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Microbiology Year 2 > Immunology > Flashcards

Immunology Flashcards

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1
Q

What does the immune system defend against?

A

infectious pathogens [bacteria, viruses, fungi, parasites (protozoa)]

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2
Q

What does the type of immune response depend on?

A

Type of immune response depends on pathogen

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3
Q

What are the two systems of the immune system?

A

Innate and Adaptive (acquired)

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4
Q

What are 4 differences between the innate and adaptive immune systems?

A

1) Innate
>Born with
>Broad specificity of recognition of pathogens
>Not affected by prior contact
>Rapid response (minutes-hours)

2) Adaptive (acquired)
>Adapts to pathogens we are exposed through throughout life time.
>Highly specific to a pathogen
>Enhanced by prior contact with a pathogen (can be life-long_
>Slower responses (days-weeks to develop an adaptive immune response)

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5
Q

Why do the adaptive and innate immune systems interact so much?

A

As they have evolved together.

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6
Q

What two classes of biological molecules do both immune systems primarily involve?

A

white blood cells (leukocytes) + soluble factors

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7
Q

What are the 4 elements of the innate immune system?

A

1) Barriers
>Systems preventing pathogens causing infection in first place

2) Leukocytes
>(phagocytes, and NK cells)

3) Soluble proteins
>(complement, interferons etc.)

4) Local and systemic responses/ coordinated responses
>(inflammation, fever)

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8
Q

What a) physical b) chemical barriers does skin have?

A

a) Epithelial cells joined by tight junctions making it difficult for pathogens to penetrate
>Flow of air or fluid helps to move pathogens away from epithelial surface.

b) Sebum contains fatty acids, skin has lowish pH to stop growth of some pathogens

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9
Q

What a) physical b) chemical barriers does the Gi tract have?

A

a) Epithelial cells joined by tight junctions making it difficult for pathogens to penetrate
>Flow of air or fluid helps to move pathogens away from epithelial surface.

b)Enzymes like pepsin destroy food
>Low pH
>Antibacterial peptides (defensins)

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10
Q

What a) physical b) chemical barriers does the UG tract have?

A

a) All have epithelial cells joined by tight junctions making it difficult for pathogens to penetrate
>Cilia

b) Low pH
>Antibacterial peptides (defensins)

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11
Q

What a) physical b) chemical barriers does the respiratory tract have?

A

a) All have epithelial cells joined by tight junctions making it difficult for pathogens to penetrate
>Cilia to move mucus

b) Enzyme lysosome disrupts cell wall of some bacteria
>Antibacterial peptides (defensins)

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12
Q

What makes skin hard to penetrate by pathogens and what is it produced by?

A

Keratin is produced by keratinocytes, makes skin rough so is hard to penetrate by pathogens

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13
Q

What are 3 ways Keratinised skin can be breached by pathogens?

A
  1. Wounds/ cuts
  2. Bites
  3. Some pathogens infect skin directly
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14
Q

Where does most infections occur and why?

A

Mucosal surfaces, as are semi-permeable.

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15
Q

What are the 3 mucosal surfaces which are infected commonly?

A
  1. Gastro-intestinal Tract
  2. Respiratory Tract
  3. Genito-urinary tract
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16
Q

What do all Leukocytes (white blood cells) derive from and what are the 2 main lineages?

A

Pluripotent stem cells (multipotential hematopoietic) from the bone marrow, which gives rise to two main lineages: myeloid cells and lymphoid cells

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17
Q

Are myeloid cells and lymphoid cells (leukocyte main lineages) part of the innate or adaptive immune systems?

A
  1. All myeloid cells are apart of innate immunity
  2. All lymphoid cells are apart of adaptive immunity, other than NK cells.
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18
Q

What are phagocytes particularly important to defend against?

A

Extracellular bacterial (infection caused by something outside host cells)/fungal infections

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19
Q

What are the two main types of phagocytes?

A

neutrophils, mononuclear phagocytes (e.g. macrophage)

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20
Q

What are the 3 main properties of neutrophils?

A
  1. Main phagocyte in blood from bone marrow
  2. Short-lived (24 hours), fast-moving (injury or infection, can get to the area quickly)
  3. Specialised lysosomes release enzymes, H2O2 (hydrogen peroxide) etc.
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21
Q

What are the two main forms of Mononuclear phagocytes and where are they found?

A

1) Monocyte
>In blood

2) Macrophage
>What monocytes change into when entering tissue often first encounter the pathogens in our body.

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22
Q

What is the function of Mononuclear phagocytes (Monocytes, Macrophages and dendritic cells)?

A

Help initiate adaptive responses as well as phagocytosis in the innate response.

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23
Q

What is 2 differences between neutrophils and mononuclear phagocytes (macrophages, dendritic cells, monocytes)?

A

> Neutrophils are short lived while mononuclear phagocytes are long lived (months-years)

> Neutrophils are present in blood, mononuclear phagocytes in tissues.

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24
Q

What are the names of the mononuclear phagocytes found in a) brain b) lungs c) liver?

A

a) Brain - microglial cells

b) Lungs - alveolar macrophages

c) Liver - Kupfer cells

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25
Q

What are Natural killer (NK) cells a type of?

A

Type of lymphocyte (only one apart of the adaptive immune system)

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26
Q

What is the main role of natural killer (NK) cells?

