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Biology Module 1 > Immunity > Flashcards

Immunity Flashcards

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1
Q

What does pathogenic mean

A

Disease causing

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2
Q

What is the body’s first line of defence?

A

To prevent entry of the organism

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3
Q

What are two groups defence mechanisms can be grouped into and give a brief summary of each.

A

1) Non-specific –> Not specific to individual pathogens e.g. phagocytosis
2) Specific –> Distinguishes between individual pathogens. Takes longer to work but provides long term immunity. e.g. Lymphocytes

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4
Q

What are the 4 natural barriers to pathogen entry and explain each.

A

1) Skin - Tough physical barrier, only effective when unbroken
2) Lysozyme - In tears and sweat, antibacterial which can hydrolyse bacterial cell walls. Tears wash away debris
3) Epithelial lining covered in mucus - Traps pathogens, cilia sweep pathogens back up trachea
4) HCl in stomach acid - Kills pathogens

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5
Q

What is phagocytosis?

A

Non specific, rapid immune response.

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6
Q

How does phagocytosis work?

A

During inflammatory response, capillaries become leaky thus plasma seeps into surrounding area. (raises temperature - denatures enzymes). Polymorphs arrive first, macrophages next (develop from monocytes, larger and longer lived) and engulf pathogenic bacteria.

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7
Q

Describe the process of phagocytosis

A

1) Phagocyte moves towards the pathogen attracted by the chemicals it produces
2) Phagocyte membrane invaginates
3) Pathogen engulfed, now in a phagosome
4) Hydrolytic enzymes within the lysosomes hydrolyse the pathogen
5) Soluble products absorbed

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8
Q

Define antigen

A

A substance capable of stimulating the production of specific and complementary antibodies

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9
Q

Define antibody

A

Globular proteins that are specific and complementary to particular antigens that can react with antigens leading to their destruction.

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10
Q

Why do lymphocytes not attack ‘self’ cells

A

Lymphocytes that are complementary in shape to foetal (self) cells are switched off

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11
Q

What are the two types of lymphocytes

A

B - Lymphocytes (B-cells)

T - Lymphocytes (T-cells)

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12
Q

B lymphocytes: Formed, develop, type of immune response, nature of immune response

A

1) Formed - Bone marrow
2) Develop - Bone marrow
3) antiBody-mediated (humoral) immunity
4) Produce antiBodies which respond to antigens found in body fluid - bacterial or viral

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13
Q

T lymphocytes: Formed, develop, type of immune response, nature of immune response

A

1) Formed - Bone marrow
2) Develop - Thymus gland
3) Cell-mediated immunity
4) Respond to antigen presenting body cells - viral infection

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14
Q

How are lymphocytes activated? Any differences between B and T?

A

A lymphocytes comes into contact with its complementary antigen, lymphocytes become sensitised. What is produced is different.

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15
Q

Cell mediated immunity - describe how the immune response comes about and describe the immune response.

A

T-cells stimulated by the body’s own (antigen presenting cells).
T-cells divide by mitosis to produce 4 different cells:
1) Killer T-cells –> Attach to antigens on the surface of the target, release perforin which produces pores on cell surface membrane - death. Hydrolytic enzymes also released
2) Helper T-cells –> Secrete cytokines e.g. interferon which promotes activation of other cells. e.g. B-cells - plasma cells = more antibodies. Promote phagocytosis. Attach opsonins to mark out the pathogens for phagocytosis.
3) Suppressor T-cells –> Secrete cytokines which deactivate B and T cells, thus preventing autoimmune diseases.
4) Memory T-cells –> circulate in body fluid, respond rapidly to future infection by the same pathogen. Rapidly produce T-cells = IMMUNITY.

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16
Q

Antibody mediated immunity - describe how the immune response comes about and describe the immune response.

A

Targets microorganisms that are in body fluids. Defends the body through the production of antibodies. Specific antigens sensitise specific B-lymphocytes, which divide by mitosis to produce B-plasma and B-memory cells. Plasma cells are short lived, but produce huge numbers of antibodies - neutralise pathogens via antigen-antibody complexes.

