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BM 212: Introduction to Immunology > Block A: Innate Activation, B-Cells and T-Cells > Flashcards

Block A: Innate Activation, B-Cells and T-Cells Flashcards

1
Q

When were observations that people who recovered from a disease were “protected” against it first recorded?

A

430BC
(Lecture 1, Slide 3)

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2
Q

When was variolation first carried out?

A

The 15th century
(Lecture 1, Slide 3)

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3
Q

When was vaccination first carried out and by who?

A

1796 by Edward Jenner
(Lecture 1, Slide 3)

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4
Q

What was Edward Jenner’s experiment in 1796 testing?

A

The idea that people (in this case milkmaids) with cowpox did not get smallpox
(Lecture 1, Slide 3)

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5
Q

How did Edward Jenner in test the idea that people who had cowpox did not get smallpox?

A

He inoculated a boy with scrapings from a cowpox pustule (a small blister / pimple on the skin containing pus) and then deliberately infected the boy with smallpox. The boy survived even after 20 exposures
(Lecture 1, Slide 3)

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6
Q

What did Louis Pasteur do in the 1880s?

A

He injected old cultures of vibrio bacteria into chickens and found they survived cholera
(Lecture 1, Slide 4)

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7
Q

What did Louis Pasteur’s experiment in the 1880s lead to?

A

Concepts about phagocytes and factors such as antibiotics being discovered
(Lecture 1, Slide 4)

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8
Q

What 4 types of pathogens does the immune system have to deal with?

A

Bacteria
Viruses
Fungi
Parasites
(Lecture 1, Slide 10)

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9
Q

What is a microbiome?

A

A community of organisms living within us that has a symbiotic, beneficial relationship
(Lecture 1, Slide 10)

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10
Q

When does a microorganism become parasitic?

A

When they breach tissue, causing damage or illness
(Lecture 4, Slide 10)

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11
Q

What are 3 differences in microorganisms that showcase the diversity of pathogens the immune system has to deal with?

A

Intracellular vs extracellular
Differing sizes
Different locations
(Lecture 1, Slide 11)

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12
Q

What are 5 possible routes of infection?

A

Person to Person
Orally (through food)
Contaminated water
Vector
Fomites (non-living objects)
(Lecture 1, Slide 13)

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13
Q

What 2 different arms can the immune system be divided into?

A

Innate and adaptive
(Lecture 1, Slide 15)

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14
Q

What is the innate immune system composed of?

A

Composed of non-specific mechanisms innate (since birth) to the host organism
(Lecture 1, Slide 15)

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15
Q

What is the adaptive (acquired) immune system composed of?

A

Composed of responsive and specific mechanisms that can adapt to specific organisms
(Lecture 1, Slide 15)

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16
Q

What does non-specific mean in the context of the innate immune system?

A

It can protect against foreign invaders without having to specifically recognise them
(Lecture 1, Slide 16)

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17
Q

Does the innate immune system require previous exposure to invaders?

A

No
(Lecture 1, Slide 16)

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18
Q

How does the innate immune system recognise a cell / substance as foreign?

A

It recognises a general conserved property that marks an invader as foreign
(Lecture 1, Slide 16)

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19
Q

How long does the innate immune system take to respond to a breach?

A

Can occur within minutes
(Lecture 1, Slide 17)

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20
Q

What 2 ways does the innate immune system first respond to a breach?

A

Phagocytosis and inflammatory processes
(Lecture 1, Slide 17)

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21
Q

What are the 3 reasons that receptors are important in the innate immune system?

A

Recognise invaders
Recruit different cells
Help in production of proteins that facilitate destruction of pathogens
(Lecture 1, Slide 17)

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22
Q

What are the 2 antimicrobial proteins that are produced by the innate immune system?

A

Interferon and complement
(Lecture 1, Slide 17)

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23
Q

What is the name of the process in which phagocytes engulf and destroy particles?

A

Endocytosis
(Lecture 1, Slide 19)

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24
Q

msWhat are the 5 types of professional phagocytes?

