen complex on the B-cell membrane and stimulate it by releasing IL-2 which triggers B-cell clonal selection
159
Q

Antibody mediated immunity

What types of cell does B-cell clonal selection produce?

A

Plasma cells - secrete antibodies into blood, short lived
Memory B-cells - remain inactive until next immune reaction, long lived

160
Q

Antibody mediated immunity

Which group of glycoproteins do antibodies belong to?

A

Globulins/immunoglobulins

161
Q

Antibody mediated immunity

How are antibodies structured?

A

4 polypeptide chains - 2 heavy, 2 light
Variable region for each type of antibody
2 antigen binding sites

162
Q

Antibody mediated immunity

What do antibodies combine with?

A

The antigen that triggered their production

163
Q

Antibody mediated immunity

What does the combining of an antibody with an antigen produce?

A

Antibody-antigen immune complex

164
Q

Antibody mediated immunity

How to antibodies inactivate antigens?

A
  1. Neutralising
  2. Immobilising
  3. Agglutinating and precipitating
  4. Activating complement
  5. Enhancing phagocytosis
165
Q

Antibody mediated immunity

What happens when antibodies neutralise an antigen?

A

Neutralises bacterial toxins or prevent viral attachment to cells

166
Q

Antibody mediated immunity

What happens when antibodies immobilise an antigen?

A

Binds to it on bacterial cilia or flagellae

167
Q

Antibody mediated immunity

What happens when antibodies agglutinate and precipitate an antigen?

A

Antibodies use both of their binding sites to cause a clumping of cells

168
Q

Antibody mediated immunity

What happens an antibody activates complement?

A

Antigen-antibody complexes activate the complement cascade

169
Q

What happens when antibodies enhance phagocytosis?

A

Antibody acts as a flag to attract phagocytes and aids phagocytosis via agglutination and complement

170
Q

What are the 4 different types of antibodies?

A

IgG
IgA
IgM
IgE

171
Q

IgG - location, how common, function?

A

Blood, lymph, intestines
Most abundant (80%) of blood antibodies
Protects against viruses and bacteria
Crosses placental barrier

172
Q

IgA - location, how common, function?

A

Sweat, tears, saliva, breast milk
10% of blood antibodies
Localised protection of mucous membranes
Decreases with stress

173
Q

IgM - location, how common, function?

A

Blood, lymph
10% of blood antibodies
Early immune response (first on site)

174
Q

IgE - location, how common, function?

A

Blood
0.1% blood antibodies
Allergic reactions
Binds to mast cells (to release histamine and heparin)

175
Q

What happens during the primary response of immunological memory?

A

Slow response
Antibodies start to appear after several days
Slow rise in IgM, followed by IgG

176
Q

What happens during the secondary response of immunological memory?

A

Faster response as a full immune response has been developed in the memory cells
Usually so quick, the pathogen is killed off before any signs and symptoms present

177
Q

How do vaccinations help the immune system?

A

By creating immunological memory against the specific disease the vaccination covers

178
Q

What do vaccinations contain?

A

Weakened, whole or partially-killed portions of microbes

179
Q

What happens after a vaccination is given?

A

B and T-cells are activated in a primary response
Can take several days

180
Q

In what 4 ways can you acquire immunity?

A
  1. Naturally acquired active immunity
  2. Naturally acquired passive immunity
  3. Artificially acquired active immunity
  4. Artificially acquired passive immunity

Passive because body is not generating antibodies

181
Q

What is naturally acquired active immunity?

A

Natural exposure to a disease

182
Q

What is naturally acquired passive immunity?

A

Transfer of IgG antibodies across the placenta from mother to child
Transfer of IgA antibodies from mother to child via breast milk

Passive because body is not generating antibodies

183
Q

What is artificially acquired active immunity?

A

Vaccination

184
Q

What is artificially acquired passive immunity?

A

Injection with immunoglobulins e.g. snake anti-venom

Passive because body is not generating antibodies

185
Q

What cells can be found in GALT?

A

Macrophages
B and T-cells

186
Q

Where can GALT be found?

A

Tonsils
Oesophagus
Small intestine
Large intestine

187
Q

What is a hypersensitivity reaction?

A

An excessive immune response produced by the normal immune system

188
Q

What are the 4 types of hypersensitivity?

A

Type I, II and III - antibody mediated
Type IV - cell mediated*

T-cells

189
Q

What is Type I hypersensitivity?

A

An allergy

190
Q

What is a Type I hypersensitivity mediated by?

A

IgE antibodies that bind to mast cells
Causes
* degranulation
* histamine response

191
Q

What are the 2 types of Type I hypersensitivity reactions?

A
  1. Systemic e.g. anaphylaxis
  2. Localised e.g. hay fever, eczema, irritant contact dermatitis
192
Q

How soon is there a Type I hypersensitivity response?

A

Immediate - within minutes of exposure

193
Q

What is Type II hypersensitivity?

