Immunity Flashcards

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1
Q

When is a microorganism a pathogen?

A

When it enters the host, colonizes tissue, evades host’s defenses and causes damage to host tissues

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2
Q

When does an infection occur?

A

If a pathogen enters the body and colonises the tissues

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3
Q

When does a disease occur?

A

When the infection causes recognizable symptoms

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4
Q

How does disease damage tissues?

A

Directly (viruses break down cells), or through production of toxins (bacteria release many toxins)

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5
Q

What is the body’s first line of defense

A

Prevent entry of pathogens

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6
Q

What defence mechanisms come after the first line of defense?

A

Non-specific: these are not specific to pathogens e.g phagocytosis
Specific immune response: Distinguishes between pathogens and involves lymphocytes. Longer to work but provides long term immunity

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7
Q

What natural barriers to pathogen entry are there?

A
  • Skin
  • Tears
  • Epithelial linings covered in mucus
  • Hydrochloric acid
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8
Q

How is skin a natural barrier?

A
  • Tough barrier to pathogens
  • Waterproof and produces sebum - oily substance with antiseptic properties
  • Produces sweat - mixture of chemicals including lactic acid and lysozyme
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9
Q

How are tears a barrier?

A
  • Protect eye by keeping it moist

- Contains lysozyme which hydrolyses cell walls of bacterial cells resulting in their death

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10
Q

How are epithelial linings with mucus a barrier?

A
  • Mucus acts as impermeable barrier to bacteria and other pathogens in body systems
  • Prevents penetration of underlying membranes
  • Contains lysozyme
  • Cilia sweep mucus and pathogens up trachea
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11
Q

How is hydrochloric acid a barrier?

A
  • Kills pathogens in food we consume

- Low pH denatures enzymes of pathogen

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12
Q

What is phagocytosis?

A

Rapid and nonspecific protection by phagocytes

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13
Q

What does the inflammatory response of phagocytes following infection involve?

A

Capillaries in affected area become leaky allowing plasma to seep into affected area, phagocytic WBC squeeze through capillary walls and accumulate. Inflamed area becomes swollen with puss contained phagocytes, dead pathogens and cell debris. There is inc. blood flow to area and appears red. area becomes hot to denature enzymes of pathogen

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14
Q

What does phagocytosis involve

A
  • Chemicals produced by pathogen attract phagocyte so it moves towards it
  • Phagocyte membrane invaginates to enclose membrane and engulfs it, forming vesicle (phagosome)
  • Lysosomes move towards phagosome and fuse with it -Hydrolytic enzymes in lysosome are released into phagosome which hydrolyses pathogen within phagosome
  • Soluble digested products are absorbed into cytoplasm of phagocyte
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15
Q

What do lymphocytes react to?

A

Antigens present of the surface of pathogens which they recognise as foreign or ‘non-self’

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16
Q

What is an antigen

A

A molecule found on the surface of living cells

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17
Q

What are self and non self antigens

A

Self antigens belong to the body and non self do not

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18
Q

What do lymphocytes have on their cell surface membrane?

A

Specific protein receptors that are complementary in shape to the antigen

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19
Q

Why don’t lymphocytes respond to self cells?

A

During early development, millions of different lymphocytes are produced from stem cells in the bone marrow. Each have a specific membrane receptor that allows it to respond to a different non-self antigen if encountered in the future. Lymphocytes do not respond to self cells because in the foetus the lymphocytes frequently make contact with other foetal self cells and the lymphocyte complementary in shape to self cells are ‘turned off’

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20
Q

Describe B-lymphocytes

A

Antibody-mediated immunity. Produces antibodies which respond to antigens found in body fluids. Responds to bacterial or viral infection

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21
Q

Describe T-lymphocytes

A

Cell-mediated immunity. Responds to antigens attached to body cells. Responds to body cells affected by viral infection

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22
Q

What does the activation of a lymphocyte involve?

A

It coming into contact with a non-self antigen that its receptors recognise

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23
Q

What happens with B-lymphocyte activation?

A

The B-lymphocyte recognises the antigen on the pathogen itself and becomes sensitised. When its receptors are sensitised, it will activate the gene responsible for the production of antibodies - antibody mediated response. The antibodies will be secreted into the blood stream and target the antigens on the pathogen

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24
Q

What happens if a T-lymphocyte is stimulated?

A

A number of different types of T cells are produced, each with a different job. T cells will directly destroy the cell - cell mediated response

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25
Q

What happens to sensitised B and T lymphocytes?

A

The sensitised lymphocytes divide by mitosis and differentiate into a variety of cells. This delay takes time between the contact of the antigen and the cloning of required lymphocyte and during this time the person has symptoms

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26
Q

What are antibodies?

A

Specifically shaped globular protein molecules each one responsible for destroying a specific pathogen. Called immunoglobulins

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27
Q

What does antibody mediated immunity target?

