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MCD Year 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the innate immune response?

A

Provides rapid response and depends on pre-formed and rapidly synthesised components. It has limited specificity (pattern recognition of ‘danger signals’

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2
Q

What is the acquired immune response?

A

It depends on clonal selection (expansion of cells or antibodies, selected for antigen specificity”. It is slow (starts in days) and is highly specific to foreign antigens. It provides memory

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3
Q

What are the anatomical barriers of the innate immune system, preventing infection? (3)

A

Skin- mechanical barrier
Mucus- traps microbes
Cilia- propulsion on epithelia

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4
Q

What are the physiological barriers of the innate immune system? (5)

A 
Low pH
Secretion of lysozyme
Interferons
Antimicrobial peptides
Complement
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5
Q

What triggers the innate immune system? Give examples

A

PAMPs (pathogen associated molecular patterns)
e.g. dsRNA in cytoplasm, bacterial cell wall components
DAMPs (damage associated molecular patterns)
e.g. monosodium urate, high extracellular ATP, reactive oxygen species

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6
Q

What recognises PAMPs and DAMPs?

A

Pattern-recognition receptors

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7
Q

What are types of extracellular and intracellular PRRs (pattern-recognition receptors)?

A

Extracellular danger signals detected by:
- TLRs (Toll-like receptors)
Intracellular danger signals detected by:
- NLRs (NOD-like receptors)
- RLRs (RIG-I-like receptors)
- AIM2

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8
Q

What does the innate immune system do?

A

1) Destroys invading nucleic acid (viruses) in the cytoplasm
2) Activates interleukins (e.g. IL-1b, IL-18), which in turn activate inflammatory pathways
3) Elicits type 1 interferons, for antiviral defence

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9
Q

What is an antigen?

A

Molecules that are recognised and bound by antibodies or T-cells

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10
Q

What are immunogens?

A

Antigens that can induce an immune response in the host

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11
Q

What are antibodies?

A

Proteins (immunoglobulins) found in the blood and body fluids produced in response to antigen and bind specifically to a particular antigen. They are the adaptive component of the humoral (soluble, non-cellular) immune response

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12
Q

What are lymphocytes?

A

Mononuclear cells. Subdivided into B lymphocytes and T lymphocytes. Each lymphocyte expresses a single specificity of antigen receptor on their surface to enable recognition of a specific antigen

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13
Q

What are naive lymphocytes?

A

Lymphocytes that have never encountered the antigen to which their cell surface receptor is specific for, and thus have never responded to it

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14
Q

What are memory lymphocytes?

A

A product of an immune response, ensuring that the specificity of their antigen receptor remains in the pool of lymphocytes in the body, and that an efficient response can be made after re-exposure to the antigen

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15
Q

What is active immunity?

A

The induction of an immune response within an individual by the introduction of antigen

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16
Q

What is passive immunity?

A

Immunity gained without antigen induction of a response, i.e. by transfer of antibody, immune serum or activated lymphocytes into a naive recipient

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17
Q

What is a primary immune response?

A

The response made by naive lymphocytes when they first encounter their specific antigen

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18
Q

What is a secondary immune response?

A

The response made by memory lymphocytes when they re-encounter their specific antigen

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19
Q

What are T-lymphocytes? How do they recognise antigen? What are their surface markers?

A

Lymphocytes that develop in the thymus
They only recognise processed antigen presented at the cell surface by MHC molecules
Surface markers: CD3 (all T cells), CD4 (a subset of T cells) and CD8 (a different subset of T cells)

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20
Q

What are B-lymphocytes? How do they recognise antigen? What are their surface markers?

A

Lymphocytes that develop in the bone marrow
They recognise free antigen in the body fluids or intact antigen directly on cell surfaces.
Surface markers: CD19, CD20 and surface immunoglobulin

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21
Q

What is clonal selection?

A

When T and B cells meet their specific antigen they replicate and produce effector memory cells in response, each with the same antigen receptor.

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22
Q

What are the effector arms of acquired (adaptive) immunity?

A

Cellular immunity

Humoural immunity

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23
Q

What is involved in cellular immunity

A

T lymphocytes

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24
Q

What is involved in humoral immunity?

A

B lymphocytes and antibodies

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25
Q

What part of an antigen binds to an antibody?