A

Help keep intracellular viral, some bacterial and protozoal infections in check until adaptive immunity develops

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27
Q

What is a stand out feature of natural killer (NK) cells?

A

Have distinct cytoplasmic granules containing perforin and enzymes to cause lysis (defensins)

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28
Q

What are 3 examples of soluble proteins in immunity?

A
  1. Defensins
  2. Interferons
  3. Complement
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29
Q

What are Defensins and what do they do?

A

Positively charged peptides made by neutrophils
that disrupt bacterial membranes causing lysis

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30
Q

What cells make interferons?

A

Interferons can be made by any cell in the body if infected by virus

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31
Q

What are the three ways interferons α and β interfere with viral infection?

A
  1. Interferons secreted from infected cells bind to neighbouring non-infected cells making them immune to infections (induce resistance to viral replication)
  2. Increase MHC class 1 protein expression and antigen presentation in all cells (involved in initiating T-cell responses, link innate and adaptive)
  3. Activates NK cells to kill virus-infected cells.
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32
Q

What does complement consist of?

A

Complement consists of 20 serum proteins (found in blood)

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33
Q

Why is complement called this?

A

Called complement as is a series of proteins that compliment antibodies in killing pathogens.

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34
Q

What is the order of the classical complement pathway?

A
  1. C1
  2. C4
  3. C2
  4. C3
    >C3a/ C3b
  5. C5
  6. C6
  7. C7
  8. C8
  9. C9
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35
Q

What is the central event of complement activation that occurs in all complement pathways?

A

Cleavage of C3 protein by C3 convertase to generate peptide fragments C3a (smaller) + C3b (larger) by the protease “C3 convertase”.

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36
Q

What are the 3 complement pathways and what initiates them all?

A

1) Classical pathway
>antigen: antibody complex formation

2) MB-lectin pathway
>Lectin binding to pathogen surfaces

3) Alternative pathway
>Activated intrinsically by pathogen surfaces such as LPS

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37
Q

What are the same three outcomes of the complement pathways?

A

1) Recruitment of inflammatory cells

2) Opsonization of pathogens

3) If all pathways active, direct killing of pathogens (via membrane attack complex)

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38
Q

How does complement recruits inflammatory cells in 2 ways?

A

> C5a (mainly) and C3a important for this.

  1. C5a acts as Chemoattractants, causing neurtrophils to move towards high concentrations due to C5a receptors; moving them from blood to tissue
  2. C5a binds to C5a receptors on mast cells (underlying mucosal surfaces) causing them to release inflammatory mediators like histamine (vasoactive amines)
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39
Q

How does complement cause optimization of phagocytes and which type of bacteria is this more efficient against?

A

> C3b is important for this; C3b coats bacterial surfaces allowing phagocytes to be attracted to this pathogen due to C3b receptors.

> More efficient at killing gram + bacteria as they have thick peptidoglycan so is difficult to cause lysis.

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40
Q

How do some bacteria combat against phagocyte optimization by complement?

A

Some bacteria evade opsonisation by producing a thick capsule that envelopes C3b (S. pneumonia, N. meningitides)

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41
Q

How does complement cause direct pathogen death via cell lysis and what type of bacteria is this efficient in killing?

A

> Full activation of complement pathway (C5b-C9) leads to formation of membrane attack complex; C9 polymerises to form hollow cylinders creating pores in bacterial membrane destabilising it causing lysis.

> Important in defence against gram -ve bacteria

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42
Q

What type of bacteria are resistant to membrane attack complex killing and why?

A

Gram + are resistant due to thick peptidoglycan layer not allowing C9 cylinders to form pores in membrane.

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43
Q

What is an example of a) localised b) systemic (body wide) immune response?

A

a) Inflammation

b) Fever

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44
Q

What are three events that occur during inflammation and what is its function?

A
  1. Dilation of blood vessels
    > Due to Vasoactive amines (like histamine) cause this.
  2. Increased capillary permeability
    >Endothelial cells retract becoming leaky (less tight junctions) causing swelling.
  3. Phagocytes migrate into tissues
    >Phagocytes from blood will move into tissues due to increased capillary permeability.

> Important for getting components (phagocytes and complement) of immune system to where they are needed in body

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45
Q

By which receptor do antibodies bind to pathogen?

A

Fc receptors

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46
Q

By which receptor do complement components bind to pathogens and what is the effect?

A

C3b can bind to pathogens and cause recognition by phagocytes via C3b receptors

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47
Q

What are 2 ways phagocytes recognise pathogens specifically through the adaptive immune system?

A
  1. Antibodies bound to pathogens via Fc receptors
  2. C3b (complement) bound to pathogens via C3b receptors cause recognition by phagocytes via C3b receptors
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48
Q

How do phagocytes recognise pathogens non-specifically via the innate immune system?

A

Pattern recognition receptors (PRRs) recognise microbe-associated molecular patterns (MAMPs) (broad patterns found on microbes).

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49
Q

What is an example of MAMPs for a) bacteria b) fungi c) some viruses?

A

a) LPS

b) Chitin

c) dsRNA (only in some viruses)

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50
Q

What are the 5 characteristics of MAMPs?

