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MBB163 > Partridge - Immune System > Flashcards

Partridge - Immune System Flashcards

1
Q

compare and contrast the strategies of of immune surveillance in bacteria, invertebrates and vertebrates

A

Bacteria:
- Restriction enzymes, CRISPR/Cas9
Invertebrates:
- Negative surveillance (ie cells marked with ‘self’ protein labels; unlabelled non-self cells destroyed by phagocytes)
Vertebrates:
- External barriers
- Negative surveillance by major histocompatibility proteins (MHC) - v polymorphic (it’s difficult for a pathogen to mimic these self-protein labels)
- Positive surveillance system – specific recognition of foreign cells

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2
Q

describe the features (when you get it/specificity/response/cell types/soluble factors) of the innate immune system

A
  • What you’re born with
  • Broad specificity
  • Resistance not improved by repeat infection
  • Rapid response (hrs)
  • Leucocytes: phagocytes, natural killer cells
  • Soluble factors: lysozyme, complement, interferons
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3
Q

describe the features (when you get it/specificity/response/cell types/soluble factors) of the adaptive immune system

A
  • Born with elements of it but it mainly adapts during lifetime
  • Highly specific
  • Resistance improved by repeat infection
  • Slower response (days/weeks)
  • Leucocytes: B and T lymphocytes
  • Soluble factors: antibody
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4
Q

name 5 external barriers to infection

A

Keratinized skin: keratin
Secretions: sebum, sweat, fatty acids, lactic acid, lysozyme
Mucous: cilia (respiratory tract)
Low pH: stomach pH 2.5
Commensals: friendly bacteria/fungi that prevent colonisation

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5
Q

what is a leucocyte?

A

white blood cell

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6
Q

name the types of phagocyte

A 
neutrophil
mononuclear phagocytes (monocytes and macrophages, dendritic cells)
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7
Q

name a type of lymphocyte

A

natural killer cell

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8
Q

describe the features of a neutrophil

A

Multilobed nucleus and granules in cytoplasm (slightly green, why snoosh is green)
Main phagocyte in blood
Short-lived, fast-moving
Lysosomes release enzymes H2O2 etc

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9
Q

describe the features of the mononuclear phagocytes

A 
Monocytes (when in the blood)
Macrophages (when in the tissues)
Monocytes and macrophages are the same but macrophages have slightly more complex morphology
Long-lived (months/years)
Helps initiate adaptive responses
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10
Q

describe the features of lymphocytes

A

Characteristic granules in cytoplasm
Kill virally infected cells non-specifically
Important in self/non-self recognition
May kill cancer cells (have altered properties that NKs can recognise)

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11
Q

describe the difference in pathogen recognition by innate cells (phagocytes and NKs)

A

Phagocytes:
- Have general pathogen-recognition receptors (PRRs) that recognise pathogen-associated molecular patterns (PAMPs)
Natural killer cells:
- Kill targets unless they recognise a self-protein (MHC)

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12
Q

describe the structure and function of defensins (type of soluble factor)

A
  • Peptides that have +ve charges meaning they can enter bacterial membranes and disrupt them
  • Made by neutrophils
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13
Q

describe the function of interferons (type of soluble factor)

A
  • Produced by virally infected cells and give to uninfected cells to protect them
  • Activate macrophages and NK cells
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14
Q

describe the function of cytokines (type of soluble factor)

A

‘hormones of the immune response’

  • small secreted proteins involved in cellular communication
  • eg interleukins – initiate and control immune responses
  • Produced by cells of the innate and adaptive immune system (in particular T-lymphocytes)
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15
Q

describe the function of inflammatory mediators (type of soluble factor)

A

cause inflammation eg histamine and prostaglandins

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16
Q

describe how inflammation occurs

A
  • Dilation of blood vessels (increases amount WBCs that can enter tissue)
  • Increased capillary permeability
  • Phagocytes migrate into tissues
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17
Q

what is an acute phase response?

A

a group of physiologic processes occurring soon after the onset of infection

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18
Q

state what happens during fever and how and why this occurs

A

On infection macrophages may release interleukin 1 (type of cytokine)

  • Acts on hypothalamus
  • Raises temperature
  • Stimulates phagocytosis
  • Reduces level of iron in blood (bacteria need high levels of iron to survive and replicate)
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19
Q

where are leucocytes made?