A

An epitope

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26
Q

What are the mechanisms by which an antibody can kill a virus?

A

1) Binds to virus and prevents attachment to a cell
2) Opsonisation: virus-Ab complex is phagocytosed
3) Complement-mediated lysis of enveloped viruses
4) Antibody-dependent cell-mediated cytotoxicity (ADCC), mediated by natural killer cells

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27
Q

What is opsonisation?

A

Where antigen is coated with ‘opsonin’ (e.g. antibody) which forms a complex aiding phagocytosis

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28
Q

What percentage of cells are lymphocytes out of a) circulating WBCs and b) cells in the lymph

A

a) 20-40% of circulating WBCS

b) 99% of cells in the lymph

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29
Q

What are the two types of T cell?

A

Helper T-cell

Cytotoxic T-cell

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30
Q

How long are the phases of primary and secondary immune response?

A

Primary immune response- Lag phase: 5-6 days (no response) then primary response occurs
Secondary is almost immediate

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31
Q

What is a B-cell antigen receptor? What does it bind?

A

Receptor is a membrane-bound antibody (i.e. a surface immunoglobulin)
Binds intact antigens

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32
Q

What is a T cell receptor? What does it bind?

A

T cell expresses two protein chains (α and β) which together make the T cell antigen receptor
It binds digested (‘processed’) antigen fragments

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33
Q

How does the T cell recognise antigen?

A

TCR recognises a complex of antigen peptide + HLA (MHC) molecule

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34
Q

How does the immune response actually clear a pathogen? (2)

A

1) Cytotoxic T lymphocytes (CTLs) kill infected cells

2) Antibodies bind to pathogens: the complex is destroyed or ingested by cells

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35
Q

What are three types of antigen presenting cell?

A

1) Macrophage
2) Dendritic cell
3) B lymphocyte

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36
Q

What are lymphoid organs? What is their function?

A

Organised tissue in which lymphocytes interact with non-lymphoid cells
They are sites of initiation and maturation of adaptive immune responses

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37
Q

What are the primary lymphoid organs? (2)

A

Thymus

Bone marrow

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38
Q

What are the secondary lymphoid organs?

A

Lymph nodes
Spleen (white pulp)
Mucosa- associated lymphoid tissue (MALT)

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39
Q

What is lymphopoiesis? What is it’s major location?

A

The generation of lymphocytes

Occurs mainly at primary lymphoid organs (thymus and bone marrow)

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40
Q

What happens to thymic output as a person ages?

A

Declines

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41
Q

What are Peyer’s patches?

A

Numerous areas of lymphoid tissue in the wall of the small intestine which are involved in the development of immunity to antigens present there. Contains germinal centres during immune responses
Predominantly B lymphocytes

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42
Q

How much lymph is returned to the blood each day?

A

2-3 litres

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43
Q

Where is the B cell zone and T cell zone in the lymph node and what are they called?

A

B cell zone (lymphoid follicle) around the outside of the node
T cell zone (parafollicular cortex) in the middle of the lymph node

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44
Q

What is the function of the spleen?

A

Filters the blood for antigens

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45
Q

The presence of what in the spleen show an ongoing immune response?

A

Germinal centres

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46
Q

What is mucosa-associated lymphoid tissue? Give examples of locations

A

MALT is a diffuse system of small concentrations of lymphoid tissue found in various mucosal sites of the body
e.g. gastrointestinal tract, thyroid, breast, lung, salivary glands, eye and skin

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47
Q

What immune cells are present in the skin?

A 
Langerhans cells (dendritic cells of the epidermis)
Intraepidermal lymphocyte
T lymphocytes (in dermis)
Macrophage (in dermis)
Dermal dendritic cell (APC)
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48
Q

What is the process of extravasation of T cells into lymph nodes?

A

1) Rolling: L-selectin on naive T cells binds to CD34 on the endothelium (high endothelial venules) forming weak bond allowing it to roll along
2) Activation: Binding to a chemokine causes activation of LFA-1
3) Adhesion: LFA-1 binds to ICAM-1
4) Migration: (transendothelial) naive T cell mirates through the endothelium

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49
Q

What lymphatic vessel do activated APCs enter a lymph node through?

