Immunity Flashcards

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1
Q

List some natural barriers to infection

A
Skin
Tears
Mucus
Acid
Wax
Phagocytes
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2
Q

How is skin a natural barrier to infection?

A
  • Physical barrier to entry of pathogens
  • Sebum glads - oil is antiseptic
  • Sweat - salts and lactic acids have an effect on bacterial growth
  • Lysosomes are present
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3
Q

How are tears a natural barrier to infection?

A
  • Lysosomes are present

- Can ‘wash away’ particles

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4
Q

How is mucus a natural barrier to infection?

A
  • Found in airways (nose and mouth), digestive system, vagina
  • Traps particles
  • Antiseptic properties
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5
Q

How is acid a natural barrier to infection?

A
  • Found in reproductive systems, stomach, and skin

- Hostile environment for microorganisms

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6
Q

How is wax a natural barrier to infection?

A
  • Found in ears

- Hostile environment for microorganisms

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7
Q

How are phagocytes a natural barrier to infection?

A

will destroy any microbe that enters the system

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8
Q

define antigens

A

a molecule found on the surface of living cells that are unique to each individual organism

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9
Q

What are antigens made of?

A

are usually proteins but may also be nucleic acids, polysaccharides or even inorganic molecules

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10
Q

How does the immune system relate to antigens?

A

The immune system of an organism can recognise antigens that belong to their body as self antigens, and those that are foreign as non-self antigens.

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11
Q

When does determination of self and non-self antigens begin?

A

During the development of the foetus in the uterus

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12
Q

How are antigens detected by the immune system?

A

B and T cells have a wide variety of specific receptors on their surface membranes. If the receptor’s shape is complementary to the shape of an antigen, it is recognised as a non-self antigen and the immune system is sensitised.

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13
Q

When does the antibody-mediated response occur?

A

When B-cells are stimulated due to the detection of non-self antigens present in body fluids such as blood or tissue fluid

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14
Q

When does the cell-mediated response occur?

A

When T-cells are stimulated due to the detection of non-self antigens on an infected cell

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15
Q

Define antibodies

A

specifically shaped globular protein molecules with a shape that is complementary to the antigen on the surface of a pathogen.

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16
Q

Why are proteins the ideal molecule for antibodies?

A

they can exist in a near infinite number of structures, as the change of 1 amino acid can result in a different shape of molecule.

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17
Q

Name the actions of antibodies

A

agglutination of pathogens
cell lysis
act as markers for phagocytic cells

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18
Q

Describe what happens when B-cells are sensitised

A

Sensitisation of the B-cells results in rapid clonal expansion of the B-cells into:

  • plasma cells (which produce antibodies)
  • memory cells (which circulate in the blood for a long period of time after infection, and if secondary infection occurs, they can quickly produce lots of antibodies to shorten the secondary immune response).
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19
Q

What other instance causes cell-mediated immunity other than infection?

A

Detection of abnormal self antigens (ie in the case of a cancerous cell)

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20
Q

List what is produced from the division of sensitised T-cells

A
  • memory T-cells
  • helper T-cells
  • suppressor T-cells
  • killer T-cells
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21
Q

What do killer T-cells do?

A

Destroy infected cells by attaching to the antigens on the cell surface membrane of the infected or abnormal cell and destroying it by direct enzyme action.

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22
Q

What do helper T-cells do?

A

Stimulate other cells involved in the immune response.
For example:
- Stimulate B-cells to divide (and produce the plasma cells that produce antibodies)
- Promote the process of phagocytosis through their effect on phagocytes.
- They attach opsonins to the pathogens that mark them out for the attention of the phagocytes.
- Secrete the protein interferon that helps limit the ability of viruses to replicate.

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23
Q

What do suppressor T-cells do?

A
  • These cells ‘suppress’ the immune response of other immune cells when required.
    T- hey switch off the immune response after invading microbes and infected cells have been destroyed.
  • Also important in preventing autoimmune responses, the situation where the immune system attacks ‘self’ cells in the body
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24
Q

What do memory T-cells do?

A
  • These cells circulate in body fluids and can respond rapidly to future infection by the same pathogen (presenting the same antigen(s)).
  • If a subsequent infection occurs, as the memory cells are already sensitised, they can very rapidly produce a large clone of T-lymphocytes.
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25
Q

Name the types of immunity

A
  • Passive immunity (can be natural or acquired)

- Active immunity (can be natural or acquired)

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26
Q

Compare the long-term effects of active and passive immunity

A
  • Passive - Only gives short-term immunity as antibody molecules are eventually broken down
  • Active - Will result in long-term immunity as immune system not only produces antibodies and T-cells but also memory cells
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27
Q

How does natural passive immunity come about?

A

Occurs in unborn foetus and newborn child:

  • Placental transfer - antibodies from the mother’s blood cross the placenta and enter the child’s blood stream
  • Colostral transfer - antibodies are present in the early milk (colostrum) that the mother produces
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28
Q

How does acquired passive immunity come about?