A

Microorganisms found in body fluids rather than body cells, involving production of antibodies

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28
Q

What happens when a antigen sensitises its B lymphocyte?

A

The B lymphocyte will become cloned, and produce plasma and memory cells. The initial response of the body when encountering an antigen for the first time is the primary immune response

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29
Q

What do most cloned B cells become?

A

Plasma cells, they are clones of the original B lymphocyte and secrete large amounts of antibody in response to non-self antigen

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30
Q

How do antibodies neutralise the pathogens?

A

As a consequence of antigen-antibody reactions

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31
Q

What happens to memory cells?

A

They remain in circulation for years allowing for a second infection to be dealt with. They remain inactive unless stimulated by presence of antigen again. If this happens, memory cells divide rapidly and produce large amounts of plasma cells. The plasma cells produce the antibodies to destroy the pathogen while memory cells provide long term protection. This is the secondary immune response

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32
Q

Describe the shape of antibodies

A

They have a binding site that is complementary to a particular antigen and forms antigen-antibody complex

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33
Q

What effect do antibodies have?

A
  • Cause agglutination of pathogens
  • Cause destruction of invading cells directly -cell lysis
  • Act as opsonins - attach to pathogen marking them for phagocytosis
  • Neutralise toxins produced by bacteria - called antitoxins
  • Attach to viruses preventing them from entering host
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34
Q

What is agglutination?

A

Clumping together of cells. Often the first stage in allowing efficient phagocytosis by polymorphs. Clumping of cells in one area allows polymorphs to engulf and destroy the pathogens through lysosomal digestion inside the cell. These antibodies are called agglutinins

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35
Q

What stimulates the production of T cells?

A

The body’s own cells that have been changed due to the presence of non-self material in them. These cells are antigen presenting cells

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36
Q

What are examples of antigen presenting cells?

A
  • Body cells infected by a pathogen
  • Tumor cells, many types of cancerous cells present abnormal antigens on their cell surface membranes
  • Macrophages that have engulfed and broken down a pathogen
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37
Q

What do T cells divide to form?

A

T memory, T helper, T suppressor, and T killer cells

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38
Q

What are T killer cells’ job?

A

They bind to antigen on cell surface membrane of the infected or abnormal cells and cause the lysis of cell membrane directly vie enzymes called perforins

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39
Q

What do T helper cells do?

A

They travel to other parts of the body helping the immune response in dealing with the infection. Stimulate B cells to divide and produce plasma cells. Stimulate macrophages to carry out phagocytosis. Secrete cytokines that limits virus’ ability to replicate
-Activate killer T cells

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40
Q

What do T suppressor cells do?

A

Suppress the immune response of the other immune cells when required. Switch off immune response after invading microbes and infected cells have been destroyed, preventing overreaction. Prevent autoimmune response

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41
Q

What do T memory cells do?

A

They are present in case of secondary infections. Circulate in body fluid and can respond rapidly to future infection.

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42
Q

What does passive immunity involve?

A

The transfer of antibodies from one organism to another. Provides short term immunity as antibody molecules will eventually be broken down.

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43
Q

How is natural passive immunity obtained?

A

Through placental transfer and colostrum (breast milk) transfer

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44
Q

What is artificial passive immunity?

A

The artificial injection of purified antibody from the blood of a recovering patient or previously vaccinated animal. Gives short term immunity

45
Q

How did we harvest antibodies in the past?

A

Through harvesting antibodies from an individual and injecting them into another person as a serum, or by immunizing animals and then the serum from the animals was given to people.

46
Q

What does monoclonal antibody production involve?

A

The removal of sensitized and cloned B cells from a mouse that has been infected with a particular antigen. These are hybridized with cancer cells to produce long lived lymphocytes that can produce required antibodies

47
Q

what are the advantages of monoclonal antibodies?

A
  • Can be produced in large quantities in a lab

- Can produce single type of antibody

48
Q

Why is passive immunity rapid immunity?

A

The process of B lymphocyte sensitization and plasma cell production do not need to take place first. Effective if someone is infected with a pathogen they have no defense against, or snake bite

49
Q

Why is passive immunity temporary?

A

Antibodies are broken down and individual has no memory cells to make more

50
Q

What does active immunity involve?

A

The person’s own immune system being activated to produce antibodies, resulting in production of long term immunity as B memory cells produced

51
Q

What is the major way to obtain active immunity?

A

Through experience of infectious pathogens. This can result in you being protected for life and is known as natural active immunity.

52
Q

How is artificial active immunity obtained?

A
  • Attenuated or dead pathogens
  • Toxoids - inactive toxins that switch on immune response
  • Isolated antigens separated from pathogen itself
53
Q

How do vaccinations result in immunity?