A

Blood transfusion reactions
Haemolytic disease of the newborn

194
Q

What is a Type II hypersensitivity mediated by?

A

IgG antibodies which bind to antigen and activate the complement system

195
Q

How soon is there a Type II hypersensitivity response?

A

Rapid onset

196
Q

What is a Type III hypersensitivity mediated by?

A

IgG
IgA
IgM antibodies

197
Q

How soon is there a Type III hypersensitivity response?

A

Within 4-8 hours

198
Q

In which pathologies does a Type III hypersensitivity reaction occur?

A

RA
Systemic lupus erythematosus (SLE)
Glomerulonephritis

199
Q

What happens in a Type III hypersensitivity reaction?

A

Antibody-antigen complexes form and deposit in capillaries, skin, kidneys, joints etc triggering an immune response
They activate the complement system

200
Q

What is a Type IV hypersensitivity mediated by?

201
Q

What happens in a Type IV hypersensitivity reaction?

A
  • Overreaction of T-cells to an antigen
  • Large numbers of cytotoxic T-cells activated
  • Cytokines released that can damage normal tissue
202
Q

How soon is there a Type IV hypersensitivity response?

A

48-72 hours

203
Q

What is an allergy?

A

A powerful immune response to an allergen

204
Q

What is an allergen?

A

An antigen that generates allergy
Usually harmless

205
Q

How does an immune response towards an allergy develop?

A
  1. Initial exposure causes sensitisation
    Slow response as not many cells have learnt how to respond yet to that antigen
  2. Subsequent exposure is a quicker and much, more exaggerated response
    The full immune response has been developed and antibodies are readily available.
206
Q

How does the body prepare for an allergen response?

A

Body produces IgE specially for that antigen:

  1. B-cell plasma cells activated
  2. Antibodies produced targeting that specific antigen
  3. Y-shape: one side binds to the antigen, the other side to the mast cell
207
Q

What are the symptoms of an allergy?

A

Mild to fatal!
Runny nose
Streaming eyes
Anaphylaxis

208
Q

What percentage of adults are affected by a food allergy?

209
Q

What percentage of children are affected by a food allergy?

210
Q

What is a food allergy?

A

An IgE-mediated immune response

IgE will be present in response to ingestion of food allergen

211
Q

How is food intolerance different to an allergy?

A

Food intolerance doesn’t have a defined immune response

However, poor digestion can lead to allergic (IgG mediated) reactions

212
Q

What is a food intolerance?

A

Symptoms triggered by eating a quantity of food and lacking the enzymes/probiotics/bile/HCI and other digestive factors needed to deal with the food

213
Q

What is missing if a person is lactose intolerant?

A

The enzyme lactase

214
Q

What is anaphylactic shock?

A

Severe, systemic, allergic response to an allergen exposure

215
Q

How soon can anaphylactic shock appear?

A

Within 5-10 mins

216
Q

What happens in the body to create anaphylactic shock?

A
  1. Exposure to allergen causes IgE to activate mast cells and basophils
  2. Systemic granulation of mast cells histamine is released
  3. Causes bronchoconstriction, vasodilation and oedema of tissue
217
Q

Why is anaphylactic shock dangerous?

A

Can cause occlusion of the airways

218
Q

What is the treatment for anaphylactic shock?

A

EpiPen (Epinephrine)

219
Q

What is the difference between acute and chronic inflammation ?

A

Acute inflammation is physiological (and beneficial)
Chronic inflammation is pathological

220
Q

Which cells produce antibodies ?

A

Plasma cells
(B-lymphocytes)

221
Q

Qualites of plasma cells

A
  • Secrete antibodies into the blood
  • Only produce one type of antibody
  • Secrete hundres of millions of antibodies each day (until cell dies)
  • Short-lived
222
Q

Qualities of Memory B-cells

A

Long-lived
Remembers the antigen for next time
Ready to proliferate and produce more plasma cells for a second immune reaction

223
Q

How long can memory cells last ?

224
Q

What separates GALT from microflora in the gut ?

A

Single epithilial cells
GALT is in the lamina propria
Provides learning environment for B and T cells

225
Q

Where can Type IV hypersenstive reactions be observed ?

A

Skin graft rejections
Allergen contact dermatitis
Multiple Sclerosis (MS)

226
Q

What causes vasodilation and increased permeability during inflammation ?

Not on slides

A

Histamine and heparin released by degranulated mast cells

227
Q

Which cell do macrophages and B-lymphocytes display antigens to ?

A

T-lymphocytes

228
Q

Which cells are antigen-presenting ?

A

Macrophages
B-lymphocytes

229
Q

What is antigen presentation ?

A

Where macrophages display a piece of a digested pathogen on its cell membrane
T-lymphocytes are then able to receive and learn about what foreign antigens are present in the body

230
Q

What is opsonisation ?

A

The process of coating a microbe with C3b in order to attach phagocytes

BioMed S2 (34 decks)

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