A

injection of purified antibodies from the blood of a recovering, immune or previously vaccinated patient or animal (eg. monoclonal antibodies)

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29
Q

How are monoclonal antibodies produced?

A
  • Mouse is inoculated with purified form of the antigen (or lab grown cancer cell is used)
  • Sensitised B-cells that are making the correct antibodies are hybridised
  • ‘Hybrid’ cells can be grown continuously under optimal conditions, providing a continuous supply of antibodies for medical applications
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30
Q

What are monoclonal antibodies?

A

a laboratory-produced antibody made by cloning a white blood cell

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31
Q

How does natural active immunity come about?

A
  • Experience of infectious pathogens (having the disease) eg mumps, chicken pox, measles
  • Can result in life-long protection
32
Q

How does acquired active immunity come about?

A
  • Vaccinations eg. Edward Jenner
  • Done now through use of attenuated or weakened pathogens, isolated antigens or inactive toxins (toxoids) that stimulate the immune response without harming the body.
33
Q

Name some vaccination programmes in the UK

A

MMR, HPV

34
Q

Name the benefits of vaccinations

A
  • Less people contracting serious illness
  • Infant mortality rates decline
  • Less people hospitalised - less strain on hospitals and more people at work
35
Q

What is the primary response?

A

The immune response triggered by the body’s first ever contact with a particular antigen, either through vaccination or by encountering the pathogen

36
Q

Why is the primary immune response slow and what consequences does this have?

A
  • As there has been no previous contact, there are no memory cells for that particular antigen and therefore the response is slow because the matching B/T lymphocyte must divide to produce many plasma cells
  • Slowness of response means the pathogen has time to multiply and cause disease symptoms before being destroyed
37
Q

Why is the secondary immune response relatively fast and what consequences does this have?

A
  • During the primary response, memory cells are produced that are specific to that particular antigen, so upon secondary infection the memory cells can be rapidly cloned, and in the case of B cells, large amounts of antibodies produced in a short space of time.
  • Due to the fast action of the secondary response, the infected individual may not be aware that they have contracted the infection for a second time
38
Q

What are the differences between the primary and secondary immune responses?

A
Primary response:
- slower to start
- smaller max production
- lasts for shorter time
Secondary response:
- Quicker to start
- larger max production
- lasts for longer time
39
Q

What do booster injections achieve?

A

In the case of vaccination programmes, a booster injection may be required to develop a much higher antibody concentration, which results in longer term protection.

40
Q

Why does organ rejection occur?

A
  • Occurs when the recipient’s immune system recognises the donated organ as having foreign non-self antigens.
  • The cell mediated immune response is activated, as T-lymphocytes are sensitised by the antigens.
  • Clonal expansion follows and the killer T-cells attack and destroy the cells of the donated tissue.
41
Q

Name the techniques to reduce the chances of organ rejection

A
  • Tissue matching
  • Immunosuppressant drugs
  • X-ray irradiation
42
Q

How do immunosuppressant drugs reduce the chances of organ rejection?

A
  • Following donation, the recipient will have drugs prescribed that scale down the action of the immune system.
  • Many of these drugs interfere with the DNA replication of the T and B cells, therefore reducing their number.
  • This allows the donated organ to function without any major damage being inflicted by the immune system.
43
Q

Describe the process of tissue matching for organ transplants

A
  • Before any organ is donated for transplant it is screened using the HLA (human leucocyte antigen) system
  • This determines the genetic similarity in the genes directly involved in antigen production
  • The fewer the differences between the donor’s and the recipient’s HLA genes, the more likely the transplant will be a success.
  • This explains why close relatives are the first source for a donor organ
44
Q

How does x-ray irradiation reduce the chances of organ rejection?

A
  • The radiation from X-rays can be targeted onto bone marrow

- This results in the recipient producing fewer B and T immune cells

45
Q

What are the problems with immunosuppression?

A
  • Recipient is far more vulnerable to infection, so must be carefully monitored to ensure their general health doesn’t become too much of an issue
  • Will be dependent on immunosuppressant drugs for the life of the transplant
46
Q

Define agglutinogens

A

The A and B antigens that are found on the cell surface membranes of red blood cells, and used in ABO blood typing

47
Q

Define agglutinins

A

a and b antibodies found in the blood plasma that are involved in the ABO blood typing system

48
Q

What is agglutination?

A

Clumping of red blood cells when matching antibodies and antigens come into contact (eg. A and a, B and b, etc)

49
Q

Why is agglutination dangerous>

A

blood vessels may become blocked, which can lead to heart attacks or strokes as oxygen and glucose can’t get to those tissues.

50
Q

what separates agglutinins from other antibodies?

A

They are not produced in response to an antigen - they are present in the plasma at all times.

51
Q

Describe what is present in the blood of someone with blood group A.

A

Antigen A on RBCs

Antibody b in plasma

52
Q

Describe what is present in the blood of someone with blood group B.

A

Antigen B on RBCs

Antibody a in plasma

53
Q

Describe what is present in the blood of someone with blood group AB.

