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MBChB Year 3 > Week 0 - Immune Intro > Flashcards

Week 0 - Immune Intro Flashcards

1
Q

What are the 2 soluble factors in the innate immunity?

A
  1. Antibacterial factors

2. Complement system

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2
Q

What is the cellular factor of the innate immunity?

A

Scavenger Phagocytes

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3
Q

What is a lysozyme?

A

Enzyme present at mucosal surfaces that breaks down the gram positive cell wall

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4
Q

What does lactoferrin do (protein found at mucosal surfaces)?

A
  • Chelates iron & reduces soluble iron in the GI/respiratory tract
  • Inhibits growth of bacteria
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5
Q

What are the 3 pathways in the complement system of innate immunity?

A
  1. Classical Pathway
  2. MB-Lectin Pathway
  3. Alternative Pathway
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6
Q

Describe the classical pathway of the complement system?

A

Antigen : Antibody complexes

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7
Q

Describe the MB-Lectin Pathway of the complement system?

A

Lectin binding to pathogen surfaces

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8
Q

Describe the Alternative pathway of the complement system?

A

Activated through pathogen surfaces

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9
Q

What 3 things does complement activation do?

A
  1. Recruit inflammatory cells
  2. Opsonization of pathogens
  3. Killing of pathogens
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10
Q

What does MB-Lectin stand for?

A

Mannose-binding lectin

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11
Q

What are the 2 key roles of macrophages?

A
  1. Clearance of micro-organisms

2. Summon help (releasing cytokines)

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12
Q

What is the difference between monocytes and macrophages?

A
  • Monocyte= blood

- Macrophages= tissue

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13
Q

Describe phagocytosis?

A
  • Specialises in destruction of pathogens

- Removes harmless debris

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14
Q

Describe antigen presentation?

A

Processes engulfed particles, travels to draining lymph nodes & presents to T cells in MHC II

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15
Q

What 3 things are pattern recognition receptors able to do?

A
  1. Recognise molecules found in micro-organisms
  2. Recognise extracellular & intracellular threats
  3. Respond to bacteria, fungi and yeasts
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16
Q

Why is the immune system not enough at times?

A
  1. Highly pathogenic bacteria

2. Structural failure

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17
Q

What % of neutrophils are in white blood cells?

A

50-70%

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18
Q

Neutrophils provide a _____ response to infection?

A

Rapid

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19
Q

What are the 4 factors of neutrophils?

A
  1. Chemotaxis
  2. Phagocytic
  3. Degranulation
  4. Die locally
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20
Q

Describe neutrophil chemotaxis?

A

Migrate towards bacterial products (LPS), chemokines & “danger signals” (complement components)

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21
Q

Describe neutrophil phagocytosis?

A

Ingest & destroy pathogens using proteases, reactive oxygen species, lysozyme etc.

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22
Q

Describe neutrophil degranulation?

A

Release toxic granules extracellularly

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23
Q

Describe how neutrophils die locally?

A

By producing characteristic pus

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24
Q

Eosinophils have a pathological role in _____?

A

Allergy

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25
Q

What are the 3 factors of eosinophils?

A
  1. Chemotaxis
  2. Degranulation
  3. Cytokine production
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26
Q

Describe eosinophil degranulation?

A

Release toxic substances onto surface of parasites e.g. Major Basic Protein, Eosinophil Cationic Protein, Eosinophil Peroxidase

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27
Q

What does eosinophils classically respond to?

A

Parasites

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28
Q

What is the difference between basophils and mast cells?

A
  • Basophils= blood

- Mast cells= tissues

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29
Q

What are basophils/mast cells important in?

A

Allergy

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30
Q

What are the 2 factors of Basophils/Mast cells?

A
  1. Degranulation

2. Cytokine release

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31
Q

Describe Basophil/Mast cell degranulation?

A

Rapid release pre-formed granules containing cytokines & mediators

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32
Q

What is the typical reaction caused by basophils/mast cell degranulation?

A

Histamine Wheal & Flare reaction

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33
Q

What are the 3 factors of dendritic cells?

A
  1. Phagocytosis
  2. Migration
  3. Antigen presentation
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34
Q

Describe dendritic cell phagocytosis?