A

Afferent

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50
Q

What lymphatic vessel do activated lymphocytes leave the lymph node through?

A

Efferent

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51
Q

What are cluster of differentiation markers used for?

A

CD markers
Bind to cell surface molecules (antibodies) to discriminate between cells of the haematopoietic system (e.g. B and T cells)

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52
Q

What are CD4+ cells?

A

T helper cells (2/3 of cells)

Regulatory T cells that secrete cytokines

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53
Q

What are CD8+ cells?

A

Cytotoxic T cells (1/3 of cells)

Lyse infected cells, secrete cytokines

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54
Q

APCs initiate what kind of immune response?

A

Acquired (adaptive)

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55
Q

What is the only type of APC to present to B cells?

A

Follicular dendritic cells

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56
Q

What type of immune response recognises PAMPs and DAMPs using PRRs?

A

Innate immunity

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57
Q

Is the innate immune system enhanced during second exposure?

A

No

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58
Q

Is the acquired immune system enhanced during second exposure?

A

Yes

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59
Q

What is the process of leukocyte extravasation?

A

1) Rolling: Selectin ligand on leukocytes bind to selectin on endothelium
2) Activation: Chemokines activate integron on leukocytes
3) Adhesion: Integrin bind to integrin ligand on endothelium
4) Migration: PECAM-1 (CD31) binds on leukocyte and endothelium and leukocyte moves through gap between cells in vessel wall

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60
Q

What causes neutrophil extravasation?

A

Release of chemokines (e.g. TNF-α, IL-1) from macrophages

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61
Q

What are the two types of neutrophil killing mechanism?

A

Oxygen-dependent

Oxygen-independent

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62
Q

What are the types of oxygen-independent neutrophil killing mechanism? (4)

A

Enzymes
Lysozyme
Hydrolytic enzymes
Antimicrobial peptides (defensins)

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63
Q

What are the types of oxygen-independent neutrophil killing mechanism? (7)

A 
Respiratory burst: toxic metabolites
Superoxide anion
Hydrogen peroxide
Singlet oxygen
Hydroxyl radical
Reactive nitrogen intermediates
Nitric oxide
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64
Q

What receptors do macrophages express? (6)

A 
Mannose receptor
CD11b/CD18
Scavenger receptor
Glycan receptor
CD11c/CD18
LPS receptor (CD14)
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65
Q

What occurs when bacteria bind to a macrophage?

A

Release of cytokines

Engulf and digest bacteria

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66
Q

What different type of cytokine are there and what is their function? (5)

A 
Interleukins (IL-x): between leukocytes
Interferons (IFN): anti-viral effect
Chemokines: chemotaxis
Growth factors
Cytotoxic tumour necrosis factor (TNF)
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67
Q

What does IL-1 do?

A

Alarm cytokine
Fever
Diapedesis

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68
Q

What does TNF-α do?

A

Alarm cytokine

fever, apoptosis, inflammation

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69
Q

What does IL-6 do?

A

Acute phase proteins

Liver

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70
Q

What does IL-8 do?

A

Chemotactic for neutrophils

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71
Q

What does IL-12 do?

A

Directs adaptive immunity

Activates NK cells

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72
Q

What is the complement system? Where are the components produced?

A

A complex series of ∼30 proteins and glycoproteins. When triggered an enzyme cascade system causes cleavage to form complement which causes a rapid amplification of the immune response

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73
Q

What are the complement activation pathways that lead to complement activation?

A

Classical pathway: initiated by Ag-Ab complexes
Alternative pathway: direct activation by pathogen surfaces
Lectin Pathway: Lectins binding to carbohydrates only found on pathogens
ALL CONVERGE AT C3 which leads to →
Common pathway: late phase of complement activation
Ends with formation of: Membrane Attack Complex (MAC)

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74
Q

What are the functions of complement? (4)

A

Lysis
Opsonisation
Activation of inflammatory response
Clearance of immune complexes

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75
Q

What is secreted by mast cells?

A

Histamine

other inflammatory mediators including cytokine

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76
Q

What complement product can activate mast cells?