A

Neutrophils
Monocytes
Macrophages
Mast cells
Dendritic Cells
(Lecture 1, Slide 19)

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25
Q

How do phagocytes move to an area they are needed?

A

Chemotaxis
(Lecture 1, Slide 19)

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26
Q

What are resident phagocytes called and where are they found?

A

Resident phagocytes are called sentinels and are found in most tissues
(Lecture 1, Slide 20)

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27
Q

What phagocytes are the first responders in inflammation?

A

Neutrophils (White blood cells)
(Lecture 1, Slide 20)

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28
Q

How do neutrophils respond within minutes to inflammation?

A

They are recruited to sites of infection
(Lecture 1, Slide 20)

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29
Q

What type of phagocyte arrives shortly after neutrophils in inflammation?

A

Macrophages
(Lecture 1, Slide 20)

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30
Q

What do mast cells produce?

A

Histamine
(Lecture 1, Slide 20)

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31
Q

How do dendritic cells have an important role late in the adaptive response?

A

They act as a bridge between innate and adaptive systems
(Lecture 1, Slide 20)

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32
Q

How does inflammation start?

A

Infected and injured cells release chemicals that stimulate inflammation
(Lecture 1, Slide 24)

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33
Q

What are the 2 purposes of inflammation?

A

To prevent the spread of infection and to heal damaged tissue following pathogen clearance
(Lecture 1, Slide 24)

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34
Q

How are phagocytes activated at the onset of infection?

A

By Pattern Recognition Receptors (PRRs) that recognise a broad range of molecules shared by pathogens - these are called Pathogen-Associated Molecular Patterns (PAMPs)
(Lecture 1, Slide 24)

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35
Q

What happens in inflammation after PAMPs are recognised by PRRs?

A

Inflammatory mediators are released by the cells
(Lecture 1, Slide 25)

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36
Q

What are the 2 types of inflammatory mediators released by cells?

A

Cytokines and chemokines
(Lecture 1, Slide 25)

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37
Q

What do cytokines mediate in inflammation and what do they cause?

A

They mediate the inflammatory response and cause fever
(Lecture 1, Slide 25)

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38
Q

What do chemical factors (such as histamine, serotonin, leukotrienes etc) cause in inflammation?

A

They cause vasodilation of blood cells
(Lecture 1, Slide 25)

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39
Q

What 2 things does vasodilation of blood cells in inflammation attract and what do these do?

A

Neutrophils to clear pathogens
Fluid containing beneficial proteins to the site of injury for healing purposes
(Lecture 1, Slide 25)

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40
Q

What do neutrophils summon in inflammation?

A

More leukocytes (white blood cells) including lymphocytes
(Lecture 1, Slide 25)

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41
Q

What do endothelial cells secret during inflammation?

A

Nitric oxide
(Lecture 1, Slide 26)

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42
Q

Is interferon a cytokine or chemokine?

A

Cytokine
(Lecture 1, Slide 28)

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43
Q

What does interferon do to a host cell?

A

It inhibits viral replication inside host cells
(Lecture 1, Slide 28)

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44
Q

Is interferon specific to a particular virus?

A

No
(Lecture 1, Slide 28)

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45
Q

What is the function of complement?

A

It can kill microbes without phagocytosis
(Lecture 1, Slide 28)

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46
Q

How does complement kill microbes without the use of phagocytosis?

A

It uses membrane attack complex (MAC) to create channels and burst the plasma membrane
(Lecture 1, Slide 28)

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47
Q

What do host cells produce if they end up getting infected by a pathogen?

A

“Distress” Ligands
(Lecture 1, Slide 30)

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48
Q

What recognises distress signals that are produced by host cells?

A

Natural Killer (NK) cells
(Lecture 1, Slide 30)

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49
Q

What do natural killer cells also have a part in detecting?

A

Cancer
(Lecture 1, Slide 30)

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50
Q

How is the innate immune system acquired?

A

It is inherited
(Lecture 2, Slide 3)

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51
Q

Is the innate system specific or non-specific?

A

Non-specific
(Lecture 2, Slide 3)

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52
Q

What are the motifs that damaged host cells express called?