A
  1. Found commonly on microbes.
  2. Conserved (Is difficult for pathogens to change)
  3. Shared by many microbes
  4. Distinct from self (Distinct from mammalian cells)

5) Critical for survival/function of pathogens (so is difficult for pathogen to mutate).

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51
Q

What are 4 examples of Pattern recognition receptors (PRRs) on phagocytes?

A
  1. Mannose receptor
  2. LPS receptor
  3. Glucan receptor
  4. Scavenger receptor
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52
Q

What is the overall effect of PRRs binding to MAMPs?

A

Recognition of MAMPs, once bound to PRRs on phagocytes can induce behavioural changes (phagocytosis, chemotaxis or signalling).

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53
Q

What do chemotactic pattern recognition receptors recognise and an example and what behaviour does this cause for phagocytes?

A

Recognise Chemoattractants such as C5a binding to C5a receptors or recognising peptides commonly produced by bacteria. Causing chemotaxis of bacteria.

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54
Q

What are Toll-like receptors (TLRs) and what is the effect of binding to MAMPs?

A

Pattern recognition receptors (PRRs), When binding to MAMPs triggers expression of new genes, Signalling induces expression of inflammatory cytokines and interferons

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55
Q

What shape of Toll-like receptors (TLRs)?

A

Hook like structure protrude form membrane

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56
Q

Where are Toll-like receptors (TLRs) found, why are they found here and an example?

A

> Usually cell-surface receptors or endosomal (as viruses can get inside cells/ intracellular MAMPs).

> E.g. TLR-3 on endosomes inside cells and recognises dsRNA which is often found in viruses.

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57
Q

If a phagocyte recognises a MAMP, how does it respond in 2 ways?

A
  1. If recognised MAMP through TLR it can start expressing new genes
  2. If recognising through other MAMPs, it triggers phagocytosis.
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58
Q

What are the 5 stages of phagocytosis and at what stage would a bacteria like TB thrive?

A
  1. Bacteria binds to surface of phagocytic cell via pattern recognition receptors.
  2. Phagocyte pseudopods extends and engulfs organism, tips of pseudopods fuse.
  3. Invagination of phagocyte membrane traps the organism within the phagosome.
    >Some bacteria thrive here like TB.
  4. A lysosome fuses and deposits enzymes into the phagosome forming phagolysosome. Enzymes cleave macromolecules and generate reactive oxygen species (ROS) destroying the organism.
  5. Debris is released.
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59
Q

What are 6 bactericidal agents that phagocytes contain inside lysosomes?

A
  1. Acidic proteins
  2. Toxic oxygen-derived products
  3. Toxic nitrogen oxides
  4. Anti-microbial peptides
  5. Enzymes
  6. Competitors
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60
Q

What are toxic nitrogen oxides and toxic oxygen-derived products most commonly used by?

A

Used by monocytes, macrophages and neutrophils to kill pathogens.

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61
Q

What are the 2 most important killing mechanisms contained in lysosomes in phagocytes, and what is the advantages of using them?

A

Toxic oxygen-derived products and Toxic nitrogen oxidases are free radicals contained within phagolysosomes, and are short lived so only damage bacteria (and not our cells).

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62
Q

How do natural killer (NK) cells recognise infected host cells from non-infected host cells?

A

> Inhibitory receptors recognise MHCI (“self”) proteins present on all nucleated cells

> Alterations in MHCI expression (due to viruses and cancers) prevents inhibitory signalling, so when MHCI expression on a host cell is low, then NK cells doesn’t get inhibited and kills host cell.

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63
Q

What proteins are present on all nucleated cells and provide evidence as “self”?

A

MHCI (“self”) proteins

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64
Q

How do natural killer cells kill an infected host cell and the advantage of this method?

A

> Makes a protein called perforin, similar to membrane attack complex

> Perforates membrane of target cell, acts as a channel so NK cell can secrete enzymes (granzyme) into target to trigger apoptosis pathway (leaves no cell material or release of viruses/ bacteria inside so infection doesn’t spread)

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65
Q

What do the many granules in natural killer (NK) cells contain?

A

> Granzymes (trigger apoptotic pathway in infected host cell, can also kill directly sometimes too).

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66
Q

What are the similarities and differences between hormones and cytokines?

A

> Like hormones, regulate immune responses by changing cell behaviour or gene expression

> Most act locally (unlike hormones), but can have systemic effects e.g. can act on hypothalamus and induce fever response.

> Also short lived response unlike hormones

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67
Q

Why is is advantageous for cytokines to be short lived?

A

As are toxic.

68
Q

What are the 5 steps of the mechanism of action of cytokines?

A
  1. Stimulus e.g. MAMP on bacterium
  2. Recognised by cell which produces cytokines
  3. Causes expression of cytokine genes, secreted
  4. Cytokines bind to cytokine receptor on target cell
  5. Target cell either change behavoiur or express different genes for overcoming infection.
69
Q

What are 4 important groups of cytokines and their functions?