A

bone marrow stem cells

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20
Q

where are the 2 types of lymphocyte made? where do they mature?

A 
B-Lymphocytes:
- Mature in bone marrow
- Receptor is antibody
T-Lymphocytes
- Mature in thymus 
- They then go to the peripheral lymphoid tissue and undergo antigen-dependent differentiation (lymph nodes/spleen)
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21
Q

what type of immune response do the 2 types of lymphocytes have?

A

B-lymphocytes:
- humoral (antibody)
T-lymphocytes:
- cell-mediated (stimulate release phagocytes, other T-cells and cytokines)

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22
Q

who came up with the clonal selection hypothesis? describe this theory

A

When we get an infection (with an antibody that recognises the antigen) there is clonal expansion

  • This is the proliferation of correct antibody on B-cell
  • The plasma B-cells produce soluble antibodies
  • Some plasma cells differentiate into memory cells – used in 2ndry infection
  • Lymphocytes that recognise self are deleted in early development
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23
Q

name the 2 ways in which a vaccine is made

A

Types of vaccine:

  • Subunit eg toxoid (derived from toxin)
  • Attenuated strains
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24
Q

briefly describe the primary and secondary responses to infection

A

Primary response: takes longer to respond and [Ab] is not as high (this is what vaccination stimulates as well)
Secondary response: takes less time to respond and [Ab] is much higher (infection)

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25
Q

describe the cell-mediated and humoral (antibody) responses

A

Cell-mediated (T-cell) immune responses:
When a T-cell meets an antigen, it undergoes clonal selection/expansion and then differentiation therefore giving the cell immunological memory.
T-cells can only recognise antigen bound to host cells
Humoral (antibody) immunity:
Antigen stimulates B-cells which differentiate into plasma cells which produce soluble antibodies
(B-cells packed full of ER –> make loads of soluble antibodies)
Widely used in research and medicine

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26
Q

what type of protein is an antibody?

A

glycoprotein

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27
Q

name the 5 types of antibody, their heavy chain and their structure (eg monomer, dimer etc)

A

IgG – γ (monomer):
IgM – μ (pentamer – linked by disulphide bonds):
IgA – α (monomer in serum or dimer in secretions):
IgD – δ (monomer):
IgE- ε (monomer):

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28
Q

what do the 5 classes of antibody do?

A 
IgG:
- Main class in serum and tissues
- Important in secondary/memory responses
- Crosses placenta (only one that can do this)
IgM:
- Important in primary responses
IgA:
- In serum and secretions
- Protects mucosal surfaces
IgD: (don’t really know what it does)
IgE:
- Present at very low levels
- Protective against extracellular parasites
- Involved in allergy
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29
Q

what are the two types of light chain an antibody can possess?

A

2 light chain types: κ (kappa) and λ (lambda)

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30
Q

how are the variable and constant regions encoded?

A

they are encoded by different exons, and can therefore recombine in different combinations to match specific antigens

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31
Q

which antibodies are released in the priamry and secondary immune system response?

A

Primary response – IgM and then IgG a few days later
Secondary response – IgG (loads & lasts ages because of long half-life) and then some IgM
Secondary response can also include IgA or IgE depending on infection type

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32
Q

which antibodies can neutralise viral toxins

A

IgG and IgA

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33
Q

which antibodies can immobilise motile microbes?

A

IgM

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34
Q

which antibodies can prevent binding and infection of host cells?

A

IgM, IgA

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35
Q

which antibodies can activate complement?

A

IgG, IgM

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36
Q

which antibodies can bind phagocytes by their Fc region?

A

IgG, IgA

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37
Q

which antibodies can bind mast cells by their Fc region?

A

IgE

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38
Q

which antibodies can bind NK cells by their Fc region?

A

IgG

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39
Q

what are the 3 main biological activities of complement?

A

1) Activation of WBCs: induces neutrophils to move out of bloodstream into tissues, also induces inflammation – peptides C5a and C3a can act as chemoattractants to neutrophils. Mast cells (WBC) also have C5a/C3a receptors – induce anaphylatoxin (histamine) release
2) Opsonisation: C3b binds bacterial surface, phagocytes have C3b receptors and therefore can recognise them and take up bacteria more efficiently
3) Cell lysis: Membrane attack complex: C9 –> polymerize –>hollow cylinders which form pores in bacterial membranes. Bacteria is porous and molecules escape = osmotic shock and death

40
Q

what is complement?

