Immunology Flashcards

1
Q

A normal immune response is composed of which three sequential phases?

A
  1. Immediate innate immunity- definsins, physical barrier
  2. Early induced innate immunity- PAMP/PRR interactions, mast cell activation, realise of pro-inflammatory mediators
  3. Adaptive immune response- activation of naive T and B cells, production of antibodies and antigen-specific cells
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2
Q

What is vaccination?

A

Deliberate exposure to a pathogen-related antigen to induce immunological mediated response and to acquire immunological memory

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3
Q

What do memory cells allow for?

A

A rapid response when the same pathogen invades a second time
Symptoms will be eradicated or dampened down in second exposure
Memory cells can remain dormant and reactivate when foreign antigens previously detected are present
Effector cells are more quickly produced this way via clonal proliferation and diffraction of memory cells

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4
Q

What must occur of antibodies to be produced?

A

An antigen specific cells must be encountered

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5
Q

What is the first antibody produced in response to infection?

A

IgM

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6
Q

IgM production will change to production of what other antibody class during the adaptive response?

A

IgG

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7
Q

What is the reason for the change between IgM production to IgG production?

A

IgG has the same, but added functionality to IgM

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8
Q

What is the lag period?

A

This is the time when antibody levels are low as they gradually build
Pathogen proliferation is very high at this stage
Symptoms will likely be experienced at this stage

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9
Q

Where do long-lived plasma cell retreat after infection is eradicated and what do they do?

A

They retreat to the bone marrow

They will secrete antigen specific antibodies for an extended period of time

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10
Q

In a secondary response to an infection, which antibody class(es) are activated from the beginning?

A

IgG and IgM

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11
Q

How can IgG activate complement?

A

Via the classic pathway

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12
Q

Why is it often effective to switch to IgA production during the secondary response?

A

IgA can form dimers which can cross epithelial tissues and that are able to block bacterial attachment to mucous membranes

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13
Q

What is unusual about the immune system combats diphtheria?

A

The toxin produced by the infection is targeted- not the microorganism
This means the toxin can be cleared, by the individual will still be a carrier

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14
Q

What happens to effector cells (non memory B and T cells) when no antigen is present for binding?

A

They will undergo apoptosis

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15
Q

Why can memory B cells produce more functional differentiation than in the primary response?

A

They have already undergone Ig class switching (IgM to IgG) and hypermutation

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16
Q

How are memory cells superior to primary B cell produced ?

A
  • They have already undergone Ig class switching
  • They have enhanced cell adhesion
  • They have enhanced chemotaxis properties
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17
Q

Why do memory cells encounter antigens faster?

A

They are present in secondary lymphoid tissues unlike naive cells
This is because they have receptors on their surface which allows for binding with chemokines which causes entrapment within such tissues

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18
Q

What is active immunity?

A

This is protection obtained solely from an individual’s own immune system and can be stimulated by vaccine or occur naturally

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19
Q

What is passive immunity?

A

This is temporary immune protection transferred form one individual to another such as secretory IgA in breastmilk

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20
Q

Describe the methodology behind inactivated vaccines?

A
  • These are termed attenuated vaccines
  • This involves the vaccine being made up of components that were never alive such and only exist to mimic the real antigen- they can be “edited~” versions of the real antigen
  • This will not produce immunity as effective as a live pathogen would
  • The the immune response will be mostly B cell mediated and less activity of T cells will be present as a line pathogen is absent
  • Immunological memory will likely not last as long and repeat vaccine may be required
21
Q

Why will there be a relatively weak T cell response to attenuated vaccines?

A

There are no live components for which T cells can act upon

22
Q

How can an attenuated vaccine be created?

A
  1. Chemical fixatives- the structure can be preserved by formalin
  2. Heat denaturation
  3. irradiation
23
Q

What are the two main problems associated with attenuated vaccine preparations?

A
  • under-inactivation- pathogen is not inactivated correctly and viable pathogens remain present
  • Over-inactivation- antigens on over-inactivated pathogens are too difficult from the real pathogen and do not confer immunity against it
24
Q

What are the main benefits to attenuated vaccines?

A
  1. Made quickly
  2. May elicit good antibody responses
  3. Easy to store and do not require refrigeration
  4. Usually safe to give to anyone- even the immunosuppressed
25
Q

What are the main disadvantages to attenuated vaccines?

