Health and disease (Immunity) Flashcards

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1
Q

What are primary defences in the immune system?

A

Primary defences are mechanisms that prevent pathogens from entering the body in the first place to cause disease.

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2
Q

How is the body protected overall?

A

A majority of our body is protected by skin. The outer layer of our skin is called the epidermis and is made from keratinocytes which are dead cells made from keratin in the process of keratinisation. Pathogens are unable to penetrate this tough layer and thus are unable to enter the body via the skin.

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3
Q

How are the eyes protected?

A

Tears produced by the eyes are natural antiseptics. They contain enzymes designed to break down pathogens before they enter the body.

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4
Q

How are the ears protected?

A

Our ears produce earwax, which is designed to act as a barrier to pathogens that try to enter the body.

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5
Q

How is the airway protected?

A

Goblet cells on the inner lining of the airway produce a sticky substance called mucus which traps pathogens in the air before they are able to enter the lungs. Ciliated epithelial cells then use their cilia to waft the mucus up the airway to the back of the mouth where it can be swallowed into the stomach and the pathogens destroyed by stomach acid.

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6
Q

How is the digestive system protected?

A

All food consumed needs to go through the stomach which is a highly acidic environment. This acidity usually kills most pathogens by denaturing enzymes before they enter the rest of the digestive system to cause diseases.

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7
Q

What are secondary defences in the immune system?

A

These are non-specific immunological responses to foreign bodies in the body usually carried out by phagocytes.

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8
Q

How do phagocytes work?

A
  1. Antibodies in the blood attach to antigens on the surface of pathogens.
  2. Antibodies are detected by phagocytes and phagocytes bind onto pathogen by receptors via the antibodies.
  3. Phagocytes wrap their membrane around the pathogen to form a phagosome on the inside of the phagocyte.
  4. Lysosomes fuse with the phagosome and releases digestive enzymes.
  5. Digestive enzymes break down the pathogen into a mixture of nutrients that can be absorbed into the cytoplasm of the phagocyte safely.
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9
Q

What types of phagocytes are there?

A
  • Neutrophils have a distinctive lobed nucleus to allow them to squeeze through tiny pores in the walls of blood vessels. They travel around the blood and accumulate in areas of infection but have short life spans.
  • Microphages are less mobile compared to neutrophils and usually settle in organs such as the lymph nodes where they play a role in the specific immune response.
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10
Q

What are antigens?

A
  • A protein or glycoprotein unique to a specific pathogen which can be detected by the immune system to stimulate an immune response.
  • Our own cells also have antigens, but our immune system has been trained to recognise our own antigens and not react to them.
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11
Q

What are antibodies?

A
  • Antibodies are proteins (also known as immunoglobins) with a complementary shape to and thus can only bind to one antigen.
  • Antibodies are specific to one type of pathogen, so our body manufactures one for each type of pathogen detected.
  • Antibodies are manufactured by lymphocytes.
  • Antibodies attach to antigens on a pathogen and through some mechanism, neutralises them.
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12
Q

What is the structure of antibodies?

A
  • All antibodies are Y-shaped with 2 distinct regions.
  • Antibodies are proteins with a quaternary structure consisting of 4 polypeptide chains held together by di-sulfide bonds.
  • There is a constant region which is the same for all antibodies as it attaches to phagocytes during phagocytosis.
  • There is a variable region consisting of the bonding region as a result of different primary structures that is different for different types of antibodies.
  • There’s 2 identical bonding regions for every antibody that have complementary shapes to a certain antigen on a certain pathogen and can only bind to it.
  • There are hinge regions at the base of the branch which allows the arms to be moved further apart for bonding more than 1 antigen.
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13
Q

What is neutralisation?

A
  • The antigen on the pathogen may be used for another function related to causing disease, e.g. binding onto host cells.
  • Antibodies attach to these antigens and deactivate them, preventing the pathogen from performing its normal pathogenic processes that causes disease.
  • The pathogens have been neutralised by the antibodies.
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14
Q

What is agglutination?