A

Anaphylatoxins

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77
Q

Summarise a typical inflammatory respose to a localised infection (e.g. glass in skin)

A

1) Tissue damage leads to the formation of complement products that act as opsonins, anaphylatoxins, and chemotactic agents. Bradykinin and fibrinopeptides induce by endothelial damage mediate vascular changes. Mast cell degranulation causes release of histamine
2) Neutrophils migrate to tissue (diapedesis) in response to chemotactic agents
3) Monocytes and lymphocytes then arrive

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78
Q

What occurs in a systemic acute phase response?

A

Accompanies local inflammatory response after 1-2 days
Fever, increased production of white blood cells, production of “acute phase” proteins in the liver; induced by cytokines

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79
Q

Give examples of acute phase proteins (4)

A

C-reactive protein (CRP)
Mannan-binding lectin (MBL)- opsonin for monocytes
Complement
Fibrinogen

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80
Q

What are NK cells? What do they do?

A

Large granulated cytotoxic lymphocytes
Lyse target cells and secrete IFN-γ
No Ag-specific receptor but express both activating and inhibitory receptors
Has receptors which bind to antibody coated cells (ADCC)
Important in defence against tumour cells and viral infections (especially herpes)

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81
Q

Chronic granulomatous disease (CGD) causes a defect in innate immunity. What defect?

A

Reactive oxygen based killing is defective

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82
Q

Leukocyte adhesion deficiency (LAD) causes a defect in innate immunity. What defect?

A

Lack of migration of neutrophils out of blood vessels

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83
Q

Interferon-γ receptor deficiency causes a defect in innate immunity. What defect and what does this cause increased susceptibility in?

A

Poor macrophage activation

Increased susceptibility to tuberculosis

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84
Q

In cellular immunity what cell kills bacteria?

A

Phagocytes

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85
Q

In cellular immunity what cell kills viruses?

A

NK cells

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86
Q

In humoral immunity what is the response to bacteria?

A

Complement activation

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87
Q

In humoral immunity what is the response to viruses?

A

Interferons

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88
Q

What cell produces antibodies?

A

B lymphocytes

89
Q

What is the structure of an antibody?

A

Two heavy chains in the middle (both the same) with a light chain either side (light chains are both the same)
Disulphide bridges form between light and heavy chains
N polypeptide terminal (at even end)
C polypeptide terminal (at uneven end)
Fab portion = V
Fc portion = I

90
Q

Describe the antigen binding site

A

Made up of 3 hypervariable regions- CDRs (complemenarity determining regions)

91
Q

What forces are involved between antibody and antigen? (4)

A

Hydrogen bonds
Ionic bonds
Hydrophobic interactions
van der Waals interactions

92
Q

What is antibody affinity?

A

The strength of the total non-covalent interactions between a single antigen binding site and a single epitope on the antigen

93
Q

What is antibody avidity?

A

The overall strength of multiple interactions between an antibody with multiple binding sites and a complex antigen with multiple epitopes

94
Q

Is antibody affinity or antibody avidity a better measure of binding capacity in biological systems?

A

Antibody avidity

95
Q

What is antibody cross-reactivity? Give two examples

A

Antibody elicited in response to one antigen can sometimes recognise a different antigen of similar structure
e.g. Cowpox vaccination induces antibodies which are able to recognise smallpox
Antibodies made against microbial antigens on common intestinal bacteria may cross-react with carbohydrates on erythrocytes

96
Q

What are the heavy chain and light chain antibody isotypes?

A

Heavy chain: α, δ, γ, ε, μ

Light chain: κ, λ

97
Q

What are the antibody allotypes?

A

The allele of the antibody chain found in the population

98
Q

What are the different antibody classes?

A 
IgA
IgG
IgE
IgD
IgM
99
Q

How many Ch domains do the different antibody classes have?

A 
IgG: 3
IgA: 3
IgM: 4
IgD: 3
IgE: 4
100
Q

In antibodies is the chain which decides the class (e.g. γ in IgG) the light chain or the heavy chain?

A

Heavy chain

101
Q

What is the most abundant immunoglobulin?

A

IgG

102
Q

How many subclasses of IgG are there? And what are they?

A

4

IgG1, IgG2, IgG3 and IgG4

103
Q

What subclasses of IgG are major activators of the complement pathway?

A

IgG1 and IgG3

104
Q

What is the most abundant IgG subclass?

