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2X Study > 5 - Microbes and the Immune System > Flashcards

5 - Microbes and the Immune System Flashcards

1
Q

What makes up the microbiome and the three types?

A

The microbiome consists of a large and mixed populations of microorganisms which coexist - microbes are rarely found in isolation or pure culture.
Types: bacterial, virome and mycobiome (fungal).

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2
Q

What is mutualism and give two bacterial examples.

A

Mutualism - mutually rely on one another, both benefit.
(1) Colonic bacteria is provided with a niche, and the host receives synthesised vitamin K and folate for metabolism.
(2) Ruminococcus spp. breaks down cellulose which aids the gut flow, and bacteria gains place to live.

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3
Q

What is commensalism and give two examples.

A

Commensalism - one benefits and the other remains unchanged.
(1) Bacteroides benefit from e. coli in humans.
(2) staphylococcus is shed of with dead skin cells which it utilises.

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4
Q

Give a fungal example of mutualism.

A

Mycorrhizae is a fungal mycelium which is associated with plant roots - it attaches to the root to allow for extension, and it gains nutrients via hyphenating in return. Fungus also gives nutrients, decomposition of organic matter, disease resistance and removal of heavy metal toxicity.

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5
Q

What is parasitism and its effects, giving examples?

A

Parasitism - one benefits (not necessarily a parasite) and the other is harmed.
They live on or in the host and may multiply, causing damage to the host - can lead to severe illness and even mortality.
Examples: Ebola, malaria, anthrax, histoplasmosis.

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6
Q

When would someone gain a fungal infection?

A

You must already be immunodeficient - unlikely for an exception to occur.

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7
Q

What are opportunistic pathogens and give examples.

A

These typically do not cause disease as they colonise us all the time, but if exposed to stress they will act.
e.g. herpes, candidiasis.

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8
Q

What are Koch’s postulates and their purpose (4)?

A

Criteria for identifying a pathogen.
1 - suspected pathogen must be absent in healthy and present in diseased.
2 - pathogen must be isolated and grown in pure culture from diseased.
3 - pathogen must cause same disease if used to inoculate a healthy host.
4 - same organism must be re-isolated from inoculated diseased.

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9
Q

What are the limitations of Koch’s postulates (4)?

A

1 - some diseased forms are asymptomatic
2 - mice are not representative
3 - viruses cannot be cultured (specific conditions)
4 - other microbes are difficult to culture

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10
Q

How and who updated Koch’s postulates?

A

Stanley Falkow adapted Koch’s theory by looking at the isolation of genetic material - enables pathogen identification.

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11
Q

What is pathogenicity, virulence factors and virulence - and their association?

A

Pathogenicity - the ability to cause disease.
Virulence factors - molecules which are required to cause disease.
Virulence - degree of pathogenicity.
They do not necessarily work together or at the same rate e.g. common cold has a high infection rate but low intensity.

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12
Q

What does phenotypic switching do and describe the process of an opportunistic pathogen?

A

Phenotypic switching can allow for increased adherence, biofilm development and invasion.
Process: budding yeast becomes a true hyphae which penetrates and invades the skin, causing vascular dissemination and colonisation of epithelial cells.

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13
Q

What issues do we face when identifying microbes (3)?

A

1 - weeks to grow
2 - agar plates restrict growth
3 - lab conditions not replicative of reality/natural environments

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14
Q

What are the two techniques used for identifying microbes?

A

Microarray - allows us to measure fluorescence and determine what genes are expressed using cDNA.
Transcriptomics - look at specific genes of interest (isolation of mRNA).

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15
Q

What is a viruses aim and its structure?

A

Its aim is to replicate within a cell, and it can either be made up of RNA or DNA, with a protective protein shell.

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16
Q

Give an example of positive and negative RNA strand viruses.

A

+ = HIV-1, Zika
- = Influenza, Rabies

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17
Q

Give the general differences between DNA and RNA.

A

DNA - uracil, ss, nuclear and cytoplasmic, OH at 2’, high intrinsic ability, error correction, long-term storage, low mutation rate.
RNA - thymine, ds, nuclear, H at 2’, smaller due to instability, no error correction, short-term storage, high mutation rate.