A

Triggers the primary immune response, memory cells produced, enabling body to produce a secondary response quickly is required

54
Q

What are societal benefits of vaccination?

A

Fewer sick people, healthy children miss less school and perform better, extend life expectancy

55
Q

What are economic benefits of vaccinations?

A

Lower treatment costs to treat the ill, employees don’t take time off work so productivity increases, parents don’t take time off work to look after kids

56
Q

When does organ rejection occur?

A

When the immune system recognises the non-self antigens

57
Q

Outline the process of organ rejection

A
  • T lymphocytes sensitized by non-self antigens present on transplanted tissue
  • T cells are cloned by mitosis and produce killer T cells
  • Killer T cells destroy transplanted tissue and over time organ will lose function
  • If the donor and recipient have different blood types, B lymphocytes will be involved and produce antibodies
58
Q

How do we reduce the change or organ rejection?

A

1) Tissue typing
2) immunosuppressant drugs
3) X-ray irradiation

59
Q

How does tissue typing reduce the chance or organ rejection?

A

It involves matching the donor and the recipient cell surface markers, so there is as close a match as possible. Before an organ is donated it is screened using HLA system, which determines genetic similarity on genes directly involved in antigen production. The fewer differences in HLA genes, the more likely it is to be successful.

60
Q

How do immunosuppressant drugs reduce chance of organ rejection?

A

They will be given drugs to scale down action of immune system. Many of these drugs will inhibit the DNA replication of T and B lymphocytes reducing their number. This slows or stops rejection process and allows donated organ to function without damage from immune system

61
Q

How does X-ray irradiation prevent rejection?

A

The radiation from X-rays can be targeted onto bone marrow or lymph tissue. This inhibits the production of lymphocytes so the patient produces fewer B and T cells

62
Q

What problems are associated with X rays and immunosuppressant drugs?

A

The recipient is much more vulnerable to infection because their immune system is compromised and they need to be monitored to ensure their general health isn’t an issue

63
Q

What other strategies support the patient to prevent infections?

A

Antiviral drugs, antibacterial mouth rinses, and use of monoclonal antibodies to target and reduce effect of T cells involved in rejection

64
Q

Why do the antigen markers on RBC not trigger an immune response?

A

The individual will not have antibodies that correspond to the antigens on their RBC because the lymphocytes responsible for these blood antibodies are switched off during early development

65
Q

What does the blood group systems depend on?

A

On knowing differences in the antigens on the cell surface membranes of the RBC

66
Q

What is the ABO blood system based upon?

A

Two different antigens - A and B, these are called agglutinogens

67
Q

What are the agglutinins?

A

There is 2 different antibodies - a and b - found in the blood plasma

68
Q

What happens when antibody a comes into contact with antigen A?

A

IT causes the red blood cells carrying antigen A to stick together or agglutinate. This also happens if b comes into contact with B

69
Q

Why is agglutination dangerous?

A

Blood vessels can become blocked and heart attacks or strokes may occur as oxygen and glucose cannot be transported to the tissues

70
Q

What are A and B in the RBC?

A

The antigens

71
Q

What are a and b in the RBC?

A

The antibodies

72
Q

When is knowledge of blood group needed?

A

When blood donations or transfusions are taking place

73
Q

Why is the antigen crucial knowledge when a blood transfusion is given?

A

If the antigens come into contact with matching antibodies in the plasma of recipient’s blood, this will cause clumping of the donated blood cells, causing blockages

74
Q

Why does the donated blood not have to be the same blood type as the recipient?

A

It is only important that it doesn’t have the antigens on the surface of the RBC that would be recognized by any of the antibodies present in recipient’s plasma

75
Q

Why does donated blood sometimes trigger an immune response?

A

The donated blood is recognized as non-self so it is treated as an invading pathogen and attacked

76
Q

Why is blood group O the universal donor?

A

There are no antigens on the red blood cells and can be given to any blood group

77
Q

Why is blood group AB the universal recipient?

A

There are no antibodies in the plasma and so can safely receive blood from any other blood group

78
Q

What other blood group system is important?

A

The rhesus system

79
Q

What does the Rhesus blood group system involve?

A

A group of antigens known as the Rhesus factor / group D antigens

80
Q

What are people with group D antigens described as?

A

Rhesus positive Rh+

81
Q

What are people without group D antigens referred to as?

A

Rh-

82
Q

When will anti-D antibodies be produced?

A

Only when a Rhesus negative individual is exposed to Rhesus positive RBC containing D antigen

83
Q

Why can Rhesus negative people have 1 transfusion of Rh+ blood?

A

They do not have antibodies against the Rh antigens. The persons’ B cells will only make the antibodies following the transfusion (this is sensitization).

84
Q

What happens if a Rh- person receives a second Rh+ blood transfusion?