A

IgG1 (70%)

105
Q

What antibody can cross the placenta?

A

IgG

106
Q

What is the second most abundant immunoglobulin?

A

IgA

107
Q

Does IgG occur on it’s own or as multiple bound antibodiea?

A

As a monomer

108
Q

Does IgA occur on it’s own or as multiple bound antibodies?

A

As a monomer in the blood

As a dimer in secretions

109
Q

What is the major secretory immunoglobulin?

A

IgA

110
Q

What antibody is found protecting mucosal surfaces?

A

IgA

111
Q

What joins two IgA antibodies when they form a dimer?

A

J chain + secretory component

112
Q

How does IgA cross from the submucosa into the lumen?

A

1) Released from a plasma cell as a dimer
2) Binds to poly-Ig receptor
3) Endocytosed
4) Enzymatic cleavage
5) Exocytosed into lumen (secreted)

113
Q

Does IgM occur on it’s own or as multiple bound antibodies

A

As a large pentameric molecule

114
Q

Where is IgM found?

A

Mainly confined to the blood (80%)

115
Q

What is the first immunoglobulin synthesised after exposure to an antigen, providing primary antibody response?

A

IgM

116
Q

What antibody is efficient at agglutination?

A

IgM

117
Q

What antibody activates complement?

A

IgM

118
Q

What antibody is involved in B cell development and activation?

A

IgD

119
Q

What antibody is produced in response to parasitic infections?

A

IgE

120
Q

What antibody is produced in allergy?

A

IgE

121
Q

What antibody cross-links with antigen to cause mast cell degranulation?

A

IgE

122
Q

What antibodies are found in the blood?

A

IgG

IgM

123
Q

What antibody is found in extracellular fluid?

A

IgG

124
Q

What antibody is found in breast milk?

A

IgA

125
Q

What antibodies occur as monomers?

A

IgG
IgD
IgE
IgA

126
Q

What type of epitope do T cells recognise?

A

Linear epitopes

127
Q

What type of epitope do antibodies recognise?

A

Structural epitopes

128
Q

What cells prevent repeat infections?

A

Memory B cells

129
Q

How is a lymphocyte activated?

A

Interaction between a foreign molecule and specific receptor

130
Q

What is the B cell receptor?

A

A membrane immunoglobulin molecule associated with a disulphide linked heterodimer of Ig-α and Ig-β

131
Q

How does signal transduction occur in the BCR?

A

Through the Ig-α/Ig-β heterodimer which interacts with intracellular signalling molecules

132
Q

How many different antibody molecules can be generated?

A

10,000,000,000

133
Q

How is antigen receptor diversity generated?

A

Recombination

134
Q

What are the three regions that are rearranged in recombination?

A

Variable: V
Diversity: D
Joining: J

135
Q

How many VJC regions are there?

A

V: 65
D: 27
J: 6

136
Q

What VDJ segment do light chains not have?

A

D

137
Q

What enzyme complex is needed for recombination? What proteins does it contain?

A

VDJ recombinase

Rag1 and Rag2

138
Q

What is the process of recombination to produce an antibody heavy chain?

A

Start with germline DNA

1) Somatic recombination- DJ joined together
2) Somatic recombination- VDJ joined together: Rearranged DNA
3) Transcription- Primary transcript RNA
4) Splicing- mRNA
5) Translation- Formation of heavy chain

139
Q

What is the process of recombination to produce an antibody light chain?

A

Start with germline DNA

1) Somatic recombination- VJ joined together
2) Transcription- Primary transcript RNA
3) Splicing- mRNA
4) Translation- Polypeptide chain

140
Q

What do naive lymphocytes require to be activated?

A 
Antigen
Accessory signal (directly from microbial constituents or from a T-helper cell)
141
Q

What antibodies are produced by B cells in thymus-dependent production? What provides the signal? Does it provide memory?

A

All Ig-classes
Signal: T helper cell
Memory

142
Q

What antibodies are produced by B cells in thymus-independent production? What provides the signal? Does it provide memory?

A

Only IgM produced
Signal: Microbial constituents
No memory

143
Q

What is the process of B cell activation from a T helper cell?