A
  1. Interleukins (IL-1, IL-38?)
    > Not structurally or functionally related so have a range of functions (usually made by T-cells)
  2. Interferons (IFNs)
    >important for viral infections e.g. IFNα, IFNβ (made by any cell in response to viral infection); cell activation of macrophages and T-cells by IFNγ (only made by monocytes, macrophages and T-cells).
  3. Chemokines
    >cell movement or chemotaxis e.g. IL-8 (CXCL8) inducing neurotrophies to move out of blood stream.
  4. Tumour necrosis factors (TNFs)
    >pro-inflammatory, can kill some cells
    Toxic cytokine, kills tumour cells but also kills non-infected cells. ○ Important for sepsis (blood stream infection)
    and localised areas.
70
Q

What are 2 advantages of the adaptive immune system that the innate doesn’t provide?

A

> Allows for pathogen-specific immunity; B and T lymphocytes recognise antigen via receptors

> Enhanced by second exposure - memory

71
Q

What are the 2 arms of adaptive immunity?

A
  1. Humoral (mediated by antibody which are soluble found in blood, saliva) immunity
  2. Cell-mediated immunity (mediated by T-cells or by cells of innate immune system activated by cytokines released by T-cells)
72
Q

What is the pathway of action for humoral immunity?

A

B lymphocytes recognise antigen through antibody receptors present on B cell surface → differentiate into plasma cells that secrete soluble antibody that labels antigen (in body fluids)

73
Q

What is the pathway of action for cell-mediated immunity?

A

T lymphocytes recognise antigen via T-cell receptors → differentiate into cytotoxic T cells that kill infected host cells or helper T cells that control the immune response by producing cytokines

74
Q

Where are the a) antibody receptors (humoral immunity) b) T-cell receptors (cell-mediated immunity) acquired?

A

a) Antibody receptor acquired in the bone marrow

b) T-cell receptor acquired in the thymus

75
Q

What is an antigen?

A

An antigen is a molecule (protein, carbohydrate etc.) that induces the production of antibodies (antibody generating material).

76
Q

What is a single antibody specific to?

A

Binds to only one antigen

77
Q

Why is it called the clonal selection hypothesis?

A

Called clonal selection as a single B cell is selected and gives rise to a clone of identical daughter cells.

78
Q

What is the clonal selection hypothesis in 3 steps?

A
  1. B cells acquire antibody membrane receptors independently of antigen in primary lymphoid tissue
  2. B cell antibody receptors bind to antigen in secondary lymphoid tissue (lymph bodes, spleen, etc.)
  3. Bound B cells differentiate and divide, secreting soluble copies of the antibodies that were bound to their surface specific to the antigen that triggered division.
79
Q

What is a clinical use of antibodies?

A

Diagnostic of infection (if present in blood shows if they have or have had infection of a specific pathogen)

80
Q

What region of an antibody is for a) Antigen recognition b) Antigen elimination?

A

a) Antigen recognition: Fab
>2 arms that grab onto antigen

b) Antigen elimination: Fc
>Tail

81
Q

What is the hinge region of an antibody, what’s its advantage and how does it do this?

A

> Hinge region is flexible

> Due to lots of proline residues, allowing Fab arms to move.

82
Q

What is a typical immunoglobin G (most common in serum) antibody structure?

A

> 2 light chains (containing 2 light domains each)

> 2 heavy chains (containing 4 heavy domains each)

> Joined by disulphide bonds and a hinge region.

83
Q

What is the a) Constant b) Variable region of an antibody and where are they found on the structure?

A

a) CONSTANT (C) regions
>Same for antibodies of a given Heavy chain class or Light chain type.
>The Whole Fc region and the bottom two domains in the Fab region.

b) VARIABLE (V) regions
>Bind antigen. Differ between antibodies with different specificities.
>The N terminal domains of the heavy and light chains in the Fab region (the two end points of the arms)

84
Q

What is an advantage to having variable regions on antibodies?

A

Allows antibodies to bind to different antigens, due to varying Fab regions.

85
Q

What is the effect of variable and constant regions of an antibody being encoded by separate exons?

A

Somatic recombination: Multiple V region exons in genome can recombine early in B cell differentiation; massively increasing number of antibodies we can produce (allows response to quickly mutating pathogens).

86
Q

What differentiates the immunoglobin classes of antibodies?

A

Differ in the amino acid sequence of the constant regions of their heavy chains

87
Q

What are the 5 main heavy chain immunoglobin classes of antibody, their structure and function?

A
  1. IgG (γ)
    >Main class in serum (blood) and tissues important in secondary responses
    >Single Y shaped molecule
  2. IgM (μ)
    >Important in primary responses (always produce first)
    >Found as a pentamer (5 Y shaped antibody units linked by disulphide bonds at Fc region) and peptide called J-chain associated important for catalysing pentamer formation.
  3. IgA (α)
    >In serum & secretions protects mucosal surfaces
    >Single Y shaped molecule in serum or blood (monomer form)
    >When secreted occurs as a dimer, 2 Y shaped antibody units linked end to end and with a J chain, also secretary component wrapped around Fc regions, involved in transport of IgA onto mucosal surfaces and protects from digestion from enzymes.
  4. IgD (δ)
    >?
  5. IgE (ε)
    >Present at very low levels involved in allergy + protection against large parasites (role in immune response)
    >Single Y shaped molecule
88
Q

What are the two light chain types of antibody and 2 examples?

A

> Light chain types: kappa (κ) and lambda (λ).

> These are not heavy chain class restricted i.e. can have IgGκ or IgGλ antibodies.