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18
Q

Describe viral heterogenicity.

A

This is driven and dependent on the mutation rate, and viral fitness will drive selection - positive selected for.

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19
Q

What is antigenic variation driven by?

A

Mutation rate and positive mutation selection.

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20
Q

What is antigenic drift?

A

This is a stochastic process in which antigens accumulate small mutations - and if any are advantageous, it will become predominant through selective pressure - e.g. resistance will be selected for.

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21
Q

What is antigenic shift?

A

This is a major alteration in the antigen sequence by genome reassortment (segmented virus) or inter-strain recombination.

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22
Q

What are segmented viruses and an issue which can occur?

A

These have a genome whose encoded genes are divided across two or more molecules of RNA/DNA - all must be incorporated in viral particle for it to be infective.
Issues occur when multiple viruses are multiplying within a cell and they cannot tell segments apart - genome recombination.

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23
Q

What is recombination?

A

Major alterations which gain new or functionally altered protein through exchange of genetic material between viruses or with the host - can lead to antigenic shifts and allows for genomic diversification.

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24
Q

What is mimicry?

A

Viruses can mimic the receptors preventing the immuno-modulators from acting - no signal - e.g. dsDNA can produce decoys.

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25
Q

What is latency and its benefits?

A

DNA viruses can wait (sleep) until the body is immunosuppressed to act - yields a bigger effect, whereas RNA viruses act as soon as they enter.
This benefits DNA infections as they last longer as there is a lack of immune response when infected cells are in a latent state - recurring infections.

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26
Q

What is a phage?

A

A virus which infects a bacteria.

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27
Q

What can mutations alter (3)?

A

1 - efficacy of antibiotic by alteration of target site
2 - receptor recognition
3 - recognition by host

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28
Q

What is natural transformation (acquire new genes)?

A
  • Uptake and incorporation of naked DNA
  • Occurs when bacteria is naturally competent and ssDNA is released during bacterial lysis
  • DNA can be combined with similar existing DNA
  • Evolved to allow repair and exchange of DNA in communities (biofilm etc)
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29
Q

How do bacteria become competent?

A

In response to quorum sensing signals as these increase the expression of competency factors - these modify bacterial membrane and allow uptake of ssDNA.

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30
Q

What is conjugation (acquire new genes)?

A
  • The genetic exchange between bacteria via sex pilus (protrudes from donor)
  • F+ strain (has desired gene) includes conjugative plasmid
  • Several proteins required
  • Associated with multi-resistant strains
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31
Q

What is transduction (acquire new genes)?

A

The exchange of genes which occurs as a consequence of phage predation.

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32
Q

What is the lytic cycle - transduction?

A
  • Results in replication of a bacterial genome and destruction of bacteria
  • Virus binds to surface receptor and genome inserted in virus head
  • Hijacks machinery producing multiple genome copies
  • Intact molecules escape via lysis
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33
Q

What is the lysogenic cycle - transduction?

A
  • Results in integration of bacteriophage DNA into bacterial chromosome
  • DNA genome injected and integrated into chromosome
  • Remains here, becoming a normal part
  • If stress or differing conditions occur, bacteriophage reverts to lytic cycle
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34
Q

What is the difference between generalised and specialised transduction?

A

General - DNA may or may not integrate, and site of integration is defined by sequence packaged
Special - transduction occurs at much higher frequencies - DNA will integrate

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35
Q

How can we tell that traits have been acquired via horizontal transfer?

A

Scars created in the chromosome following homologous recombination events.

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36
Q

What are pathogenicity islands?

A

Large pieces of DNA which encode for multiple genes that are integrated into the chromosome - virulence traits.

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37
Q

Why may introduced DNA not persist in a bacterium?

A

Due to restriction sites like CRISPR-Cas9 which recognise and destroy foreign DNA.

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38
Q

Why is gene expression key to a bacterium (2)?

A

It regulates the capacity to sense and respond via mechanisms - tightly controlled. It also is essential in avoiding waste of limited (small size) resources.

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39
Q

What is quorum sensing?