A

1) Ag cross-links mIg generating signal= increased expression of MHC II and costimulatory B7
2) Internalisation and presentation of Ag
3) T helper cell recognises Ag and costimulation = activation of T helper cells
4) T helper cell expresses CD40L
5) CD40L interacts with CD40 on B cell = signal 2
6) B7-CD28 (B cell-Th cell) interaction = costimulation for T helper cells
7) B cells expresses cytokine receptors
8) T-cell derived cytokines bind to receptors on B cell
9) B cells enters DNA synthesis and differentiation

144
Q

After collaboration with T helper cell what are the two possible outcomes for B cell?

A

Plasma cell

Memory cell

145
Q

What are the proliferation cytokines?

A

IL-2
IL-4
IL-5

146
Q

What are the differentiation cytokines?

A

IL-2, IL-4, IL-5
IFN-γ
TGF-β

147
Q

What is an effector B cell?

A

Plasma cell- produces antibodies

148
Q

What is the process of B cell activation to produce plasma and memory cells?

A

1) Antigen stimulated B cells migrate into germinal centres- reduce surface Ig expression and undergo rapid cell division and mutation (rearranged V-region genes in dark zone)
2) Migrate to light zone and increase surface Ig expression (called centrocytes)
3) B cells with high-affinity surface Ig interact with follicular dendritic cells and bind antigen
4) B cells with low-affinity surface Ig die by apoptosis
5) Those that pass antigen selection receive a second survival signal from T helper cells and differentiate into memory B cells or plasma cells

149
Q

What MHC class do CD4 co-receptors see antigen on?

A

MHC class II

150
Q

What MHC class do CD8 co-receptors see antigen on?

A

MHC class I

151
Q

How do CD8 cells detroy their targets?

A

Induce apoptosis

152
Q

How do CD4 cells destroy their target?

A

Recruit effector cells of innate immunity, help activate macrophages
Amplify and help Tc and B cell responses

153
Q

Where are the immature and mature thymocytes located in the thymus?

A

Immature- cortex

Mature- Medulla

154
Q

What are the recombination events that occur in production of TCR?

A

VJ cleavage for α chain

VDJ cleavage for β chain

155
Q

What DNA regions are used to code for the α chain?

A

Variable and joining

156
Q

What DNA regions are used to code for the β chain?

A

Variable, diversity and joining

157
Q

What checks are performed on the αβ chain to ensure if is functional?

A

Is it functional? (Can it bind MHC? yes)
Is it functional? (Can it bind weakly to MHC? yes)
Is it dangerous/autoreactive? (Can it bind strongly to MHC? no)

158
Q

What is the difference between Th1 and Th2 cells?

A

Th1 cells produce IFN-γ and IL-2

Th2 cells produce IL-4, IL-5, IL-6, IL-10 and IL-13

159
Q

What antigen is presented on MHC class I?

A

Transplantation antigen

160
Q

What MHC class is mainly involved in immune response?

A

MHC class II

161
Q

What are the four regions on an MHC molecule?

A

Peptide-binding region
Immunoglobulin-like region
Transmembrane region
Cytoplasmic region

162
Q

What size peptides does MHC class I accommodate?

A

8-10 amino acids long

163
Q

What size peptides does MHC class II accommodate?

A

> 13 amino acids long

164
Q

What cells express MHC class I

A

All nucleated cells (although at various levels, may be altered during infection or by cytokines)

165
Q

What cells express MHC class II

A

Only on professional antigen presenting cells (may be regulated by cytokines)

166
Q

What subunits make up the structure of MHC class I?

A

α1, α2, α3 and β2-microglobulin

167
Q

What subunits make up the structure of MHC class II?

A

α1, α2, β1 and β2

168
Q

How many subunits are in the transmembrane region and cytoplasmic region of MHC class I? Which?

A

One (α3)

169
Q

How many subunits are in the transmembrane region and cytoplasmic region of MHC class II? Which?

A

Two (α2 and β2)

170
Q

What are the two pathways of antigen presentation?

A 
Endogenous antigen in MHC class I is restricted to CD8 T cells
Exogenous antigen in MHC class II is restricted to CD4 T cells
171
Q

What is endogenous antigen?

A

Antigen synthesised in the cytoplasm

172
Q

What is exogenous antigen?

A

Antigen captured from external environment

173
Q

What type of antigen do MHC class I present and on which cells?