A

Immune defence against bacteria (and viruses slightly). 20 serum proteins activated via an enzyme cascade.

41
Q

name the 3 ways in which complement can be activated

A

the classical pathway, the MB-lectin pathway or the alternative pathway

42
Q

name the complement factors in compliment, which is the most abundant?

A

C1, 4, 2, 3, 5, 6, 7, 8, 9 (in order but you don’t need to know the order)
C3 is the most abundant

43
Q

describe the classical pathway

A

the globular heads of C1 can bind to the Fc region of 2 IgG molecules or 1 Fc region of IgM. C1, 2, 3, 4 activated to form the membrane attack complex

44
Q

why is IgM a more potent activator of compliment?

A

IgM can form a pentamer therefore there are more Fc regions

45
Q

how do IgG and IgA act as opsonins?

A

IgA/M bound to a bacterium bind to Fc receptors on phagocyte. This creates pseudopods which engulf and fuse around the antibody coated bacterium. This creates a phagosome (vesicle containing bacterium) which then fuses with the lysosomes forming a phagolysosome. The bacteria is then destroyed by acid/peptides/proteins/toxic oxygen derivatives/enzymes

46
Q

what are mast cells? where are they usually found?

A

mononuclear phagocytes involved in the release of inflammatory mediators. usually found underlying mucosal tissue

47
Q

which antibody(s) can bind to NK cells?

A

IgG

48
Q

describe antibody dependent cell-mediated cytotoxicity

A

NKs are lymphocytes which recognise infected host cells (not phagocytic)
Fc receptor on NK binds antibody bound to antigen on an infected host-cell
NK starts to make perforin (protein) – perforates membrane of infected cell (structure like membrane attack complex)
This doesn’t kill the host cell, the NK uses it as a channel in which it pumps granules full of enzymes to make the infected cell undergo apoptosis

49
Q

how are Fc receptors on mast cells used in an allergic response?

A

initial exposure to the allergen means it (the allergen) binds to IgE and causes a large amount of IgE to be produced. During a second exposure IgE binds to Fc receptors on mast cells. The IgE cross-link and trigger the response of the mast cell which undergoes degranulation. Inflammatory mediators are released and cause local inflammation. This is beneficial in response to parasites.

50
Q

whats the difference between polyclonal and monoclonal antibodies?

A

monoclonal: A Monoclonal antibody, by contrast, represents antibody from a single antibody producing B cell and therefore only binds with one unique epitope
polyclonal: antibodies that are secreted by different B cell lineages within the body. They are a collection of immunoglobulin molecules that react against a specific antigen, each identifying a different epitope.

51
Q

how are polyclonal antibodies produced?

A
  • Immunise animal with pure preparation of molecule you’re interested in
  • primary and secondary response occurs
  • Take a sample of blood, allow to clot to remove clotting factors, take clear solution left (contains antibodies
52
Q

how are monoclonal antibodies produced?

A
  • Derived from single B-cell fused with a tumour cell line
  • Tumour cell is a type of mutant plasma cell which can’t make its own antibodies
  • Hybrid cells make antibody and divide indefinitely
53
Q

name the 4 ways in which antibodies are used in research, diagnostics and therapy

A

1) Identifying and labelling molecules in complex mixtures
2) Serotyping pathogens – the differentiation between different bacterial strains
3) Characterising cell surface proteins, identifying cell types
4) Humanised antibodies are used in therapy - antibodies from non-human species whose protein sequences have been modified to increase their similarity to antibody variants produced naturally in humans.

54
Q

name the 2 major subgroups of T cells and what they do

A 
T-helper cells (CD4 +ve):
- Help B cells make antibodies
- Activate macrophages and NKs
- Help development of cytotoxic T cells
T-cytotoxic cells (CD8 +ve)
- Recognise and kill infected host cells
55
Q

describe the structure of the T lymphocyte receptor

A

Receptor only ever on the membrane, never secreted
α-helix allows the receptor to cross the membrane
Two domain structure, linked by disulphide link (α and β units)
Similar to Fab arm of antibody
- Has variable and constant regions (constant closest to membrane)

56
Q

how do T and B cells differ in antigen recognition?