A
  1. Can be difficult to stimulate an immune response
  2. Poor at eliciting T cell response
  3. May not give lasting immunological memory and require boosters
26
Q

What are adjuvants?

A

A mixture of inflammatory substances to kick-start the immune system to activate B and T cells
This is required because a foreign antigen alone is not enough

27
Q

What is the main downsides to the use of adjuvants in vaccines?

A
  • Toxicity
  • Altered immune response- the immune response may be directed against the pathogen/ adjuvant conjugate rather than solely the pathogen
  • CD4+ cells may only be able to recognise the carrier and not the free vaccine
28
Q

What is sub-unit vaccination?

A

Recombinant DNA technology allows for the genes for a sole antigen to be isolated
This involves using a sole antigen, meaning disease cannot be caused

29
Q

What are polysaccharide vaccines?

A
  • These are vaccines directed against pathogens encapsulated by polysaccharide sugars
  • The polysaccharide sugar is the antigenic material
  • To improve immune response, adjuvant toxoids can be added to the coating
  • This is important in allowing both B and T cell responses to the toxoid
  • This aids better class switching and antibody production
30
Q

How can live attenuate vaccines be obtained?

A

Passaging
This is the process whereby attenuated stains are grown through repeated subculturing
The pathogen will become adapted to the environment it is grown in meaning it can be led down certain paths of adaption to make it less effective in human tissues

31
Q

What are the advantages to live attenuated vaccines?

A
  • Similar to natural infection
  • Both B and T cells are properly activated
  • There is a strong immune response initiated
  • Good immunological memory is conferred
32
Q

What are the main disadvantages to live attenuated vaccines?

A
  • if immunocompromisation, patients can become very ill
  • Any circulating antibody can interfere with the immune response
  • The vaccine is fragile and refrigeration is key
  • The pathogen can acquire new mutations and become virulent again
33
Q

What are the two types of passive immunity?

A
  1. Naturally acquired

2. Therapeutic

34
Q

What is naturally acquired passive immunity?

A

This is when a foetus or baby obtains maternal antibodies

Secretory IgA is given to babies through breastmilk

35
Q

What is therapeutic passive immunisation?

A

This involves injecting antibodies to specific pathogens

This is effective but cannot last long since the antibodies cannot be produced by the body

36
Q

When may it be difficult to produce vaccines?

A
  • The body can never clear infection (TB and HIV)

- When there are many different strains of a pathogen

37
Q

Which acronym is used to remember types of infection associated with immunodeficiency ?

A

SPUR

  • Serious (unresponsive to oral antibiotics)
  • Persistent (can cause structural damage and becomes chronic)
  • Unusual (may include opportunists pathogens)
  • Recurrent
38
Q

What is primary immunodeficiency?

A

This is caused due to the immune system having components “missing” or functioning incorrectly
This is most often due to genetic disorders

39
Q

What is secondary immunodeficiency ?

A

This is caused by environmental factors

Most often due to immunosuppressant drugs

40
Q

Which cells make up the innate immune system?

A
  • Macrophages
  • Neutrophils
  • Mast cells
    _natural Killer cells
  • Dendrite cells
41
Q

Which proteins are involved in the innate immune system?

A
  • Complement
  • Acute phase proteins
  • Cytokines
42
Q

What do macrophages do at the end of infection?

A

Produce cytokines and other molecules which promote wound healing and tissue repair

43
Q

Which pathogens are likely to cause recurrent infection?

A
  • Staph aureus
  • Burkholderia cepacia
  • Mycobacteria TB
  • Fungi- candida and aspergillus
44
Q

Where are neutrophils produced?

A

Bone marrow

45
Q

Which cells produce which pro-inflammatory mediators and cytokines that allow activation of specific adhesion molecules (on endothelium) and neutrophils to occur?

A

Macrophages and mast cells

IL-1, IL-6 and TNF-a

46
Q

Which cells secrete which cytokine to superactivate macrophages?

A

NK cells and T cells

Interferon y

47
Q

What is Kostmann syndrome?

A

A syndrome affecting only the end part of the myeloid lineage that allows for neutrophil differentiation

48
Q

How is Kostmann syndrome treated?

A

Since the immune system is weakened (no neutrophils) prophylactic antibiotic and antifungals can be given
Stem cell transplants can also occur
Granulocyte colony stimulating factor can allow for maturation of neutrophils

49
Q

What are some types of PRRs?

A
  • Toll like receptors
  • Scavender receptors
  • Lectin receptors