Non-Specific Defences Flashcards

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1
Q

What are the two types of innate (non-specific) defence?

A

Internal and external.

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2
Q

Compare specific and non-specific defences.

A

Non-specific defences are not selective, and occur during the early immune response. They are ready to go from the moment of birth. Specific defences are the opposite, they need to know what exactly they are dealing with (so they can know if they are capable of dealing) and do not begin to work until after the non-specific defence has tried to eliminate the threat. They must also be trained by lymphocytes to act on threats, are present, but not ready, at birth.

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3
Q

What are the specific defences mediated by?

A

Lymphocytes drive the specific response.

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4
Q

What are the cells/ processes involved in the non-specific defence?

A
  1. Cytokines.
  2. Complement.
  3. Inflammation.
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5
Q

What are the cells/ processes involved in the specific defence?

A
  1. Cytokines.
  2. Antibodies.
  3. B & T lymphocyte cells.
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6
Q

What is the ‘self’ and what happens if our immune system targets it?

A

The self is out body, our tissues and cells. The immune system should not target the self as it is US, and if it does, it is referred to as an auto-immune disease e.g. T1 diabetes targets beta cells in the pancreas.

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7
Q

What is the ‘non-self’ and what happens if our immune system targets it?

A

The non-self are foreign cells/ organisms within or on our bodies. If they are perceived as harmful, they are targeted and destroyed by our immune system.

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8
Q

List the central lymphoid tissues.

A
  1. Bone marrow.

2. Thymus.

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9
Q

Give the functions of the central lymphoid tissues.

A
  1. Leukocytes are formed in the bone marrow.

2. T-lymphocytes are trained in the thymus.

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10
Q

List the peripheral lymphoid tissues.

A
  1. Spleen.
  2. Tonsils & adenoids.
  3. Peyer’s patches.
  4. Lymph nodes.
  5. Appendix.
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11
Q

What is an antigen?

A

An antigen is any threat, which is then targeted & destroyed by our immune system.

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12
Q

What is an antibody?

A

An antibody is a protein made by B-lymphocytes to get rid of harmful things.

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13
Q

What is humoral immunity related to?

A

Humoral immunity relates to the blood, and is associated with antibodies and B lymphocytes.

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14
Q

What does cell-mediated immunity relate to?

A

Cell-mediated immunity relates to the physical contact with an antigen that is required to remove it. T -lymphocytes require hands-on contact with antigens to destroy them. There is no antibody association here.

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15
Q

How long should acute inflammation last?

A

Up to three days- longer than this is a sign of chronic inflammation.

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16
Q

What is the function of acute inflammation?

A

Acute inflammation has a beneficial function, it acts to protect against disease & enable the healing of tissue.

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17
Q

Why is chronic inflammation harmful?

A

Chronic inflammation (inflammation lasting more than three days) is harmful as it results in lasting damage to inflamed tissues. It is also a feature of many diseases, e.g. rheumatoid arthritis, cancers and any lung diseases.

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18
Q

What triggers inflammation?

A
  1. Microbial invasion.

2. Tissue damage.

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19
Q

List the five main events occurring in inflammation.

A
  1. Phagocytosis of pathogens.
  2. Dilation & permeability of capillaries.
  3. Containment of foreign matter.
  4. Leukocyte migration & proliferation.
  5. Continued leukocyte activity.
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20
Q

What is the purpose of pathogen phagocytosis as part of inflammation?

A

Pathogen phagocytosis around the site of tissue damage reduces the damage that pathogens can potentially do- bacteria and viruses are nipped in the bud.

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21
Q

What is the purpose of the dilation of capillaries during inflammation?

A

The dilation of capillaries (and other blood vessels) as part of the inflammation process results in an increase of blood flow to the area of damage, thus allowing more leukocytes, defensive proteins and healing cells to access the damaged tissue.

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22
Q

What is the purpose of leaky capillaries during inflammation?

A

Capillaries are always permeable, but during inflammation they become more so. This allows for leukocytes to exit the bloodstream, and enter the site of damaged tissue in order to aid in repair.

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23
Q

What drug triggers the dilation of capillaries and increased permeability? Where does this drug come from?

A

Histamine, which is released from mast cells on the skin (if the skin is the tissue damaged), or from basophils (if the damage is internal).

24
Q

What is the process of capillary dilation and increased permeability referred to?

A

Vascular change.

25
Q

Is it only capillaries which dilate and become more permeable during inflammation?

A

No, all blood vessels surrounding the damaged tissue become more dilated and permeable.

26
Q

What are the four characteristic features of inflammation, give their causes.

A
  1. Redness due to an increase in blood flow.
  2. Heat due to an increase in blood flow.
  3. Swelling due to an increase of blood flow, as well as capillary permeability (more fluid in vessels).
  4. Pain due to oedema (fluid accl from permeability- has nowhere else to go), bradykinin stims nearby sensory neurons.
27
Q

Is pain beneficial as part of the inflammation process, and if so why?

A

Pain, while an unnecessary side effect, is beneficial to us during periods of inflammation as it warns us that there is some sort of tissue damage.

28
Q

What is the purpose of the containment of foreign matter during inflammation?

A

Foreign matter is contained so as to prevent the spread of antigens to other body parts, thus reducing damage.