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17
Q

Describe the action of antibodies and B-memory cells

A

1) The antibodies latch onto complementary antigens clumping the bacteria together, this causes agglutination or clumping as an antigen-antibody complex. It is then engulfed by polymorphs and other phagocytes. They can also act as opsonins by attaching to pathogens and marking them out for phagocytosis.
2) Memory cells remain in body fluids. Once stimulated divide rapidly by mitosis to produce vast numbers of plasma cells - Secondary immune response.

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18
Q

What do T cells also attack

A

Transplanted tissues as they are non self and caner cells

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19
Q

What is passive immunity?

A

Individuals receiving antibodies form another source

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20
Q

What is active immunity?

A

Individuals achieve immunity through the production of their own antibodies.

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21
Q

How can you gain passive immunity?

A

1) Antibodies passing from mother to baby across the placenta / mothers colostrum - crucial for a baby.
2) Antibodies made in another individual, harvested and injected as serum (from convalescing individual)
3) Monoclonal antibodies from another species.

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22
Q

How do you obtain monoclonal antibodies? What are the advantages.

A

Removal of sensitised and cloned B-Lymphocytes from a mouse that has been infected by a particular antigen. Then hybridise them with cancer cells. Put in a fermented and they divide rapidly.

Produced in large quantities in a lab.
Can produce a single type of antibody

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23
Q

Advantages and Disadvantages of passive immunity

A

Advantage - Rapid as antibodies are injected

Disadvantage - Temporary

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24
Q

Describe active immunity. Primary and Secondary responses.

A

Primary response is slow - individual suffers the disease as it takes a while for B-lymphocytes to produce antibodies, but once it is in place it is long lasting.
Secondary response is stronger and larger as there are many memory cells.

25
Q

Describe vaccinations

A

Trick the immune system into thinking its been infected by a particular disease.
Usually contain either:
1) Killed / weakened pathogens
2) Modified toxins produced by the pathogens
3) Isolated antigens separated from the pathogens itself.
Sometimes a booster is given - produces a stronger and larger secondary response.

26
Q

Importance of vaccinations to society

A

Fewer sick people and lives of many people extended.
Less strain on hospitals - economic
Employees less time taken off work - increased productivity

27
Q

What is herd immunity?

A

If a high enough proportion of the population is vaccinated, those who are not vaccinated are unlikely to catch a particular disease. Important for those unable to be vaccinated e.g. newborns.

28
Q

What can happen if you transplant tissue? Are there any exceptions?

A

The tissue contains non-self antigens which can produce an immune response. Except if its from the same person (skin graft) or from an identical twin.

29
Q

What is transplant rejection?

A

1) T-lymphocytes stimulated by non self antigens
2) T-cells cloned by mitosis to produce Killer T-cells
3) Killer T-cells destroy the transplanted tissue.

Can also be B-cells if its a blood donation and the blood groups don’t match

30
Q

What strategies try to prevent transplant rejection and are there any drawbacks to any of the strategies?

A

1) Tissue typing - matching donor and recipient cell surface markers
2) Immunosuppressant techniques - e.g. drugs to inhibit DNA replication thus the cloning of lymphocytes. Slows down the rejection process. Compromises the recipients immune system –> makes the individual susceptible to infection.
3) X-Rays - Irradiation of bone marrow or lymph tissue. Unpleasant side effects.

31
Q

What is the ABO system?

A

There are four different types of blood groups A,B,AB,O and everyone belongs to one of the groups. This is a polymorphism - a situation where there are several distinct categories or forms.

32
Q

What happens if a non-matching blood group is transfused

A

An antigen-antibody reaction will occur which will cause the blood to agglutinate, this can block arteries thus can cause death.

33
Q

Draw out the table for the blood group, antigens and antibodies in plasma.

A

In book

34
Q

Draw out the table of whether a reaction will occur.

A

In book

35
Q

Which blood group is the universal donor and why?

A

Blood group O as it has neither A or B antigens.

36
Q

Which blood group is the universal recipient and why?

A

Blood group AB as it has neither anti-A or anti-B antibodies.

37
Q

What would happen if i transfused blood from blood group A into someone who was blood group B

A

A person who is blood group B will have anti-A antibodies. The blood being transfused will have A antigens of the RBCs. Antigen-Antibody reactions will occur which will cause the blood to agglutinate in the recipient.