A

B-cells recognise soluble, free, native (antigen that hasn’t been processed in anyway) antigens
T-cells recognise cell-associated (attached to body’s own cells), processed (broken into peptides) antigen

57
Q

what are Major Histocompatibility Proteins (MHCs)?

A

small proteins that bind to processed antigen in order for infected host cells to be recognised by T-cells

58
Q

how are Major Histocompatibility Proteins (MHCs) encoded?

A

Encoded by the Major Histocompatibility gene Complex (MHC) on chromosome 6

59
Q

what is the significance of MHCs being highly polymorphic?

A

their polymorphism (variability of alleles at each gene) means they can bind a wide range of processed antigens (peptides) and therefore have a broad specificity.

60
Q

which cells express MHC I and which cell do they present to?

A

Expressed by all nucleated cells

Display antigen to CD8 +ve (cytotoxic) T-cells

61
Q

which cells express MHC II and which cell do they present to?

A

Expressed by macrophages, dendritic cells, B-cells

Display antigen to CD4 +ve (helper) T-cells

62
Q

how do MHC I processed antigens reach the cell membrane? how does the specific T-cell deal with the infected host cell?

A

Virus-infected cell –> viral proteins, broken down in cytosol (proteosomes)
Peptides transported to ER, bind MHC I –> cell surface
Activated cytotoxic T-cells kill the infected cell (via perforins etc) by inducing apoptosis

63
Q

how do MHC II processed antigens reach the cell membrane? how does the specific T-cell deal with the infected host cell?

A

Macrophage/dendritic cell/B-cell intenalises and breaks down foreign material
Peptides bind to MHC II in endosomes –> cell surface
Activated T helper cells help B cells make antibodies, produce cytokines that activate/regulate oter leucocytes

64
Q

cytokines are produced and act locally, why is this?

A

Cytokines are toxic in high concentrations therefore need to act locally

65
Q

what are the 4 main groups of cytokines

A

interleukins
chemokines
colony stimulating factors
interferons

66
Q

which cells usually produce interleukins? roughly how many interleukins are there?

A

usually T cells

approx 38 of them

67
Q

when are interferons released? which ones are released when?

A
  • Viral infections eg IFNα, IFNβ

- Immune system cell activation eg IFNγ

68
Q

what do chemokines do?

A

cell movement (chemotaxis)

69
Q

what do colony stimulating factors do?

A

stimulate leukocyte production

70
Q

what happens when a cytokine binds to its receptor?

A

Binding of a cytokine to its receptor can cause cell activation and changes in gene expression

  • Many are dimeric enzyme-coupled receptors
  • Chemokine receptors are G-protein coupled receptors
71
Q

name the 2 subgroups of CD4+ve cells

A

TH1 and Th2 cells

72
Q

what do TH1 and TH2 cells do?

A 
TH1 cells:
- Produce IL-2, γ-interferon and TNFβ.
- Activate macrophages
- Induce B-cells to make opsonizing antibodies (IgG)
TH2 cells:
- Produce IL-4, 5, 6, 10, 13. 
- Induce B-cells to make IgE
73
Q

what do T regulatory cells (TREGs) do?

A

Produce IL10, IL35 – suppress other T-cells

74
Q

what is the hygiene hypothesis and who came up with it?

A

the lack of exposure to ‘dirt’ (bacteria). Insufficient exposure to certain types of infection skew TH1/TH2 balance towards TH2 (which is parasite/allergy TH cell type)
BUT negative correlation between helminth (parasite) infections and allergic disease
Infection releases both TH1&2 as well as TREGs therefore insufficient exposure to infection prevents TREG development

75
Q

how does lymph travel through the body?

A

Lymph is an extracellular fluid that accumulates in tissues and is carried by lymphatic vessels back to through the lymphatic system to the thoracic duct and into the blood

76
Q

what happens when bacteria enter the skin and it becomes infected? (ie describe the activation of adaptive immunity in the draining lymph node)

A

1st: bacteria are phagocytosed by macrophages; and presented on dendritic cells
2nd: dendritic cells and macrophages enter the lymphatic system and travel to lymph node
3rd: if T-cell comes across dendritic cell with foreign antigen => T cell activation (production cytokines)
4th: Cytokines stimulate B cells to divide and differentiate into plasma cells => antibody production
5th: Antibodies and T cells exit lymph node to circulate

77
Q

what type of virus is HIV?