89
Q

What antibody dominates the a) Primary response b) Secondary response>

A

a) Primary responses= dominated by IgM

b) Secondary responses= dominated by IgG

90
Q

How is it possible that the primary response is dominated by IgM and then the secondary response by IgG?

A

As class switching allows antibodies to alter into a different class.

91
Q

What is the advantage of class switching?

A

Class switching gives flexibility to immune response as can produce different types of antibodies with different functions relevant on the infection.

92
Q

What antibody would the secondary immune response be dominated by if the infection was a mucosal pathogen?

A

IgA

93
Q

Where are each of the 4 (not IgD) heavy chain immunoglobin classes of antibody found in the body?

A
  1. IgG – present in blood (serum), extracellular fluid, can cross the placenta
  2. IgM – usually restricted to blood, can enter extracellular fluid (get into tissues) if inflammation makes cells leaky
  3. IgA monomer – blood, extracellular fluid
    >IgA dimer – mucosal secretions, tears, saliva, breast milk important in protecting new born if breast fed.
  4. IgE – mainly associated with mast cells beneath epithelial surfaces (respiratory tract, GI tract, skin)
94
Q

Which class of antibody protects new born babies against infection and why?

A

IgG is the only antibody which can cross the placenta.

95
Q

When does class switching occur and what takes place during it?

A

> Occurs when an antibody has been stimulated by antigens (secondary lymphoid tissues)

> The same V region gene recombines with different C region genes, this allows the same antigen specificity (variable region) to be linked to different Fc functions/locations

96
Q

What is affinity maturation of antibodies, how is it done and what is its effect?

A

> During an immune response, the affinity of the antibodies to an antigen increases

> Occurs due to somatic hypermutation of V region genes in B cells responding to antigen

> Mutations (are generated at random) that increase binding affinity are selected (as only the antibodies that bind survive, like natural selection of B cells.

97
Q

What are 4 direct methods antibodies stop pathogens and which immunoglobin classes do which?

A
  1. Block adherence (IgM, IgG, IgA)
    >Stops pathogens binding to host cells in the first place, so can’t infect.
  2. Neutralise toxins (IgG, IgA)
    >After undergoing affinity maturation, can bind tightly to toxins neutralizing them.
  3. Agglutination of bacteria, inhibits movement (IgM, dimeric IgA)
    >Clumps of bacteria can’t move well, uses multiple Fab arms, so can’t spread through body easily.
  4. Block uptake of nutrients (IgG)
    >High affinity antibodies stop uptake so they can’t grow or reproduce.
98
Q

What are Fc effector functions and why are they called this?

A

> Antibodies interact with innate immune system via their Fc regions.

> The Fab (variable) regions bind to specific pathogens and the constant Fc regions bind to Fc receptors guiding the innate immune system.

99
Q

What are 3 examples of Fc effector functions?

A
  1. Complement mediated lysis (bacteria and enveloped viruses (viruses that take lipid envelope from host cell))
    >Via classical complement pathway
  2. Enhancement of phagocytosis (opsonization)
  3. Enhanced killing of infected cells by NK cells
100
Q

How do antibodies activate the complement classical pathway?

A

C1q (first compliment/ C1) must interact with 2 Fc regions which are bound to a foreign surface (Antibodies have to be adjacent at the right distance so two heads of C1q can interact)

101
Q

What is the most efficient antibody for activating complement and why?

A

IgM more efficient activator than IgG, as IgM is a pentamer and is easier to achieve the two Fc regions at the right distance to interact with the heads of C1q.

102
Q

How do antibodies act as opsonins for phagocytes and what 2 classes of antibody are important for this?

A

> As phagocytes have receptors for Fc regions of some classes of antibodies on their surface. (phagocyte binds to Fc regions of antibodies surrounding a pathogen and phagocytose the pathogen)

> IgG, monomer IgA are important for this (recognised by Fc receptors on phagocytes)

103
Q

What is a method that bacteria, such as Staphylococcus aureus and Streptococcus sp., use to evade phagocytosis or complement?

A

> Some bacteria have proteins which bind to the Fc regions of antibodies, if the bacteria has bound to the Fc regions, then the Fc regions can’t interact with Fc receptors on phagocytes and for complement activation

104
Q

What is antibody dependent cell-mediated cytotoxicity (ADCC) and which antibody mediates this?

A

> Infected host cells may express foreign proteins on their cell surface (e.g. virus envelope proteins), if we have previously made IgG antibodies against these virus proteins it allows specific recognition of infected host cells by cells such as NK cells with appropriate Fc receptors.

> Only IgG can do antibody dependent cell-mediated cytotoxicity (ADCC)

105
Q

What is the only way NK cells can kill infected red blood cells and why?

A

> Antibody dependent cell-mediated cytotoxicity (ADCC), as the red blood cell is coated in viral proteins which IgG antibodies bind to and NK cells can bind to the Fc regions and then go on to kill there blood cell via apoptosis.

> Normally can’t as don’t have MHCI receptors on surface. (important for malaria as red blood cells are infected)

106
Q

Which antibody class has a particularly long half life in serum?

A

IgG

107
Q

What are thymus a) dependent b) independent antigens?

A

a) B cell responses to most protein antigens require T cell help (thymus-dependent or TD antigens). E.g. virus proteins

b) Some microbial antigens can induce B cell responses in the absence of T cells (thymus-independent or TI antigens)

108
Q

What help by T cells is needed by thymus dependent antigens?