A

Their blood would agglutinate as they know have antibodies against rhesus factor

85
Q

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

A

There is a chance their blood will mix and the mother’s B cells will become sensitized and make antibodies against it. If the mum falls pregnant with a Rh+ baby again there is a high risk of haemolytic disease of the newborn

86
Q

What is haemolytic disease of the newborn?

A

When there is massive destruction of the child’s red blood cells. The baby will be anaemic and short of breath as it cannot transport enough oxygen to its tissues.

87
Q

Why is haemolytic disease of the newborn rare now?

A

Rh- mothers are treated during pregnancy by being given an injection of anti-D antibodies. These attach to any antigen D containing foetal RBC fragments that may cross the placenta and enter mother’s circulation, before mother’s B lymphocytes are stimulated to produce anti-D antibodies

88
Q

What are antibiotics?

A

Drugs developed to kill bacteria

89
Q

What are antimicrobial substances derived from?

A

They are either synthetic (sulphonamides), come from animals (lysozymes), or from plants

90
Q

What’s the difference between antibiotics and antimicrobials?

A

Antibiotics are specific against bacteria, antimicrobials include agents against all agents that act against all types of microorganisms

91
Q

How do antibiotics work?

A

They either disrupt cell wall formation or inhibit metabolic processes

92
Q

How does cell wall disruption kill bacteria ?

A

They disrupt cell wall formation by inhibiting an enzyme involved in the process. The bacteria are killed as the cell bursts, as it cannot resist osmotic pressure due to a weakened cell wall

93
Q

When are bacteria antibiotic resistant?

A

When one or more antibiotics no longer have any effect on the bacteria and are rendered useless

94
Q

What leads to antibiotic resistance?

A

Mutations in the bacterial genome lead to metabolic changes within the bacteria so antibiotics no longer have any effect, Bacteria reproduce rapidly so one resistant bacteria can quickly become a large population

95
Q

How have penicillin resistant bacteria evolved to be resistant?

A

1) produce penicillinase to break down penicillin
2) Exporting the active ingredient in penicillin out of the cell before it works
3) alternative metabolic pathways in cell wall formation can render penicillin ineffective

96
Q

How else can we reduce antibiotic resistance?

A

By taking the full course of antibiotics. We also seldom use some antibiotics and are kept as a last resort

97
Q

Where may we find new antibiotics?

A
  • Ocean sediments
  • Soil bacteria
  • Human nasal cavity
98
Q

What fruits and veg have antimicrobial effects?

A

Apple and spinach contain antimicrobial and antifungal compounds

99
Q

What herbs and spices are antimicrobial?

A

Caraway and thyme have antibacterial, antiviral and antifungal compounds

100
Q

What does how rapidly a disease spread depend on?

A

How easily it spreads between people, how likely someone falls ill once infected, whether there is a vaccine, % uptake for vaccine

101
Q

Why are viruses more likely to cause epidemics?

A
  • They have very small genomes prone to mutations
  • Many disease causing viruses have RNA which is less stable than DNA
  • Antibiotics aren’t effective against viruses
102
Q

What are animal species that harbor viruses that cause disease called?

A

They are reservoirs of that virus

103
Q

Why are bats reservoirs for disease that infect humans?

A
  • Mammals with similar physiology to humans
  • Social animals in close contact to many others, ensuring high number of bats are carriers
  • Fly large ranges and are therefore potentially in contact with other organisms distances away from their base
104
Q

What are ELISA tests?

A

A lab technique that uses antibodies, enzymes, and other molecules as biomarkers to detect the presence of particular molecules in the body.

105
Q

How are ELISA tests carried out?

A

In a lab using 96 well plate and centrifuged blood. The blood is centrifuged to remove red blood cells as any antibodies present in a person’s blood will be in the plasma. The removal of the red blood cells allows detection of colour change in a positive test

106
Q

What can ELISA tests test for?

A
  • Pathogens in the body
  • Cancer cell markers
  • Cardiac disease markers
  • Pregnancy
107
Q

How do ELISA tests detect prostate cancer?

A

If the prostate gland becomes cancerous, abnormally high levels of the protein PSA may occur in the blood. This is tested by using a specific monoclonal antibody, with an enzyme attached to allow the presence of the antibody to be detected

108
Q

How do ELISA tests detect pregnancy?

A

Following the implantation of an egg in the uterine wall, increased levels of the hormone hCG can be detected in blood or urine. In a home pregnancy test hCG antigens are detected by hCG monoclonal antibodies. The formation of the antigen-antibody complex results in a linked enzyme reacting to produce the characteristic colour change associated with pregnancy tests

109
Q

How can ELISA tests detect a pathogen?

A

An ELISA plate impregnated with the viral antigens is coated with blood serum from the patient. If the patient’s blood contains complementary antibodies then the antigen-antibody complex triggers an enzyme reaction leading to a colour change