A
  • Not specialised in destruction of pathogens

- Functions mainly as antigen presenting cells

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35
Q

Describe dendritic cell migration?

A
  • In tissues constantly sampling environment

- When activated will travel to draining lymph nodes

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36
Q

Describe dendritic cell antigen presentation?

A

Presents to CD4 T cells & can initiate an adaptive immune response

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37
Q

What are the 2 types of adaptive immunity?

A
  1. Humoral

2. Cellular

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38
Q

What is the humoral adaptive immunity mediated by?

A

B cells

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39
Q

What does the B cells do in humoral adaptive immunity?

A

Release antibodies (immunoglobulins) which targets extracellular pathogens ie. bacteria

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40
Q

What 2 things mediate the cellular adaptive immunity?

A
  1. CD4 T cells

2. CD8 T cells

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41
Q

What do the CD4 T cells in the cellular adaptive immunity do?

A
  • Directs B cells & CD8 T cells

- Cytokine secretion

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42
Q

What are CD4 T cells also known as?

A

“Helper” T cells

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43
Q

What are DC8 T cells also known as?

A

“Killer” or “Cytotoxic” T cells

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44
Q

Describe the 2 regions on an antibody?

A
  • Fab region: antigen binding

- Fc region: binds to Fc receptors on phagocytes & activates complement

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45
Q

What are the 3 functions of antibodies?

A
  1. Opsonise for phagocytosis
  2. Activate complement for lysis
  3. Neutralise toxins & pathogen binding sites
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46
Q

Describe IgM?

A
  • Main antibody of primary immune response
  • Low affinity
  • Activates Complement
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47
Q

Describe IgG?

A
  • Main antibody of secondary immune response
  • Higher affinity as part of secondary response
  • Activates Complement, binds Fcg receptor on phagocytes (opsonsises)
  • Crosses placenta
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48
Q

Describe IgA?

A
  • Present in secretions & lines epithelial surfaces

- Neutralises by blocking binding of pathogens

49
Q

Describe IgE?

A
  • High affinity binding to Mast cells through Fc receptor

- Role in allergy

50
Q

The antibody isotopes differ in ______?

A

Fc regions

51
Q

Describe the primary B cell response?

A
  • 5-10 days
  • Smaller peak
  • IgM>IgG
52
Q

Describe the secondary B cell response?

A
  • 1-3 days
  • Larger peak
  • Increase in IgG & sometimes IgA / IgE
53
Q

List the 5 things that T cells can encourage in the immune system response?

A
  1. Clonal expansion of specific B cells
  2. Progression to antibody secreting cells (plasma cells)
  3. Progression to memory B cells
  4. Isotype switching to IgG, IgA & IgE
  5. Affinity Maturation
54
Q

Where are B cells developed?

A

Bone marrow

55
Q

How do B cells die?

A

If B cell receptor binds strongly to “self” antigen in bone marrow it dies by apoptosis

56
Q

Where are T cells developed?

A

Bone marrow and migrate to thymus

57
Q

How do T cells die?

A

If T cell receptor binds strongly to “self” antigen in thymus it dies by apoptosis

58
Q

T cells only see antigen in context of ____?

59
Q

Describe Class I MHC?

A
  • Presents to CD8 T Cells
  • Found on all nucleated cells
  • Presents intra-cellular antigen
60
Q

Describe Class II MHC?

A
  • Presents to CD4 T Cells
  • Presents extra-cellular derived antigen (phagocytosed)
  • Found on Antigen Presenting Cells
61
Q

List 3 antigen presenting cells?

A
  1. Dendritic cells
  2. Macrophages
  3. B cells
62
Q

What are the 2 primary organs of the adaptive immune system?

A
  1. Thymus

2. Bone marrow

63
Q

What are the 3 secondary organs of the adaptive immune system?

A
  1. Lymph nodes
  2. Spleen
  3. Mucosal Associated Lymphoid Tissue of GI Tract (MALT) & Bronchial Tract (BALT)
64
Q

What is the function of the spleen?

A

Filters blood of senescent cells &

blood borne pathogens

65
Q

List the 4 functions of the adaptive immune system?