A

Somatic hypermutation, which is needed for class switching and tighter binding to antigen.

109
Q

What antibody class will be most prevalent in a mouse without a thymus and why?

A

IgM, as this is the main antibody in the primary response and if class switching cannot occur (without a thymus) then IgM cannot swap to IgG.

110
Q

Where do T cells mature, and what is meant by them “maturing”?

A

Mature in thymus, where they gain specific T cell receptors allowing them to bind to antigen.

111
Q

What are the 2 major subpopulations of T lymphocytes, what receptor protein is found on their surface and which is found more in healthy individuals?

A
  1. T-helper cells (CD4 protein)- main group in healthy individuals.
  2. T-cytotoxic cells (CD8 protein)
112
Q

What distinguishes T-helper cells and T-cytotoxic cells from each other?

A

Different receptor proteins on surface.

113
Q

What are the roles of 1) T-helper cells (CD4) 2) T-cytotoxic cells (CD8)?

A

1) Help B cells make antibody, activate macrophages and natural killer cells (help innate immune system), help development of cytotoxic T cells.

2) Recognise and kill infected host cells (intracellular pathogens)

114
Q

What does TCR stand for?

A

T lymphocyte receptor.

115
Q

How are T lymphocyte receptors (TCRs) structurally similar to the Fa arm of an antibody in 2 ways?

A

1) 2 chains (alpha and beta) with variable regions at the ends that bind to antigens, and constant domains which anchor into cell membrane of T lymphocyte.

2) Multiple V region exons can recombine during early T cell differentiation (similar to somatic recombination in B cells).

116
Q

What is a structural difference between TRCs and antibodies?

A

TRCs are never secreted while B cell receptors can be secreted (antibodies).

117
Q

What is the difference in how B cells and T cells recognise antigen?

A

Unlike B cells, T cells can only recognize host cell-associated (antigen presenting cell), processed antigen (only recognises process proteins, degraded into short peptides).

118
Q

What are MHCs (Major Histocompatibility proteins) and what is their function?

A

Transport processed antigen (peptides) from inside the cell to the surface of host cells.

119
Q

What are the 2 types of MHC protein (Major Histocompatibility proteins), where they expressed and what is their function?

A

1) MHC1: >Expressed by all nucleated cells (Self-label on all nucleated cells, recognised by NK cells too to determine self or not self) >Function: bind and display endogenous (protein that has been synthesised inside the antigen presenting cell) antigen to CD8+ve (cytotoxic) T cells

2) MHC2L >Expressed by macrophages, dendritic cells (have high levels, very good at presenting antigen to CD4 helper T cells), B cells >Function: display exogenous (antigen presenting cell has taken something up from environment then transports peptides from this external antigen to surface) antigen to CD4+ve (helper) T cells

120
Q

Why are dendritic cells efficient at contacting with T cells?

A

Dendritic cells have many projections (dendrites) giving big surface area.

121
Q

How do CD8 T cells recognise antigen and kill pathogens in 7 steps?

A
  1. Virus infects host cell ->
  2. host cell produces virus proteins ->
  3. some viral protein is broken down in the cytosol by proteosomes ->
  4. these peptides are transported to ER -> bind MCHI ->
  5. transported to cell surface ->
  6. TRCs on Cytotoxic T cell bind to peptide presented (CD8 stabilises this) ->
  7. induces apoptosis of host cell.
122
Q

What is the role of CD8 proteins for cytotoxic T cells?

A

CD8 helps stabilise the interaction between TRC and peptide presented by MHCI???? (or is CD4 what actually binds to the protein)

123
Q

What are the 5 steps to CD4 T helper cell function?

A
  1. Macrophage/ dendritic cell/ B cell internalize and break down bacterial protein ->
  2. in endosomal compartments the broken-down proteins bind MHCII ->
  3. transported to cell surface ->
  4. TRCs on T helper cells bind to bacterial proteins presented by MHCII (stabilised by CD4) ->
  5. helps make antibody, produce cytokines that activate/ regulate other leucocytes.
124
Q

What is the role of CD4 proteins for T helper cells?

A

CD4 helps stabilise the interaction between TRC and peptide presented by MHCI

125
Q

What is a Naïve T cell and where are they found?

A

T cells without specific TRCs for a pathogen. Found in the Thymus.

126
Q

What drives production of different sub-sets of T-helper cells, and what is the effect f having these different sub-sets?

A

In the secondary lymph nodes Naïve T helper cells (CD4) interact with different types of pathogen triggering development into different subsets that produce cytokines appropriate for that specific pathogen response.

127
Q

What type of Naïve T helper cell recognises peptide + MCII?

A

TH0 T cell is a Naïve CD4 T cell that recognises peptide + MCII

128
Q

How many different T helper cell subtypes can TH0 differentiate into and what are their names?

A

5 different subtypes: TH1, TH2, TH¬17, TFH, Treq

129
Q

What do the 5 different T helper cell subtypes of TH¬0 produce, their function, and what pathogen do they treat?