A

Damage-Associated Molecular Patterns (DAMPs)
(Lecture 2, Slide 7)

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53
Q

What are 3 types of pattern recognition receptors?

A

Toll-like receptors (TLRs)
C-type lectin receptors (CLRs)
NOD-like receptors (NLRs)
(Lecture 2, Slide 8)

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54
Q

What type of receptors are TLRs?

A

Endosomal or plasma transmembrane receptors
(Lecture 2, Slide 9)

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55
Q

What 2 domains are TLRs composed of?

A

Leucine rich pathogen recognition domain and a signalling domain
(Lecture 2, Slide 9)

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56
Q

How many TLRs are there in the human body?

A

13
(Lecture 2, Slide 11)

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57
Q

What are cytokines?

A

Small hormone-like secreted proteins
(Lecture 2, Slide 13)

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58
Q

What are 5 things included in cytokines?

A

Chemokines
Interferons
Interleukins
Lymphokines
Tumour necrosis factors
(Lecture 2, Slide 13)

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59
Q

What do cytokines act through?

A

Cell surface receptors
(Lecture 2, Slide 13)

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60
Q

What do cytokines allow?

A

They allow communication between cells so that the right cells can be activated to destroy invading pathogens
(Lecture 2, Slide 14)

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61
Q

What 2 changes can cytokine interaction have on a target cell?

A

Changes in expression of adhesion molecules and chemokine receptors
(Lecture 2, Slide 14)

62
Q

What does the changes in expression of adhesion molecules and chemokine receptors due to cytokine receptor lead to?

A

It allows these cells to move location
(Lecture 2, Slide 14)

63
Q

What 2 things can cytokines instruct a target cell to do?

A

Increase / Decrease enzyme activity
Instruct a cell to die
(Lecture 2, Slide 14)

64
Q

What does the term “chemokines” specifically refer to?

A

A subpopulation of cytokines that cause immune cells to move
(Lecture 2, Slide 16)

65
Q

What are chemokines also known as?

A

Chemoattractants
(Lecture 2, Slide 16)

66
Q

What do chemokines do in innate immunity?

A

They attract cells to the site of infection
(Lecture 2, Slide 16)

67
Q

What is extravasation?

A

A multi-step process of the emigration of cells from the blood stream into the tissue
(Lecture 2, Slide 17)

68
Q

Why is extravasation a key step?

A

Without cells crossing the blood barrier, the immune response would come to a halt
(Lecture 2, Slide 17)

69
Q

What is the first step of leukocyte extravasation called?

A

Chemoattraction
(Lecture 2, Slide 18)

70
Q

What happens in the chemoattraction stage of leukocyte extravasation?

A

TLR activation leads to cytokine and chemokine release, resulting in the chemokines attracting leukocytes
(Lecture 2, Slide 18)

71
Q

What is the second step of leukocyte extravasation called?

A

Rolling adhesion
(Lecture 2, Slide 18)

72
Q

What occurs in the rolling adhesion stage of leukocyte extravasation?

A

Carbohydrate ligands on leukocytes cause them to bind with a slight affinity to selectin molecules on endothelial cells
(Lecture 2, Slide 18)

73
Q

What is the third step of leukocyte extravastation called?

A

Tight adhesion
(Lecture 2, Slide 18)

74
Q

What occurs in the tight adhesion stage of leukocyte extravasation?

A

Chemokines produced by macrophages cause integrin molecules to become activated
(Lecture 2, Slide 18)

75
Q

What is the fourth stage of leukocyte extravasation called?

A

Endothelial transmigration
(Lecture 2, Slide 18)

76
Q

What does the endothelial transmigration occur through in leukocyte extravasation?

A

Through pseudopodia
(Lecture 2, Slide 18)

77
Q

How are different cells recruited to different tissues?

A

By using different chemokines
(Lecture 1, Slide 21)

78
Q

What does different combinations of selectins result in?

A

Selective recruitment of cells
(Lecture 2, Slide 21)

79
Q

What 2 things do PAMPs activate?

A

Phagocytes (through TLRs)
The complement system
(Lecture 2, Slide 23)

80
Q

What is complement?