A

retrovirus

78
Q

what does the HIV nucleocapsid contain?

A

Nucleocapsid contains 2xssRNA, RT, protease, integrase

79
Q

how does HIV replicate?

A

Virus binds cell receptor – virus recognises membrane proteins
Virus envelope fuses with plamsa membrane
Nucleocapsid enter cytoplasm
Viral RNA reverse transcribed into dsDNA
Viral DNA trasnported to nucleus and integrates into host cell genome – forms a provirus
- Provirus is not replicating or making proteins

80
Q

HIV infections can be classed into 3 groups: latent, permissive, lytic. Describe each of these groups

A

Latent:
- Provirus
Permissive:
- Small amounts of transc/transl and the host cell is kept alive
Lytic:
- Lots of proteins being made, cell death by lysis

81
Q

which immune cell is susceptible to HIV infection?

A

CD4+ve cells (T helper cells) susceptible to infection (GP120 protein binds to CD4+ve receptor)

82
Q

how do latent HIV proviruses become activated?

A

T cell stimulation activates HIV provirus transcription

  • Number of T cells infected increases with each round of viral replication
  • Will eventually lyse cells
83
Q

what is the significance of monocytes becoming infected with HIV?

A

Monocytes may traverse the blood/brain barrier –> CNS involvement

84
Q

what happens if there are no chemokine receptors on CD4+ve cells when HIV has entered the body?

A

CD4+ve expression not sufficient for HIV infection – must be expression of coreceptor (chemokine receptors) on cell surface for HIV to use
- In an experiment a human CD4+ve receptor was expressed in a mouse without coreceptors, the mouse’s cells weren’t infected by HIV

85
Q

why do young and healthy people take longer to develop AIDS?

A

they produce lots of chemokine which occupy chemokine receptors meaning HIV can’t bind

86
Q

how are T helper cells depleted by HIV?

A

Direct lysis by virus
Killed by cytotoxic T cells or other immune mechanisms
Apoptosis

87
Q

what happens if the T helper cell conc decreases below:

  • 500 T cells per μl
  • 200 T cells per μl
A
  • 500 T cells per μl: symptoms develop

- 200 T cells per μl: AIDS

88
Q

what are some of the symptoms associated with AIDS?

A

Opportunistic infections
Reactivation of latent viruses
Rare cancers
CNS involvement, dementia

89
Q

state the origin, lineages and severity of HIV-1

A

Origin = Central Africa
4 lineages (M, N, O, P) each transmitted independently from primates to humans
- M is the pandemic form
- Likely source is a subgroup of chimpanzees
- Cross-species transmission in ’10-‘30
- 9M subtypes that predominate in different locations

90
Q

state the origin and severity of HIV-2

A

Origin = W Africa
Predates HIV-1
Likely source = sooty mangabees
Less virulent and less easily transmitted

91
Q

how is HIV transmitted? when are you most infectious if you have HIV?

A 
Most infectious immediately after infection
Unprotected sex
Blood/blood products 
Breats-feeding
Mother to foetus
92
Q

name the 5 methods of preventing and/or treating HIV

A 
vaccines
drug therapy
immunisation (kick and kill)
passive immunisation
gene editing(? - this is one for the future)
93
Q

name the problems associated with vaccination and HIV

A

High mutation rate of virus
Humoral immunity may not be protective you need to induce the cytotoxic T cells
Several vaccine trials (some failures but also some recent successes)
Success: RV144 pox virus (inactivated) + HIV proteins (30% success rate)

94
Q

name the problems associated with drug therapy and HIV

A

High mutation rate
Toxicity (side effects)
Viral latency (person doesn’t express symptoms so early treatment isn’t possible and late treatment is significantly less effective)
Cost

95
Q

what is combination therapy?

A

3 different drugs used in tandem; HIV can’t mutate fast enough to overcome them

96
Q

name 4 examples of drug therapy

A

AZT (prevents viral replication)
Inhibitors of reverse transcriptase
HIV protease inhibitors
Fusion inhibitors

97
Q

describe the kick and kill method of treatment

A

Vaccine stimulates cytotoxic T cells – boosts own immune system so they start killing the virally infected T helper cells.
Then drugs are used to induce the infection (activate latent infection)
The vaccine-stimulated cytotoxic T cells then kill the infected T helper cells

MBB163 (12 decks)

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