A
  • Results in changes in gene expression due to signalling at a population-level
  • Bacteria sense their population size and coordinate behaviour in response
  • These changes depend on low or high bacterial density and the accumulation of auto-inducer proteins
  • Controls expression of several traits
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40
Q

How does the accumulation of autoinducer proteins occur?

A

They are in naturally low levels in both the bacteria and the environment, but as the population grows, the constant diffusion causes an increase in environmental levels.

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41
Q

Give an example of quorum sensing.

A
  • Bacteria in squid produce fluorescent light to hide the shadow cast - preventing predation
  • Occurs via production of auto-inducers encoded by lux gene which diffuse out of the cell
  • As population grows there is an increase in lux expression so more autoinducers in the environment - once too high they diffuse back into the cell (gradient)
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42
Q

What is environmental sensing?

A
  • Results in changes in gene expression within an individual bacterium
  • Two component signal transduction in response to environmental signals
  • Relies on interaction between two proteins in response to a stimulus
  • Upon stimulus, transmembrane sensor kinase undergoes conformational change that indicates autophosphorylation of kinase domain, then it interacts with second response regulator, transferring P group and activating transcription regulator - transphosphorylated and acts to enhance/repress gene expression
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43
Q

Give three examples of environmental sensing systems.

A

Goldilocks syndrome - regulates pore size via turning on/off
CheAW/Y - flagella movement towards nutrients
phoPQ - enhances virulence via expressing Salmonella traits

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44
Q

What are the different sources of energy and carbon for microbes and associated names?

A

Energy:
Light - photo
Chemical oxidation - chemo
Carbon:
CO2 - auto
Organic compounds - hetero
We are chemoheterotrophs.

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45
Q

What is a psychrophile and how does it deal with the conditions?

A

Optimum growth in <15 degrees, and the membrane will become too solid so the unsaturated fat content increases to keep it interactive and fluid.

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46
Q

What is a hyperthermophile and how does it tolerate the conditions?

A

Survival requires >70 e.g. Taq. The membrane will become too liquid so the fats solidify by increasing fat content.

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47
Q

What is a mesophiles optimal conditions?

A

Body temperature.

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48
Q

What are cryoprotectants?

A

These are cold/heat shock proteins which assist by preventing proteins from unfolding/denaturing and maintain correct structure.

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49
Q

What is the difference between the neritic and oceanic zone?

A

Neritic - diverse life, easy light access, low pressure, nutrient-rich.
Oceanic - pressure increases with depth, home to chemotrophs (unstable zone).

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50
Q

What is red snow caused by?

A

Chlamydomonas nivalis.

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51
Q

Give two examples of how microbes are used in technology.

A

Restriction enzymes - used for protection and defence from viral infection.
CRISPR-Cas9 - binds with new infection, protein Cas9 cuts DNA at specific site allowing insertion, deletion, expression etc.

52
Q

Give two examples of how microbes can be used for vaccines.

A

Recombinant vaccines - HBV infection causes chronic liver disease - vaccine expresses HepB antigen in yeast cells.
COVID - spike proteins used and produced, triggering immune response, hence destroying cells.

53
Q

Give two uses of microbes in medicine.

A

Cancer - cervical, gastric and bladder.
Antibiotics - inhibit cell wall biosynthesis etc.

54
Q

What is the microbiota?

A

This is a stable interdependent community of microbes that are mainly found in the colon, but also in the lungs, skin, teeth etc.
Most are non-culturable.

55
Q

State three methods we could use to study non-culturable microbes.

A

16S sequencing, whole genome sequencing/metagenomics, and computation.

56
Q

What is 16S sequencing and its four properties?

A

Ribosomal RNA only made by 16S region - a sequence found in every bacteria and so if we only sequence this we can identify the bacterium. It is highly conserved and only differs minorly between species.
1. Identification of species and relative frequencies
2. Phylogenetic view of community composition
3. Low cost
4. Inferred functions

57
Q

What is whole genome sequencing and its 4 properties?

A

This is when we sequence all DNA from a bacterial population to generate more data but requires power software.
1. Identification of variants and polymorphisms
2. Accurate function
3. Better identification than 16S
4. High costs

58
Q

How/when do we develop a microbiota - what microbes?