A

It’s a series of proteolytic cascades containing more than 30 proteins in the plasma and on cell surfaces
(Lecture 2, Slide 24)

81
Q

What are the 3 main pathways of activation of complement?

A

Classical
Alternative
Lectin
(Lecture 2, Slide 24)

82
Q

What activates complement in the classical pathway?

A

Antigen-antibody complexes
(Lecture 2, Slide 25)

83
Q

What activates complement in the lectin pathway?

A

Lectin binding to pathogen surfaces
(Lecture 2, Slide 25)

84
Q

What activates complement in the alternative pathway?

A

Pathogen surfaces
(Lecture 2, Slide 25)

85
Q

What are the 3 main roles of complement?

A

Recruitment of inflammatory and immunocompetent cells
Opsonization (tag pathogens for elimination)
Killing of pathogens
(Lecture 2, Slide 25)

86
Q

How is a bridge formed between innate and adaptive immunity?

A
  1. Breakdown of pathogens generates lots of antigens
  2. These antigens can be presented on phagocytic cells as well as released into the body
  3. Antigens can then be recognised by cells in the adaptive immune system
    (Lecture 2, Slide 27)
87
Q

Is adaptive immunity specific or non-specific?

A

Specific
(Lecture 2, Slide 27)

88
Q

How long can adaptive immunity take to become established?

A

Can take days or even weeks
(Lecture 2, Slide 28)

89
Q

What does adaptive immunity create?

A

An immunological memory for long-term protection
(Lecture 2, Slide 28)

90
Q

What is the first stage of adaptive immunity?

A

Recognition of antigen
(Lecture 2, Slide 29)

91
Q

What is the second stage of adaptive immunity?

A

Activation of lymphocytes (B and T cells)
(Lecture 2, Slide 29)

92
Q

What is the third stage of adaptive immunity?

A

Attack against antigen and creation of memory
(Lecture 2, Slide 29)

93
Q

Where do B and T lymphocytes develop?

A

In the bone marrow
(Lecture 3, Slide 8)

94
Q

What cell does development of B and T lymphocytes start from?

A

A haematopoietic stem cell (HSC)
(Lecture 3, Slide 8)

95
Q

What does the haematopoietic stem cell produce after a series of divisions?

A

Common lymphoid progenitors (CLPs)
(Lecture 3, Slide 8)

96
Q

What do common lymphoid progenitors (CLPs) give rise to?

A

Either B or T cells
(Lecture 3, Slide 8)

97
Q

How do B and T cells get their names?

A

The cells which remain in the bone marrow are called B cells, whereas the ones that migrate to the thymus are called T cells
(Lecture 3, Slide 8)

98
Q

Where do mature B cells move?

A

The periphery (lymphoid organs)
(Lecture 3, Slide 8)

99
Q

Why do re-arrangements of immunoglobin in B cell maturation take place within in cell?

A

So that by the immature B cell point, a unique cell surface IgM immunoglobulin (BCR receptor) is formed
(Lecture 3, Slide 10)

100
Q

What does each B cell in the bone marrow have?

A

A unique IgM molecule thats a receptor on its surface - a BCR or B cell receptor
(Lecture 3, Slide 11)

101
Q

What does the BCR on a b cell cell do?

A

It recognises antigens
(Lecture 3, Slide 12)

102
Q

How are B cell receptors (BCRs) made?

A

By a recombination of inherited genes
(Lecture 3, Slide 12)

103
Q

What chains is Immunoglobulin (Ig) composed of?

A

2 long heavy chains
2 short light chains
(Lecture 3, Slide 13)

104
Q

What 5 classes of immunoglobulins do mammals have?

A

IgA, IgD, IgE, IgG and IgM
(Lecture 2, Slide 13)

105
Q

What class of immunoglobulins do all vertebrates have?

A

IgM
(Lecture 3, Slide 13)

106
Q

What 2 immunoglobulin classes are the most common in mammals?

A

IgM and IgG
(Lecture 3, Slide 15)

107
Q

What is the function of IgM and IgG immunoglobulins?