A
  1. Provides specific antibodies to innate immune system, enhancing pathogen clearance
  2. Provides cytokines to innate immune system to upregulate activity
  3. Finishes off clearing pathogens
  4. Develops memory to prevent future infection
66
Q

List the 5 immune cells in the secondary immune response?

A
  1. Memory B cells
  2. Memory T cells
  3. Memory lymphocytes
  4. Preformed antigen specific IgA
  5. Preformed high affinity IgG
67
Q

Describe the role of memory lymphocytes in the secondary immune response?

A

Have lower threshold for activation & actively patrol sites of previous pathogen entry

68
Q

What happens to B cells in an immune response?

A

Enters lymphoid follicle to form germinal centre & undergo affinity maturation

69
Q

What is the classification framework called for the adaptive immune system?

A

Coombes and Gell Classification

70
Q

Describe type I hypersensitivity response?

A
  • Immediate, atopic
  • IgE mediated bound to mast cells
  • Increase in severity with repeated challenge
71
Q

Describe type II hypersensitivity response?

A
  • Cytotoxic, antibody dependent
  • IgM or IgG bound to cell/matrix antigen
  • Uncommon cause of allergy
72
Q

Describe type III hypersensitivity response?

A
  • Immune complex
  • IgM or IgG bound to soluble antigen
  • Aggregate in small blood vessels
73
Q

Describe type IV hypersensitivity response?

A
  • Mediated by action of lymphocytes infiltrating area

- T cells (CD4+ & CD8+)

74
Q

What is type I hypersensitivity responsible for?

A

Most allergies

75
Q

List the 6 stages of type I hypersensitivity/ an allergic response?

A
  1. Sensitisation
  2. Mast cells primed with IgE
  3. Re-exposure to antigen
  4. Antigen binds to IgE associated with mast cells
  5. Mast cells degranulate
  6. Pro-imflammatory process stimulates and amplifies future responses
76
Q

List 6 things that mast cells release when degranulating in an allergic response?

A
  1. Toxins (i.e. histamine)
  2. Tryptase
  3. Pro-inflammatory cytokines
  4. Chemokines
  5. Prostaglandins
  6. Leukotrienes
77
Q

What 2 things does the early phase tissue effects in type I hypersensitivity result in?

A
  1. Smooth muscle contraction

2. Increased vascular permeability

78
Q

What 2 things does the late phase tissue effects in type I hypersensitive result in?

A
  1. Sustained smooth muscle contraction/ hypertrophy

2. Tissue remodelling

79
Q

What is anaphylaxis?

A

Severe, systemic type I hypersensitivity

80
Q

Describe anaphylaxis?

A
  • Widespread mast cell degranulation caused by systemic exposure to antigen
  • Vascular permeability is principle immediate danger:
    ie. Soft tissue swelling threatening airway, loss of circulatory volume causing shock
81
Q

What is type II hypersensitivity a common cause of?

A

Autoimmune disease

82
Q

List the 3 stages of type II hypersensitivity?

A
  1. Sensitisation
  2. Opsonisation of cells
  3. Cytotoxicity: Complement activation, inflammation, tissue destruction
83
Q

What can happen in some cases of type II hypersensitivity?

A

Direct biological activation with antigen (i.e. receptor activation, impaired enzyme action)

84
Q

What 2 things is type III hypersensitivity a cause of?

A
  1. Autoimmune disease

2. Drug allergy

85
Q

What 3 things can happen due to type III hypersensitivity aggregating in small blood vessels?

A
  1. Direct occlusion
  2. Complement activation
  3. Perivascular inflammation
86
Q

What is type IV hypersensitivity also known as?

A

Delayed type hypersensitivity

87
Q

Give an example of type IV hypersensitivity?

A

Dermatitis

88
Q

What is the exception for autoimmune disease?

A

Autoimmune diseases which fit into a single category of hypersensitivity

89
Q

What is the definition of an autoimmune disease?

A

Harmful inflammatory response directed against ‘self’ tissue by the adaptive immune response

90
Q

Describe type I diabetes?