A

1) TH1 (inflammatory CD4 cells):
>Produce: interferon-γ (IFN- γ).
>Function: IFN- γ activates macrophages causing inflammation, B cells to make IgG (opsonizing antibodies), cytotoxic (CD8) T cells for intracellular infections.
>Treats: Extracellular bacteria (due to increasing IgG), microbes that persist in macrophage vesicles (e.g. mycobacteria) , viruses (due to CD8 T cell activation).

2) TH2 (most common in blood):
>Produce: IL-4.
>Function: IL-4 induces B cells to make IgE.
>Treats: Large parasites like Helminths (due to IgE), involved in allergens (IgE)

3) TH17 (mucosal surface CD4 cells):
>Produce: IL-17.
>Function: Found under mucosal surface IL-17 induces epithelial cells to make antimicrobial peptides, recruits neutrophils, pro-inflammatory.
>Treats: Extracellular bacteria (e.g. Klebsiella pneumoniae) and fungi (e.g. Candida albicans).

4) TFH (Follicular helper T cells):
>Produce: IL-21.
>Function: IL-21 helps induce B cell differentiation to plasma cells, class switching from IgM (class switching for secondary response), and affinity maturation of antibodies.
>Treats: Most microbes (important for most infections that need B cells to make antibodies)

5) Treg (regulatory T cells):
>Produces: IL-0, TGF- β (transforming growth factor).
>Function: IL-10 and TGF- β suppress inflammation by acting on other T cell subsets and suppress B cells to down regulate immune response once infection is dealt with.
>Protects: Self-molecules and natural flora against rogue NK cells.

130
Q

Why would someone with more TH1 than TH¬2 in their blood have more allergies?

A

TH¬1 is found in higher concentrations in a healthy person’s blood, if TH¬2 is found more then that would mean more B cells would switch to produce IgE which is responsible to overreaction to allergens.

131
Q

An overexpression of which T helper cell subtypes would lead to greater risk of autoimmune disease and why?

A

Overexpression of TH17 due to its pro-inflammatory nature

132
Q

What are follicles and which T helper cell subtype is found here?

A

Follicles are sections of lymph nodes close to B cells.

133
Q

Under-expression of which T helper cell subtype makes an individual more prone to developing autoimmune disease and why?

A

Treq as if less is present then the immune response is not downregulated as quickly, and more rogue NK cells will kill self-molecules.

134
Q

Once bound to an infected host cell, how do cytotoxic T cells (CD8) kill pathogen?

A

When bound to a host cell, secretes perforin to pierce a pore making perforin channels into infected host cell, secretes granzymes (like proteases) which activates caspase cascade to induce apoptosis.

135
Q

Why is it advantageous for NK cells and cytotoxic (CD8) T cells to kill pathogen via the apoptosis pathway instead of lysis?

A

Apoptosis means cell shrivels up and is cleaned up by macrophages, so no pathogen proteins are released for more infection.

136
Q

What is meant by Cytotoxic (CD8) T cells being efficient at killing pathogen?

A

A single cytotoxic T cell can kill 100s of infected targets. Once they’ve killed the infected host cell they quickly leave.

137
Q

When can B cells respond on their own to pathogen, and when do they need help of T cells?

A

B cells can respond on their own if it is a thymus independent antigen but if is a protein antigen needs help of T cells

138
Q

In 8 steps describe activation of adaptive immunity in a draining lymph node after infection from a bacterium.

A
  1. Infection through cut, bacteria enters
  2. Dendritic cells and macrophages in the tissues contact pathogen, they bind, break down and then present processed bacterial peptides on the surface.
  3. Travel through lymphatic vessels to nearest draining lymph node
  4. Lymph node contains naïve B and T cells, they leave quickly if no infection present, if infection they stay for longer
  5. Activation of T cells first, by dendritic cell presenting processed bacterial peptides on surface.
  6. T cells interact with B cells to divide and differentiate into plasma cells to create specific soluble antibodies.
    >B cells can respond on their own if it is a thymus independent antigen but if is a protein antigen needs help of T cells
  7. T cells and antibodies leave through lymphatic vessels to tissue to where they deal with the infection
    >T follicular helper cells are found a lot in lymphoid, help B cells class switch from IgM.
  8. Lymph node, generation of memory cells, migrate to bone marrow and stay around for a while to deal with re-infection quicker.
139
Q

After a vaccine against a pathogen, when infected what immune response is triggered?

A

Secondary immune response

140
Q

What are the 2 aims of vaccination?

A

Aim 1: Try Eradicate disease e.g. small pox (which caused 400 million deaths in 20th century) officially eliminated in 1979.

Aim 2: If can’t eradicate a disease completely, instead reduce incidence/transmission of disease

141
Q

What are 6 factors which favour global eradication of infectious disease by vaccinations?

A
  1. Disease limited to humans
    >No re-invasion by microbe from animal
  2. No long term carrier state
  3. Few unrecognised clinical cases
    >So surveillance is possible
  4. One or few stereotypes
    >Single vaccination is adequate
  5. Stable, cheap and effective vaccination available.
  6. Eradication programme is cost-effective
142
Q

When would herd immunity not apply and give an example?

A

Not for disease NOT spread by person-to-person contact e.g. tetanus

143
Q

What is herd immunity and its effect?

A

> When most of the population is immunised

> Spread of infection between person to person is constrained which protects immunocompromised people that can’t have vaccines.

144
Q

Describe an overview of how vaccines cause an immune response?