A
  • Begins from birth (microbes from post-natal life have biggest impact)
  • Adult diet reached at 3 years (adult-like microbiota)
  • Post-natal factors: breast-feeding, environment, host genetics, pet ownership etc.
  • Microbiota most similar to those from our formation years
  • Environment determines bacteria - oil, dry skin etc.
  • We each have characteristic species - bacterial fingerprint
  • Co-dependent (we evolved with them)
59
Q

How would our stable microbiota communities stray from normal?

A

Due to obesity and IBD - alters normal types.

60
Q

Why is our microbiota key for our health (4)?

A
  • Limits pathogen colonisation
  • Form epithelial barrier
  • Butyrate (generated from food we ingest by bacterial fermentation of dietary fibres) has anti-inflammatory effects (t-cells)
  • Short chain fatty acids circulate and cand decrease allergic airway inflammation
61
Q

Why do probiotics make little to no difference?

A

Our microbiota is likely already colonised by the bacteria, and our microbiota is so stable that it is unlikely to be colonised by anything else - causes no harm but has little efficacy.

62
Q

What are the links between our microbiota and IBD?

A

IBD occurs in those with host genetic factors where the immune system begins to attack intestinal bacteria (misdirected). Inflammation occurs and lesions appear on the colon due to attack of the immune system - and abnormal colonisation could contribute. Immune specialisations go wrong, causing IBD.

63
Q

What is the issues and solutions surrounding Clostridium Difficile?

A

Issue: can develop antibiotic resistance and grows a mono-culture which colonises epithelial surface and damages colon.
Solution: faecal matter transplant reintroduces good microbe culture (risks of transferring other illnesses and unknown pathogens) - less successful for intestinal bacteria in other conditions.

64
Q

What occurs during the initial immune response?

A

There is an increase in the permeability of local blood vessels and the migration into tissues of dendritic cells, macrophages, and mast cells - causes acute inflammation.

65
Q

What are PAMPs?

A

Pathogen associated molecular patterns which make microbes distinct from mammalian cells.

66
Q

What are DAMPs and what releases them?

A

Damage associated molecular patterns which are evidence of trauma or infection - damage to tissue.
These are released by dying cells such as metabolites, nucleic acids etc.

67
Q

What is the complement cascade and its three steps?

A

A series of plasma proteins that act via an enzymatic cascade to control pathogens.
1 - C3a and C5a released at infection site and enhance acute inflammation (influx of immune cells).
2 - Complement receptor accepts microbes encoded by C3b and phagocytosis occurs - faster clearance and killing.
3 - Formation of membrane attack complex killing the pathogens.
Host cells and some pathogens can evade this.

68
Q

What are the 5 PRRs (pattern recognition receptors) and their molecules/site?

A

1 - TLR - PAMPs, membrane.
2 - NLR - PAMPs/DAMPs, cytoplasm.
3 - CLR - pathogen and host carbohydrates - membrane.
4 - ALR - bacterial/viral cytoplasmic DNA.
5 - RLR - pathogen or host ss/ds DNA, cytoplasm.

69
Q

Give two examples of microbes which evade the NLRs.

A

1 - Polio virus steals host RNA caps to hide and appear as host mRNA.
2 - Listeria monocytogenes - altered cell wall.

70
Q

What are the human consequences to microbial sensing (3)?

A

1 - tell neighbouring cells (inflammatory cytokines made)
2 - tells adaptive immune system pathogens are present - phagocytosis and taken to draining lymph nodes
3 - limit microbial replication (control of resources)

71
Q

How does E.coli evade immune detection?

A

NF-kB is a transcription factor which alters gene transcription to warn of infection. E.coli virulence factors degrade NF-kB and the shigella enzymes causes degradation of NF-kB activator, downregulating inflammation.

72
Q

What is the normal response to influenza?

A

Influenza causes inflammatory cytokine release and cell death, which leads to an immune response. Type 1 IFN can reduce the viral spread by warning neighbouring cells.

73
Q

How does influenza evade immune detection?

A

It infects epithelial cells and can block the inflammatory response - inhibits activation of PRRs and reduces anti-viral response (cytokines cannot warn system and IFNs cannot reduce spread.