A

They provide the bulk of specific immunity against bacteria and viruses in extracellular fluid (body fluid not contained in cells)
(Lecture 3, Slide 15)

108
Q

What is the function of the IgE immunoglobulin?

A

They participate in defences against multicellular parasites and allergic responses
(Lecture 3, Slide 15)

109
Q

What is the function of the IgA immunoglobulin?

A

They are secreted by plasma cells in the linings of the gastrointestinal (GI) respiratory and genitourinary tracts to protect locally
(Lecture 3, Slide 15)

110
Q

What is the site on the antigen that the antibody binds to called?

A

The epitope
(Lecture 3, Slide 17)

111
Q

What is an antigen?

A

A substance capable of stimulating an immune response
(Lecture 3, Slide 18)

112
Q

What are the 3 main types of antigens?

A

Foreign antigens (heteroantigens)
Self-antigens (autoantigens)
Cancer cell derived antigens (neoantigens)
(Lecture 3, Slide 18)

113
Q

What 2 things activates the B cell receptor (BCR)?

A

They are activated by antigens and by helper T cell cytokines (T-dependant activation)
(Lecture 3, Slide 20)

114
Q

What does activation of the B cell receptor (BCR) cause the B cells to do?

A

Proliferate and differentiate into plasma cells that make antibodies and some of these form into memory cells
(Lecture 3, Slide 20)

115
Q

How do B cell receptors on the membrane ensure each lymphocyte is specific to just one type of antigen?

A

Each B lymphocyte has a membrane receptor (BCR) that binds to a specific antigen
Once this occurs the antigen is “recognised “by the lymphocyte”
(Lecture 3, Slide 22)

116
Q

Do the progeny (descendants) of a antigen-stimulated B cell express the same receptor, or a different receptor?

A

Same receptor
(Lecture 3, Slide 24)

117
Q

How can B cells also present an antigen?

A

Once the antigen binds to the receptor, the cell can internalize and degraded the antigen to peptide fragments which can then bind to MHC class II receptors and be transported to the cell surface
(Lecture 3, Slide 26)

118
Q

What are 4 the functions of antibodies?

A

Neutralisation of antigens
Opsonisation (tag foreign pathogens for elimination by phagocytes) of bacteria
Activation of complement system
Aid in killing cells (ADCC)
(Lecture 3, Slide 28)

119
Q

What does a diverse collection of T-cells allow the host to do?

A

Mount an adaptive immune response against a wide range if pathogens
(Lecture 4, Slide 6)

120
Q

How are T cells selected in the thymus?

A

Cells that recognize self MHC receive signals for survival whereas those which interact strongly with self antigens are removed
(Lecture 4, Slide 7)

121
Q

What happens to T cells after they are selected in the thymus?

A

They mature and migrate into the periphery
(Lecture 4, Slide 7)

122
Q

Where do T cells circulate?

A

Through lymph nodes
(Lecture 4, Slide 7)

123
Q

What is clonal deletion?

A

Any cells that receive too little / much of a signal and are deleted by apoptosis or are put into an inactive state called anergy
(Lecture 4, Slide 9)

124
Q

What are the 2 features of lymphocyte development that separates them from innate immunity?

A
  1. Each lymphocyte only expresses one receptor specificity
  2. Lymphocyte DNA is irreversible altered by gene rearrangement during development
    (Lecture 4, Slide 10)
125
Q

What is clonal expansion?

A

Proliferation of an individual T cell resulting in clones of lymphocytes with identical antigen receptors
(Lecture 4, Slide 10)

126
Q

What 2 protein chains are T cell receptors (TCRs) made from?

A

Usually α and β (alpha and beta)
Sometimes γ and δ (gamma and delta)
(Lecture 4, Slide 11)

127
Q

Is the T cell receptor trans-membrane or just on the surface of the membrane?

A

They are transmembrane
(Lecture 4, Slide 11)

128
Q

What tail do T cell receptors have?

A

A cytoplasmic tail
(Lecture 4, Slide 11)

129
Q

How are T cell receptors (TCRs) generated?

A

By random combination and mutation of germline DNA in both chains
(Lecture 4, Slide 12)

130
Q

How are T cells selected in the thymus?