A

Selective, autoimmune destruction of the pancreatic β-cells

91
Q

What type of hypersensitive is type I diabetes?

A

Often mix of Type II & Type IV

92
Q

What precedes symptoms of type I diabetes?

A

Inflammation of the Islets of Langerhans

93
Q

Describe Myasthenia Gravis?

A

Syndrome of fatigable muscle weakness (limbs, respiratory, head & neck)

94
Q

What is Myasthenia Gravis caused by?

A

IgG against acetylcholine receptor which therefore prevents signal transduction

95
Q

List 5 examples of systemic autoimmune disease?

A
  1. Rheumatoid arthritis
  2. Systemic lupus erythematosus
  3. Inflammatory bowel disease
  4. Connective tissue disease
  5. Systemic vasculitis
96
Q

List the signs and symptoms of rheumatoid arthritis?

A
  • Pulmonary nodules & fibrosis
  • Pericarditis & valvular inflammation
  • Small vessel vasculitis
  • Soft tissue nodules
  • Skin inflammation
  • Weight loss, anaemia
97
Q

Describe the pathophysiology of rheumatoid factor?

A
  • IgM & IgA directed against IgG Fc region

- Forms large immune complexes

98
Q

Where are the large immune complexes in rheumatoid factor located?

A
  • High conc in synovial fluid

- Also found in other tissues

99
Q

Describe the pathophysiology of rheumatoid arthritis?

A
  • Inflammation = release of PAD from inflammatory cells
  • Further chemoatraction of inflammatory cells into synovium
  • Osteoclast activation & joint destruction
  • Fibroblast activation & synovial hyperplasia
100
Q

What is common in rheumatoid arthritis?

A

Anti-citrullinated protein/ peptide antibodies

101
Q

What does PAD do?

A

Alters variety of proteins by converting alanine –> citrulline

102
Q

What 3 inflammatory cells are sent into the synovium during rheumatoid arthritis?

A
  1. Macrophages
  2. Neutrophils
  3. Lymphocytes
103
Q

What are the 3 means of treatment for autoimmune diseases?

A
  1. Steroids
  2. Inhibitors of metabolism
  3. Inhibitors of T-cell function
104
Q

What are biologic therapies?

A

Therapeutic agents synthesised biologically rather than chemically

105
Q

What is the nature of biologic agent Infliximab & what is its target?

A
  • NATURE: monoclonal antibody

- TARGET: soluble cytokine

106
Q

What is the nature of biologic agent Etanercept & what is its target?

A
  • NATURE: soluble receptor

- TARGET: soluble cytokine

107
Q

What is the nature of biologic agent Rituximab & what is its target?

A
  • NATURE: monoclonal antibody

- TARGET: surface marker

108
Q

List 3 examples of biologic therapies?

A
  1. Infliximab
  2. Etanercept
  3. Rituximab
109
Q

What are the 3 benefits of biologic therapies for treating rheumatoid arthritis?

A
  1. Reduces joint swelling & pain
  2. Decreases systemic inflammation
  3. Delays & prevents appearance of erosions & bone deformity
110
Q

What is the risk of biologic therapies for treating rheumatoid arthritis?

A

Increased risk of infection especially TB

111
Q

What can biologic therapeutics turn off in the during the inflammatory reaction in rheumatoid arthritis?

112
Q

List the 3 environmental factors which can lead to autoimmune diseases?

A
  1. Infection
  2. Geographical factors
  3. Modifiable personal risk factors
113
Q

Give 2 examples of how infection can be a factor for autoimmune disease?

A
  1. Molecular mimicry

2. Tissue damage exposing self-antigens

114
Q

Give an example of a geographical factor which can lead to autoimmune disease?

A

Vit D deficiency

115
Q

Give an example of a modifiable personal risk factor which could lead to autoimmune disease?

116
Q

What autoimmune disease is a deficiency in Vit D associated with?

A

Multiple Sclerosis

117
Q

How is smoking associated with rheumatoid arthritis?

A

Smoking is associated with conversion of alanine to citrulline

118
Q

What are the 2 different types of autoimmune diseases?

A
  1. Organ specific

2. Systemic

MBChB Year 3 (15 decks)

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