A
  • Some antibodies are bigger and have more than 2 bonding regions.
  • Each of the these bonding regions may attach to an antigen on a different pathogen.
  • A clump of pathogens is formed around the antibody.
  • This clump prevents the pathogen from performing its normal pathogenic processes and also makes the pathogens easier for phagocytes to engulf.
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15
Q

What is the process of immunisation?

A
  • During the first infection, the primary immunological response is slow because it take time for the body to select the right lymphocytes to produce the right antibodies. This means that the antibody concentration rises slowly to a level required to combat the infection.
  • During the second infection, the secondary immunological response is very quick because memory cells in the blood help the body recognise the pathogen faster and begin producing antibodies faster. The antibody concentration in the blood rises so fast that the pathogens are killed before they get the chance to reproduce and cause disease. The person is immune to that disease.
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16
Q

Why is an immune response a good example of cell signalling?

A
  • An immune response requires lots of cells to work together in a coordinated way in order to fight off an infection.
  • This communication is usually carried out by the release of chemical messengers called cytokines from certain cells. These messengers are picked up by receptors with complementary shapes at their target cells where they trigger a change.
17
Q

How are pathogens identified?

A
  1. Pathogens may enter a host cell. This process triggers the cell itself to attack the pathogens, killing some and leavings fragments to be presented on the cell surface membrane. These fragments can be detected by the correct B-cells and T-cells or act as markers for T-killer cells to destroy the infected cell.
  2. Pathogens are engulfed and destroyed by macrophages in the lymph nodes. The antigens are kept and fuse with the plasma membrane, turning the macrophage into an antigen presenting cell. This is then able to find the correct lymphocyte for the infection.
18
Q

What are cytokines?

A
  • Hormone-like proteins with a complementary shape to a specific receptor on target cells.
  • Unlike hormones, they usually act over short distances at low concentrations and have very specific target cells.
19
Q

How are cytokines used?

A
  1. Macrophages may release monokines to attract neutrophils to an infected area by chemotaxis.
  2. Macrophages may release monokines to stimulate specific B-cells to produce antibodies.
  3. Cells in the immune system can release interleukins to stimulate proliferation of B-cells and T-cells.
  4. Interferons are able to inhibit virus replication as well as stimulate cells in the immune system.
20
Q

How is the specific immune response triggered?

A
  1. Antigens of pathogens are presented by infected cells or antigen-presenting cells (macrophages).
  2. These antigens are detected by the right T-helper and T-killer cells responsible for this specific antigen (clonal selection).
  3. Detection activates these cells, causing then to proliferate and differentiate.
21
Q

What are the activities of T-helper cells post-activation?

A
  1. T-helper cells proliferate by mitosis and increase in numbers (clonal expansion).
  2. They release cytokines called interleukins which activates the correct B-cells for the specific pathogen.
  3. Some become T-memory cells that remain in the blood post-infection and stimulates immunity.
22
Q

What are the activities of T-killer cells post-activation?

A
  1. T-killer cells proliferate by mitosis and increase in numbers (clonal expansion).
  2. T-killer cells begin circulating the body in the blood, looking for infected body cells presenting pathogen fragments on their plasma membrane.
  3. Once T-killer cells detect infected cells, they secrete toxins like hydrogen peroxide into the cell, destroying it and the pathogens inside.
23
Q

What are the activities of B-cells post-activation?

A
  1. B-cells proliferate by mitosis and increase in numbers (clonal expansion).
  2. Some B-cells differentiate to form plasma cells.
  3. Plasma cells manufacture antibodies that are specific to the infecting pathogen.
  4. Some B-cells differentiate to form B-memory cells that remain in the blood post-infection, stimulating immunity.
24
Q

Why is the secondary response quicker than the primary response?

A
  • During primary response, it takes time for the right T-cells and B-cells to be selected (clonal selection) and proliferate to sufficient numbers to combat the infection as they are few in numbers initially.
  • During secondary response, T-memory and B-memory cells specific to the infecting pathogen is already present in the blood, so the pathogen is detected quicker. Clonal selection time is cut substantially, so less time overall is required for lymphocytes to reach numbers sufficient to combat infection. This is usually so quick that the pathogen doesn’t have enough time to reproduce and cause disease.