38
Q

What is the Rhesus system based on?

A

Based on the presence or absence of an antigen. (Rhesus antigen / antigen D). Rh+ve individuals have the antigen while Rh-ve individuals do not have the antigen. If you’re Rh+ve you will not have anti-D antibodies. Rh-ve don’t usually have these antibodies but will produce them if their blood comes into contact with Rh+ve blood.

39
Q

What happens when a Rh-ve mother has a Rh+ve baby.?

A

1) During birth some foetal RBC ( Rh+ve so contain anti D) leak into the mothers circulation
2) Causes Rh-ve mother to produce anti-D antibodies. No threat to current baby as by the time sufficient numbers of anti-D antibodies are produced the baby will have been born.
3) If a further pregnancy is Rh+ve, and the baby’s blood gets into the mothers circulation large numbers of anti-D antibodies will be produced quickly and cross the placenta causing agglutination of the foetal cells.

40
Q

What procedures are put in place to prevent that happening.

A

Mother injected with Anti-D antibodies –> attach to any antigen D cells that cross the placenta preventing the mothers own immune response.

41
Q

What is an antibiotic?

A

Substance produced by microorganisms that act against bacteria.

42
Q

How do antibiotics kill bacteria?

A

1) Disrupt cell wall formation, burst an die - Penicillin

2) Inhibit metabolic processes e.g. protein synthesis- Tetracycline

43
Q

How has antibiotic resistance come about?

A

Mutations in the bacterial genome lead to metabolic changes that results in antibiotics no longer being effective.

44
Q

How has penicillin become resistant?

A

Produced penicillinase to break down penicillin. Exporting the active ingredient in penicillin out of the cell before it can work.

45
Q

What is a superbug?

A

A disease that is resistant to two or more strains of antibiotic.

46
Q

How do you control the spread of antibiotic resistance?

A

1) Only use antibiotic when necessary
2) Complete the prescribed course of antibiotics
3) Strict hygiene regulations in hospitals
4) Consideration given when going to prescribe two antibiotics
5) Keep some antibiotics as a last resort.

47
Q

What are the benefits to the individual and society of discovering new antibiotics?

A

More effective treatment, less treatment costs, less time off work.

48
Q

Where are they looking for new sources of antibiotics?

A

The soil, as some microbes naturally produce antimicrobial substances as a defence mechanism.

49
Q

Define epidemic.

A

Diseases that spread rapidly through a small region and affect a higher proportion of the population.

50
Q

Define pandemic.

A

Diseases affecting many thousands of people and affect many countries at the one time.

51
Q

What makes virus more likely to spread infection?

A

1) Prone to mutation
2) Many disease causing viruses are retroviruses with RNA in the genome. These are less stable.
3) Antibiotics are not effective against viruses

52
Q

What are reservoirs of disease?

A

Animal species that harbour viruses that subsequently cause disease in humans. Generally suffer little harm themselves.

53
Q

What have bats been a reservoir of?

A

Marburg, SARS and Nipah.

54
Q

Why are bats suitable reservoirs of disease?

A

1) Similar physiology to humans.
2) Social animals, which allow a high proportion of bats to become carriers.
3) Fly large range - potentially in contact with other organisms.
4) Urbanisation means that humans are coming into contact with bats.

55
Q

What is an ELISA?

A

Enzyme-linked immunosorbent assay. Lab technique that uses antibodies, enzymes and other molecules as biomarkers of disease.

56
Q

How does an ELSIA work?

A

Body fluids from a patient added to wells on a plate. Range of antibodies added to these wells. Antigen-antibody reaction, triggers an enzyme linked with it to cause a colour change.

57
Q

What can ELISAs be used to detect?

A

Pathogens, Cancer, Cardiac diseases and pregnancy.

58
Q

How does a pregnancy test work?

A

Increased levels of HCG antigens detected by complementary HCG antibody. Antigen-Antibody complex results in a linked enzyme produces a colour change.

59
Q

How are cytokines used?

A

Chemicals released by T-helper and other cells. Small proteins that help coordinate the immune response. Found in blood and used to detect TB.

Biology Module 1 (5 decks)

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