A

Vaccine injected into muscle -> dendritic cells -> transferred to nearest draining lymph node -> activation of T cells (CD8 + CD4) and B cells (memory and plasma cells) -> effective immune response.

145
Q

What is neutralising immunity?

A

When no infection is caused as vaccines allow memory B cell formation that secretes antibodies that neutralise the pathogen on second infection.

146
Q

What are the 3 main types of vaccination, what form of pathogen is inside and is it alive?

A
  1. Attenuated pathogen
    >Virulence reduced in pathogen so causes mild infection
    >Living (can replicate to some extent)
  2. Killed pathogen
    >Unable to replicate (e.g. by heating pathogens), still express antigens but can’t replicate.
    >Unliving
  3. Subunit
    >Immunise with molecular component(s) of pathogen
    >Unliving
147
Q

What are 6 properties a vaccine needs?

A
  1. Be safe
  2. Causes protection
  3. Cause long lived protection
  4. Induce neutralizing antibodies
    >Important for e.g. polio virus which would cause permanent neuron damage, so if neutralised before infection means less damage
  5. Induces protective T cells
  6. Practical
148
Q

What are two examples of how a vaccine can be “practical”?

A
  1. Low cost per dose
  2. Heat stable so doesn’t need special storage in warmer countries.
149
Q

Why does a living vaccine only require 1 dose as well as not needed an adjuvant while a non-living requires multiple as well as an Adjuvant?

A

As live vaccines mimic a real life infection so are more effective triggering cells mediated immunity as well as humoral while an intramuscular non-living pathogen may not trigger cell mediated immunity so not as many memory cells remain for long.

150
Q

What type of vaccine is cheapest?

A

Living pahogens

151
Q

Why is a Living Polio vaccine normally given orally?

A

As a natural route of infection triggers a stronger immune response.

152
Q

What is an Adjuvant?

A

Adjuvant – ingredient added to vaccines to enhance immune response by inducing local inflammation

153
Q

Why is a living pathogen vaccine not safe for immunocompromised individuals?

A

As the pathogen could replicate still despite being attenuated (weakened)

154
Q

What antibodies are found in an immune response after a) Living vaccine b) Un-living vaccine?

A

a) IgG, IgA, Cytotoxic T cells

b) Mainly IgG (not as good at protecting mucosal surfaces) and no Cytotoxic T cells (no cell mediated immunity triggered so no class switching too)

155
Q

What are 4 methods of attenuation, and what type of pathogen are they used for?

A
  1. Serial passage through cell culture in vitro for viruses
    >Grow pathogen in cell culture giving all they need to replicate so don’t make virulence factors anymore.
  2. Serial passage in vitro for bacteria
    >Culture in agar so stop making virulence factors
  3. Adaptation to low temperatures for viruses
    >Grow at low temp and become accustomed to this, so when entering warm human body don’t replicate.
  4. Genetic manipulation for any pathogen
    >Make the pathogen not produce toxins
156
Q

Why is a killed vaccine still able to produce side effects?

A

Due to the full pathogen being present it could still cause side effects despite being dead.

157
Q

How are killed vaccines made?

A

Replication of the pathogen is inactivated by chemicals so they cannot infect cells.

158
Q

What are the advantages and disadvantages of sub-unit vaccinations?

A
  1. Advantages
    >Less side effects
  2. Disadvantages
    >Multiple injections as is shorter lived immune response.
    >Requires adjuvants
159
Q

What is a Sub-unit vaccine?

A

Uses component of pathogen not whole organism

160
Q

What are 4 types of sub-units which can be altered for sub-unit vaccines?

A
  1. Toxoid: chemically inactivated toxin e.g. diphtheria, tetanus
  2. Recombinant protein (make proteins from pathogens by cloning, can modify the proteins) like a spike protein
  3. Subcellular fractions, subcellular components from the pathogen such as polysaccharide capsule
  4. Conjugate vaccines, link polysaccharide that activates B cell to a carrier protein which can activate T cells to (mediates memory B cell formation)
161
Q

What are Recombinant Vector Vaccines and how do they work?

A

Use vector (virus) to carry DNA or RNA encoding for a protein which is present in the pathogen we want to immunise against. This subunit will promote an immune response.

162
Q

Describe an example of a Recombinant vector vaccine in recent years?

A

AstraZeneca Covid vaccine:

Used chimp adenovirus (responsible for colds) to introduce gene which encodes for “spike” protein of covid, which it uses to attach to host cells.

163
Q

What are Nucleic acid (DNA/RNA) vaccines and how do they work?

A

> Use DNA or RNA to transiently express pathogen antigen in host cells:

  1. DNA- injected directly into muscles and taken up by cells
  2. mRAN- needs to be enclosed in lipid coat so is taken up by cells.
164
Q

What is an advantage to both recombinant vector vaccines and Nucleic acid (DNA/RNA) vaccines?

A

Both recombinant vector vaccines and DNA/RNA vaccines generate immune responses similar to natural infection

165
Q

What are 5 barriers for vaccines?

A
  1. Complex life-cycle of pathogen
  2. T cell immunity needed
  3. High mutation rates
  4. Many types of pathogen
  5. Complex storage (such as needing to be kept cool)

Microbiology Year 2 (7 decks)

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