A

Endogenous on CD8 T cells

174
Q

What type of antigen do MHC class II present and on which cells?

A

Exogenous on CD4 T cells

175
Q

What is the pathway for endogenous antigen presentation?

A

Endogenous antigen synthesised in cytoplasm

1) Endogenous antigen is degraded by proteasome
2) Peptide if transported to RER via TAP
3) Class I MHC α chain binds calnexin, then β2 microglobulin. Calnexin dissociates. Calreticulin, tapasin and ERp57 bind. MHC captures peptide, chaperones dissociate
4) Class I MHC-peptide is transported from RER to Golgi complex to plasma membrane

176
Q

What is the pathway for exogenous antigen presentation?

A

Exogenous antigen captured from external environment

1) Class II MHC α and β bind invariant chain, blocking binding of endogenous antigen
2) MHC complex is routed through Golgi to endocytic pathway compartments
3) Invariant chain is degraded, leaving CLIP fragment
4) Exogenous antigen is taken up, degraded, routed to endocytic pathway compartments
5) HLA-DM mediates exchange of cLIP for antigenic peptide
6) Class II MHC-peptide is transported to plasma membrane

177
Q

To switch to effector cells what do T cells require? (3)

A

1) Antigen recognition
2) Co-sitmulation
3) Cytokines

178
Q

What MHC pathway presents viral antigen?

A

Class I and II

179
Q

What area in post-capillary venules do T cells enter the lymph node through?

A

High-endothelial venules

180
Q

Explain the process of cytotoxic T lymphocyte (CTL)-mediated killing of target cells

A

1) CTL and target cell interact via MHC class I and form a conjugate
2) CTL rearranges cytoplasm so Golgi stack and granules are towards point of contact with target cell
3) Granules released by exocytosis
4) Dissociation of conjugate
5) CTL recycled and target cell dies by apoptosis

181
Q

What enzymes are stored in cytotoxic granules for apoptosis?

A

Perforin
Granzymes
Granulysin

182
Q

What does perforin do to induce apoptosis?

A

Polymerises and forms pores

183
Q

What doe s amacrophage do once activated? (3)

A

1) Kills phagocytosed microbes
2) Increases expression of MHC molecules and co-stimulators (B7) molecules
3) Secretes cytokines (TNF, IL-1, chemokines, IL-12)

184
Q

What happens if the source of an antigen is not completely eradicated?

A

Chronic stimulation

Granuloma formation

185
Q

What is delayed type hypersensitivity?

A

Th cells encounter certain types of antigens (e.g. poison ivy) and secrete cytokines that induce a localised inflammatory reaction (large influxes of non-specific inflammatory cells- mainly macrophages)

186
Q

What are the two phases of delayed-type hypersensitivity?

A

Sensitisation phase

Effector phase

187
Q

What happens in the sensitisation phase of delayed-type sensitivity?

A 
Antigen presenting cells present antigen on MHC class II molecule to T cells (generally Th1 cells, occasionally CD8)
T cells then differentiate and proliferate
188
Q

What happens in the effector phase of delayed type hypersensitivity?

A

Second exposure to antigen
Th cells secrete a variety of cytokines and chemokines. They attract and activate macrophages and other non-specific inflammatory cells

189
Q

Give an example of DTH that occurs with Th2 cells and what happens

A

Eosinophil activation occurs
e.g. Chronic asthma
Chronic allergic rhinitis

190
Q

Give an example of DTH that occurs with Th1 cells and what happens

A

Macrophage activation

e.g. Contact dermatitis (tuberculin reaction)

191
Q

Give an example of DTH that occurs with cytotoxic T cells and what happens

A

Cell or matrix associated antigen
Direct cytotoxicity
e.g. Contact dermatitis

192
Q

What are the subsets of T helper cells and their roles?

A

Th1: Pro-inflammatory (Boost cellular immune response)
Th2: Pro-allergic
Treg: Anti-inflammatory (Limit the immune response)
Tfh: Pro-antibody
Th17: Pro-inflammatory (Control bacterial and fungal infection)

193
Q

Why is immune regulation required? (2)

A

1) To avoid excessive lymphocyte activation and tissue damage during normal protective responses to infections
2) To prevent inappropriate reactions against self antigens (“tolerance”)

194
Q

Generally, what causes autoimmunity?