29
Q

What facilitates the containment of foreign matter?

A
  1. Heparin is an anti-coagulant, and is released from mast cells (skin)/ basophils (elsewhere) to allow leukocytes to access area of injury.
  2. Clotting factors which have leaked out of BVs become active and form clusters around bacteria to inhibit their spread.
30
Q

How is a scab formed?

A

When the clotting factors are activated during inflammation, they harden to form a scab at the skins surface (if the damage is external).

31
Q

What is leukocyte proliferation?

A

The increase in production of leukocytes, carried out to aid in healing damaged tissue.

32
Q

List and describe the four steps involved in leukocyte migration

A
  1. Margination- cytokines release sticky factors onto BV walls.
  2. Attachment- leukocytes attach to BV walls and line up.
  3. Diapedesis- leukocytes travel through endothelial gaps of BV walls.
  4. Chemotaxis- leukocytes are chemically attracted to the site of injury.
33
Q

Why is leukocyte migration necessary?

A

Leukocytes do not work in the bloodstream, and so must move out of it into the damaged tissue in order to aid in repair.

34
Q

How does the continued activity of leukocytes end the process of acute inflammation?

A

Some leukocytes engage in phagocytosis to get rid of antigens, and cytokines are released to induce changes.

35
Q

What changes do cytokines bring about during stage 5 of inflammation (continued leukocyte activity)?

A
  1. Make BV walls even stickier, more leukocytes adhere and migrate.
  2. Bone marrow is stimulated to produce more neutrophils.
  3. Hypothalamus is stimulated to raise body temperature- kills off infection and stops viral activity (specificity).
36
Q

List the four steps of phagocytosis.

A
  1. Attachment.
  2. Internalisation.
  3. Degradation.
  4. Exocytosis.
37
Q

Compare the functions of histamine and heparin during inflammation.

A
  1. Histamine is works to dilate blood vessels and make them more permeable- brings about vascular change.
  2. Heparin is an anticoagulant, cells get to the site of injury more easily.
38
Q

What happens when the non-specific defence system doesn’t work?

A

The specific defence is called into action- as a late immune response.

39
Q

What are interferons and what is their function?

A

Interferons are a type of cytokine which prevent the spread of viruses (prevent viral replication).

40
Q

How do interferons work and what cells do they target?

A

Interferons are secreted by a cells which is infected by a virus. They bind to receptors on healthy cells to promote the production of anti-viral proteins within the healthy cell. These proteins then coat the healthy cell and thus reduce the chances of their infection by a virus.

41
Q

How does interferon work to help an already-infected cell?

A

Interferon can do nothing for a cell already infected by a virus, it can only prevent further infection of healthy cells.

42
Q

During what period & for how long does interferon carry out its function?

A

As part of the early immune response, and for only a limited amount of time (not indefinite).

43
Q

What are natural killer cells and what is their function in non-specific defence?

A

Natural killer cells are the only lymphocyte which is used in the early immune response. They target viruses to inhibit them and prevent further infection.

44
Q

How is a virus-infected cell destroyed by NK cells?

A

The NK cells forms holes in the membrane of a target cell, and this allows for fluid to rush into the cell & then be destroyed due to lysis.

45
Q

What is complement?

A

It is a group of approx. 20 plasma proteins which work in a cascade (pathway) to destroy orgs, esp bacteria.

46
Q

What are the two pathways in the complement cascade?

A
  1. Alternative pathway.

2. Classical pathway.

47
Q

Describe how the alternative pathway works and give its benefits in terms of timely-response to infection.

A

The alternative pathway works by complement binding directly to the carbs of a bacterium’s cell membrane and then destroying it. It is beneficial in the early immune response as B-lymphocytes and therefore antibodies are not required for this pathway.

48
Q

Describe how the classical pathway works and its relation to antibodies.

A

The classical pathway involves complement binding to antibodies which are already attached to a bacterium in order to destroy it.

49
Q

Why is complement so important in terms of antibodies?

A

Complement is required to actually destroy a target cell as antibodies cannot do this on their own- they simply identify and bind to a target cell (cannot kill it directly).

50
Q

List the precise steps involved in the alternative complement pathway.

A
  1. Complement binds to the surface of bacterial cell.
  2. Complement proteins form a MAC- Membrane Attack Complex.
  3. The MAC inserts into the cell membrane like a drill and forms a pore.
  4. Lysis of the cell occurs as fluid rushes into the cell through the pore.
51
Q

What triggers the complement cascade?

A

The binding of complement to the surface of a bacterial cell.

52
Q

Compare the targets of interferon, complement and natural killer cells.

A

NK cells and interferon target viruses, complement targets bacteria.

53
Q

When triggered what processes do the complement cascade bring about?

A
  1. Increased inflammation.
  2. Attraction of macrophages to the area.
  3. Coating of antigens to make them more obvious to macrophages.
  4. Kills intruders.
54
Q

List the phagocytic cells involved in immunity.

A
  1. Monocytes.
  2. Macrophages.
  3. Neutrophils.
  4. Occasionally eosinophils.
55
Q

When steps one, two and three of inflammation occur what overall function does this provide?

A

To protect, incur vascular change and to prevent deeper infection.