A

Antigens A and B on RBCs

No agglutinins in plasma

54
Q

Describe what is present in the blood of someone with blood group O.

A

No agglutinogens on RBCs

Both a and b antibodies in plasma

55
Q

What information is crucial to know in the case of a blood transfusion and why

A

The donor’s antigens
This is because if the donor’s antigens are treated as non-self and are attacked by the matching antibodies in the plasma of the recipient’s blood, agglutination will occur, which can kill the recipient.

56
Q

Why are the donor’s antibodies not as important to know during blood transfusion?

A

The relatively small amounts of antibody in the small volume of donated plasma are diluted by the much larger volume of the recipient’s plasma and don’t cause problems for the recipient’s red blood cells.

57
Q

What condition is required for a safe blood transfusion?

A

The recipient must not have antibodies to the donated antigens

58
Q

What blood group is the universal donor and why?

A

blood group O

because there are no antigens on the red blood cells and can therefore be safely given to any blood group

59
Q

What blood group is the universal recipient and why?

A

blood group AB because there are no antibodies in the plasma, and so can safely receive blood from any other blood group

60
Q

What antigens are considered in the rhesus blood grouping system?

A

the rhesus factor/group D antigen

Most people have this antigen and are considered rhesus positive (Rh+)

61
Q

Describe what happens in the case of Rh- individuals receiving transfusions of Rh+ blood

A
  • Rhesus negative individuals can have 1 transfusion of Rh+ blood with no complications, as they don’t have any antibodies against the Rh antigens
  • The person’s B cells will only make the antibodies following the first transfusion - this process is known as sensitisation
62
Q

Why can Rh- individuals receive one Rh+ blood transfusion?

A

No individual naturally produces anti-rhesus antibodies - they only occur if a Rh- individual is exposed to Rh+ blood cells

63
Q

Describe how haemolytic disease of the newborn occurs

A
  • If an Rh- mother has an Rh+ baby there is a chance that the blood from the baby will mix with the mother’s, usually during birth or late in pregnancy, causing the mother’s B cells to be sensitised into making antibodies against it
  • If the same mother is pregnant with another Rh+ baby, there is a high risk of massive destruction of the baby’s red blood cells.
64
Q

What are the symptoms of haemolytic disease of the newborn?

A

The baby will be anaemic and short of breath as it can’t transport enough oxygen to its tissues. It will also appear jaundiced as it breaks down the haemoglobin, producing other pigments

65
Q

How is haemolytic disease of the newborn prevented?

A

Rh- women with Rh+ partners are given a routine injection of anti-D antibodies towards the end of pregnancy. If the newborn is Rh+, a further injection is given to the mother after birth.

66
Q

From what source to many antibiotics come from?

A

Production by other organisms as a natural defence mechanism (eg. penicillin)

67
Q

what is an antibiotic’s most common modes of action?

A

usually to either disrupt the cell walls of the prokaryotic cells by inhibiting the enzymes involved in their formation, or by interfering with the process of protein synthesis in some way

68
Q

Where do bacteria gain the ability of antibiotic resistance?

A

random genetic mutations occur that allow it to be resistant in some way. These mutations are then inherited by future generations and spread through survival of the fittest

69
Q

What are superbugs?

A

Strains of bacteria that become resistant to all known antibiotics

70
Q

What would be disrupted in an antibiotically resistant world?

A
  • surgery - antibiotics are routinely given to patients after surgery to prevent sepsis
  • People would also be hospitalised/made to stay home for minor ailments that would normally cause no decrease in productivity, eg. Throat infection
71
Q

How can the likelihood of antibiotic resistance be reduced?

A
  • Less prescription of antibiotics
  • Completing antibiotic courses
  • Public health campaigns
  • ‘Deep cleaning’ of hospitals and clinics
  • Removal of use in meat industry/eating less meat
72
Q

where is a lot of research in new antibiotic discovery going in to?

A

studying strains that are in direct competition with each other - it would be a competitive advantage to produce a compound that inhibits the growth of another, allowing it to obtain resources more readily due to decreased competition

73
Q

What does ELISA stand for?

A

enzyme-linked immunosorbent assay

74
Q

Describe how ELISA works

A
  • Plastic plates with numerous small circular wells have antibodies pre-added to them.
  • The antibodies are linked to an enzyme that causes a colour change in the well
  • The antibodies added to the plates are specific to a range of biomarkers (antigens) - if there is a reaction between the antibody held in the plate and the antigen in the patient’s body fluid, then the enzyme is activated and a colour change is detected
75
Q

Describe some uses for ELISA

A

ELISA plates have been developed for a range of conditions including cancer (PSA test for prostate cancer), cardiac disease and pregnancy

76
Q

What are cytokines?

A

a group of small protein molecules that act as signals during an infection. They are most associated with T-helper cells

77
Q

How can cytokines be used in the detection of disease?

A
  • level of cytokines in the blood can be used as biomarkers for disease such as TB
  • Many cytokines promote inflammation - another biological response that can help infection. For this reason, cytokine responses form a key area of study for researchers of the progression of rheumatoid arthritis.