A

Susceptibility genes and environmental triggers

195
Q

What is allergy?

A

Harmful responses to non-infectious antigens which cause tissue damage and disease

196
Q

What antibody/cells mediates acute anaphylactic shock?

A

IgE

Mast cells

197
Q

What cells mediate delayed type hypersensitivity?

A

T cells (Th1)

198
Q

What is immunological tolerance?

A

Specific unresponsiveness to an antigen that is induced by exposure of lymphocytes to that antigen

199
Q

What does breakdown of self-tolerance result in?

A

Autoimmunity

200
Q

What is the therapeutic potential of inducing tolerance? (3)

A

1) Prevent graft rejection
2) Treat autoimmune diseases
3) Treat allergic diseases

201
Q

What is central tolerance?

A

Where self-reactive T or B cells are destroyed before they enter the circulation

202
Q

What is peripheral tolerance?

A

Where self-reactive T or B cells are destroyed or controlled if they have entered the circulation

203
Q

What is the mechanism of central tolerance? (3)

A

1) Apoptosis
2) Change in receptors (B cells)
3) Development of regulatory T lymphocytes (CD4+ T cells only)

204
Q

What is the mechanism of peripheral tolerance? (4)

A

1) Anergy
2) Apoptosis
3) Ignorance
4) Regulation

205
Q

How does a T cell that develops in the thymus encounter MHC bearing peptides expressed in other parts of the body?

A

AutoImmune Regulator
AIRE is a transcription factor that allows thymic expression of genes that are expressed in peripheral tissues. This allows thymic expression of genes from other tissues

206
Q

What is AIRE?

A

Autoimmune regulator- A transcription factor allowing thymic expression of genes expressed in periheral tissues

207
Q

What autoimmune disease results from a mutation in AIRO?

A

Autoimmune Polyendocrinopathy Syndrome type 1

208
Q

What is anergy in peripheral tolerance?

A

If a naive T cell see’s it’s MHC/peptide ligand without costimulatory protein it becomes anergic.
It will be less likely to be stimulated in the future even if co-stimulation is present

209
Q

What is ignorance in peripheral tolerance? Give examples of where this occurs

A

Where antigen is present in too low a concentration to reach the threshold for T cell receptor triggering. This subthreshold stimulation would lead to apoptosis to cells and antigen are compartmentalised
e.g. eye, brain

210
Q

What is known as the “death ligand” as it induces apoptosis?

A

Fas ligand

211
Q

What type of T cell are Treg cells?

A

T helper cells

212
Q

Defective Treg has been observed in what condition?

A

Multiple sclerosis

213
Q

What are the different types of Treg cell?

A

1) nTreg (natural
Develop in thymus and reside in peripheral tissue to prevent harmful reactions against self
2) iTreg (inducible)
Develop from mature CD4 T cells exposed to antigen in the periphery

214
Q

What are the effects of Th1 and Th2 cells on macrophage activity?

A

Th1- activates phagocytes to kill ingested bacteria

Th2- Inhibits macrophage activation

215
Q

What is the “master regulator” key inflammatory cytokine?

A

IL-10

216
Q

What is the function of IL-10?

A

Blocks proinflammatory cytokine synthesis (including TNF, IL-6, IL-8 and IFN-γ)
Downregulates macrophages

217
Q

How does class switching occur under T cell influence? What determines the class?

A

T cells release a cytokine which causes class switching. The cytokine released depends on the type of T helper cell

218
Q

What is the function of eosinophils and basophils?

A

They defend against parasites too large to be phagocytosed

219
Q

Summerise, generally, the sequence and timing of events following an infection

A 
First 12 hours: Innate immunity
Cellular and chemical barriers (e.g. skin), phagocytes, dendritic cells, complement, NK cells, ILCs (Innate Lymphoid Cells)
1 day onwards: Adaptive immunity
B lymphocytes- antibodies
T lymphocytes- T effector cells
Days 0-3: Antigen recognition
Day 7: Lymphocyte activation
Day 11-14: Antigen elimination
Day 16-19: Contraction (homeostasis)
Day 20

MCD Year 1 (10 decks)

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