A

The T cell receptor (TCR) is tested to confirm it works and that it doesn’t react with self
(Lecture 4, Slide 14)

131
Q

Are T cells with strong or weak affinity with self deleted during selection in the thymus?

A

Strong
(Lecture 4, Slide 14)

132
Q

What happens to the “useful” T cells after T cell selection in the thymus?

A

They differentiate
(Lecture 4, Slide 14)

133
Q

What 2 types of cells can T cells differentiate into after selection in the thymus?

A

CD4+ “helper” T cell or CD8+ “killer T cell”
(Lecture 4, Slide 14)

134
Q

How are antigens generated?

A

Phagocytes chew up pathogens which generates lots of short peptides from pathogen-associated proteins - this is known as an antigen
(Lecture 4, Slide 16)

135
Q

What is the first step of T cells taking the antigen to MHC class II molecules?

A

The antigens taken from the extracellular space to intracellular vesicles
(Lecture 4, Slide 17)

136
Q

What is the second step of T cells taking the antigen to MHC class II molecules?

A

Acidification of vesicles activates proteases to degrade antigen into peptide fragments
(Lecture 4, Slide 17)

137
Q

What is the third and final step of T cells taking the antigen to MHC class II molecules?

A

Vesicles containing peptide fragments fuse with vesicles containing MHC class II molecules
(Lecture 4, Slide 17)

138
Q

What does MHC stand for?

A

Major Histocompatibility Complex
(Lecture 4, Slide 18)

139
Q

What are the 2 forms of MHC and where are they found?

A

MHC class I: Expressed on all mammalian cells
MHC class II: Selectively expressed on professional anti-gen presenting cells
(Lecture 4, Slide 18)

140
Q

What MHC class receptors do helper and cytotoxic T cells have?

A

Helper T cells have both MHC class I and II (though mostly class II) receptors whereas cytotoxic T cells only have MHC class I receptors
(Lecture 4, Slide 18)

141
Q

What is the difference between MHC class I and class II receptors?

A

Class I presents antigens from inside the cell whereas class II is specialised to present pathogens from outside the cell
(Lecture 4, Slide 19)

142
Q

What is the first step of T cells becoming activated?

A

Naïve (not exposed to their antigen) T cells recirculate looking for phagocytes presenting their antigen (On their MHC Receptor)
(Lecture 4, Slide 20)

143
Q

What is the second step of T cells becoming activated?

A

Upon recognition of phagocyte presenting cognate (complementary) antigen, the T cell and anti-gen presenting cell form an interaction
(Lecture 4, Slide 20)

144
Q

What is the third (and final) step of T cells becoming activated?

A

The T cell receptor (TCR) transmits signals and the T cell becomes activated
(Lecture 4, Slide 20)

145
Q

What do activated T cells differentiate into?

A

Functional effector T cells
(Lecture 4, Slide 21)

146
Q

What do Th1 and Th2 effector T cells do?

A

Th1 cells enhance macrophage activity and activate cytotoxic T cells
Th2 cells stimulate B cells to produce antibodies
(Lecture 4, Slide 22)

147
Q

How do we get memory T cells?

A

After infection the number of T-cells specific for antigen increases dramatically then drops of, leaving a small number of “memory” T cells
(Lecture 4, Slide 24)

148
Q

How can vaccines be used to protect the body against a pathogen?

A

By exposing the body to a small amount of the pathogen, this an leave the body with memory T cells so the body is more prepared if the actual pathogen infects
(Lecture 4, Slide 24)

149
Q

Which 2 cytokines stimulate memory T cells to promote survival?

A

IL-5 and IL - 7 , which are interleukins
(Lecture 4, Slide 26)

150
Q

What do memory T cells still require to proliferate?

A

The correct signals (from their TCR)
(Lecture 4, Slide 26)

151
Q

What is a potentially disadvantage of the adaptive immune system?

A

Not all antigens are harmful and there is potential for the body to accidentally react to itself
(Lecture 4, Slide 28)

152
Q
A

BM 212: Introduction to Immunology (13 decks)

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