74
Q

What four scenarios are antibiotics used in?

A

1 - routine surgeries
2 - organ transplantation
3 - chemotherapy and other cancer treatments
4 - childbirth

75
Q

Give the 6 primary causes of antibiotic resistance.

A

1 - over-prescription
> more prescriptions = more resistant isolates in population
> education and rapid diagnostic tests to identify if antibiotics are necessary
2 - unfinished course
> take someone else’s, skip a day or not finish = infection not killed
> bacteria then grows and mutates
3 - over-use in livestock and fish farming
4 - poor infection control in clinics/hospitals
5 - lack of hygiene/sanitation
6 - lack of new antibiotics

76
Q

How does a beta-lactam antibiotic work?

A

Bind to penicillin binding proteins in bacteria and prevents cross-linking of peptidoglycan layer of cell wall. Membranes begin to bulge and lysis occurs as pressure builds.

77
Q

When was the golden era?

A

1943-1961

78
Q

What is the difference between intrinsic and acquired resistance?

A

Intrinsic - bacteria naturally resistant to antibiotics
Acquired - develop resistance via mutation or horizontal gene transfer

79
Q

What are the four mechanisms of antibiotic resistance?

A

1 - reduced drug uptake (less porins so less antibiotic in)
2 - enzymatic degradation
3 - target modification - binding site
4 - increased drug efflux - pump out

80
Q

How do parasites evade the immune system via location?

A

1 - intracellular (plasmodium - liver, toxoplasma - macrophages) Triatome bugs can suck blood and defecate parasites, which are rubbed into wound and cause damage to residing organs.
2 - cysts (toxoplasma and echinococcus) - hard shell and may burst out.

81
Q

How do parasites evade the immune system via antigenic mimicry?

A

Schistosoma burrow from skin into bloodstream covered in proteins/antigens so is disguised

82
Q

Which parasites evade the immune system via immunosuppression?

A

T. cruzi, T. brucei, filarial worms, and schistosoma.

83
Q

How do parasites evade the immune system via antigenic variation?

A

Immune system responds to antigens, not whole organism so the organism varies what parts are shown to immune system - plasmodium, T. brucei etc.

84
Q

What are trypanosomes?

A
  • T. cruzi
  • Persist in CNS and brain
  • Lack of sleep/wake control
  • Sleeping sickness
  • Tsetse flies
85
Q

How do trypanosomes evade the immune system?

A
  • Antigenic variation
  • Alter coat which the complement cannot go beyond
  • 20% genome devoted
  • Coat switched via either new expression site in ES-body or transfer of new VSG gene, changing it and expressing a new one.
  • Ribosomal genes control VSG expression.
86
Q

What is the issue with parasitic worms and the usual immune response mechanisms?

A
  • Macro-parasites
  • Complement cannot penetrate waxy cuticle
  • Macrophages cannot phagocytose worm due to size
  • Antibody binding not effective
87
Q

What is the immune response to parasitic helminths and its action?

A

IgE - evolved for helminth infection.
- IgE binds to worm and its functional tail binds to specific receptors - eosinophils.
Either:
- Secretion of major basic proteins penetrate worms cuticle
- Release of histamine relaxes blood vessels and allows immune system action due to unclogging

88
Q

Where else may we see the histamine reaction?

A

Effective to allergens - displays same IgE response to pollen (allergic reaction).

89
Q

What is the network regulatory T cells action and its link with helminths?

A
  • T cells calm the immune system and helminths also secrete these.
  • No routine systemic helminth infections in an area means no stimulation
  • This lack of regulatory T cell stimulation makes us vulnerable - inappropriate allergen responses
  • Hygiene hypothesis (germ exposure)
  • Evolution with parasitic worms (tolerate)
90
Q

What is worm therapy and give two examples.

A

> Potential to use calming molecules that worms produce.
IBD - could relieve symptoms and trigger calming via eggs or worms (whip worms - short-term)
Rheumatoid arthritis - anti-inflammatory drugs which are small chemical molecules which mimic protein (ES-62) activity as protein itself cannot be used.

91
Q

What is overvaccination?

A

No adverse effects but no positive/negative effects either. The antibody production usually always sits at a comfortable low level anyway.

92
Q

How do memory B lymphocytes compare to naïve?

A
  • longer lived, occupy specific niches, increased frequency, rapid proliferation, more Ab produced with high affinity (via maturation) and class switching
  • IgG and IgA have better effector functions than IgM
93
Q

Describe the secondary Ab response properties.

A
  • faster, higher, isotope switched, higher antigen affinity.
  • germinal centre drives affinity maturation and class switching of memory B and long-lived plasma cells
94
Q

What cells do vaccines induce?

A

Long-lived plasma cells and plasma antibody responses.

95
Q

How do memory T lymphocytes compare to naïve?

A
  • long-lived, increased frequency
  • rapid proliferation due to lower activation threshold (less signals)
  • T cells do not undergo affinity maturation (no receptor change)
  • Vaccine use for killing tumour cells
96
Q

How does vaccine attenuation work (4)?

A

1 - virus isolated and cultured on host cells
2 - virus incubated on cells from another host - select those for better growth
3 - virus grows and mutates spontaneously
4 - ensure mutated virus cannot grow on human cells as we want to shift host range efficiently

97
Q

What is a killed vaccine?

A

Chemicals/heat used to kill organism and render it non-infectious - can still induce immunity

98
Q

What is a subunit vaccine?

A

Chemically inactivate toxins called toxoids used to generate antibody response.

99
Q

What is a recombinant subunit vaccine?

A

Certain pathogens are hard to grow so are cultivated in/on another organism.

100
Q

What is a live attenuated vaccine?

A

Uses multiple attenuated master (carrier) virus which proliferates in the respiratory tract. Risks surround those with asthma, immunocompromised or of old age.

101
Q

What is the vaccine design process (3)?

A

1 - antigen identification
2 - vaccine delivery
3 - immune activation

102
Q

What are CD4 and CD8 T cells, and their function?

A

CD4T - receptor is CD4, helper T cells.
CD8T - receptor is CD8, killer T cells.
> recognise processed antigen presented on MHCs on surface of antigen presenting cells - break down proteins and small peptides via an enzyme to stimulate TCRs.

103
Q

What are B cells?

A

Humoral immune cells which produce the antibodies in serum.
> BCR binds to protein/antigen, and antigens which cross-link surface BCR provide optimal B cell activation (no accessory cells required).

104
Q

What do T and B cells have in common?

A

They have antigen receptors which differ to yield specificity to antigens. The receptors send signals via IgA and IgB and these reach the nucleus allowing for altered gene transcription.

105
Q

Which MHC class correlates with which CDT?

A

CD8T - short peptide - I
CD4T - longer peptide - II

106
Q

What is the T cell response (5)?

A
  1. Pathogens infect tissue
  2. Activated DCs move to lymphoid organs - turning pathogen into peptides for MHCs
  3. DCs activate antigen specific T cells
  4. T cells proliferate and migrate out of lymph node
  5. T cells migrate to infected tissue and some become memory T cells.
107
Q

Where are T cells found and why is this useful?

A

Paracortex or T cell zone - DCs meet naïve CD4/8 cells here - means DCs can easily find them due to set location

108
Q

Where are B cells found and why is it important that B and T cells have different locations?

A

B - B cell follicles
Importance - allows for strong separate responses to be enacted

109
Q

What are the three signals for T cell activation?

A

1 - antigen recognition
> peptide binds to MHC recognised by TCR
2 - co-stimulation
> co-stimulatory molecules on DC surface
3 - cytokine-mediated differentiation/expansion
> inflammatory cytokines and receptors for T cell activation

110
Q

What is the dendritic cell-antigen process (6)?

A
  1. PRR triggering enhances phagocytosis
  2. Bacteria digested inside endosomes
  3. MHC molecules in endosomes meet pathogen
  4. MHC molecules containing peptides from pathogen are presented on cell surface
  5. PRR triggering causes DC to migrate from tissue to draining lymph node
    > PRR triggering also causes DC to express high levels of co-stimulatory molecules and make inflammatory cytokines
  6. DC receives signals from pathogen and PRR to stimulate CD4 T cells.
111
Q

What are the endosomes?

A

They contain toxic enzymes for pathogen breakdown.

112
Q

What is clonal selection?

A

The process by which T cells select the correct TCR to recognise the peptide-MHC - leads to clonal expansion

113
Q

What is Th1?

A

Virus/intracellular bacteria
> anti-viral response and enhance function of innate immune cells via cytokines

114
Q

What is Th2?

A

Helminths/PRR signals
> enhance mucosal response and wound healing via cytokines (IL)

115
Q

What is Th17?

A

Fungi/extracellular bacteria
> Activate neutrophils and production of antimicrobial molecules via cytokines (IL)

116
Q

What is a macrophages function?

A

Take up infected killed cells, and either package them in an area where they cannot cause damage or flushed out of body.

117
Q

What is the function of CD8 T cells and the two methods?

A

Kill tumour cells and cells infected by viruses/intracellular bacteria
1. Release inflammatory cytokines (with Th1) - helps other immune cells to dispose of infected cells
2. Produce toxic granules - contain perforin which makes holes in target cells, allowing granzymes to come in and trigger apoptosis.

118
Q

What is the B cell response (8)?

A
  1. Pathogens infect tissue
  2. Smaller antigens/pathogen products drain to lymph nodes, or are carried by DCs to B cells.
  3. Picked up by macrophages or DCs which exchange intact pathogens with B cells - activation - or B cells pick them up.
  4. At follicle border, activated CD4T cells moved toward follicle and activated B cells move to T cell zone as they receive danger signals from inflammatory cytokines etc - they present peptides on MHCII to CD4 and B undergoes class switching.
  5. If successful, B and T move into B follicle to form germinal centre and CD4T becomes T follicular helper cells. T provides information that it can be activated, allowing a better BCR.
  6. B cells undergo rapid proliferation and somatic hypermutation. B cells change nucleotide sequence at genome level to allow for a variety of receptors.
  7. Best mutated present peptides from antigen to MHCII to follicular T - have been waiting in germinal for high affinity BCR/B.
  8. Formation of memory B cells and plasma cells.
119
Q

Where are the naïve cells found?

A

Secondary lymphoid organs.

120
Q

What is class switching and give an example.

A

Fragmented crystallisable (FC) region is switched
e.g. IgM -> IgA (more functional)

121
Q

Give the order of functionality for immunoglobulin classes (5) from low to high.

A

IgM > IgD > IgG > IgE > IgA

122
Q

What is somatic hypermutation?

A

The Fab (fragment of antigen binding) region is altered via changing nucleotide sequencing.

123
Q

What are the different types of Ab (4) and how are they made?

A
  • IgM - low affinity antibody with high avidity, found in B cells which haven’t class switched
  • IgG - most abundant in serum, activates complement so key for immune cell activation
  • IgE - serum in those with allergies, involved in allergy and anti-worm response
  • IgA - mucosal sites, protects body against infection via proteases in respiratory tracts - immediate protection due to location.
124
Q

How do Ab protect the host (humoral immunity) (3)?

A
  1. Neutralise pathogen - Ab blocks virus from binding to receptors, preventing entry and infection.
  2. Activate complement - C1q (complement component) is triggered setting of complement cascade - formation of C5a and C3a - increases inflammatory response and MAC formation.
  3. Enhance phagocytosis - receptor for FC and Ab help macrophages and neutrophils phagocytose the antigen.
125
Q

How do memory cells provide enhanced protection and where are they found?

A

Most of T/B cells undergo apoptosis to make room for a new immune response, but those that stay become memory cells and mean that we do not need to wait for information from DCs and macrophages, providing a faster and superior protection.
e.g. knowing which immunoglobulin class
They are useful for vaccines and memory T cells can be found in the gut, lymph nodes etc.

126
Q

What is the C5-9 complement?

A

A membrane attack complex is formed by C5-9 which binds to the membrane of a pathogen and makes holes in it so regulation cant be maintained in the pathogen, thus killing it.

127
Q

What is opsonisation?

A

The molecular mechanism whereby molecules, microbes, or apoptotic cells are chemically modified to have stronger interactions with the cell surface receptors on phagocytes and NK cells

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