3.2.4 The immune system Flashcards

1
Q

What is a pathogen?

A

An organism that causes disease

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2
Q

What is an antigen?

A

A molecule that is recognised as non-self which raises an immune response

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3
Q

What is an antibody?

A

A protein with quaternary structure, which is produced by B lymphocytes / plasma cells and they are complementary to an antigen

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4
Q

What is non-specific immunity?

A

They are immediate/ have a rapid response and they respond in the same way regardless of the type of pathogen
e.g. physical / chemical barriers (stomach acid, skin, mucus) / phagocytes

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5
Q

What is specific immunity?

A

They have a slower response and they are dependent on the antigens, found on surface of pathogen
e.g. T lymphocytes, B lymphocytes

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6
Q

What are phagocytes?

A

They are non-specific immune cells that engulf pathogens, then digest them

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7
Q

What are T lymphocytes?

A

They are specific immune cells that mature in the thymus, they are associated with cell-mediated immunity

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8
Q

What are B lymphocytes?

A

They are specific immune cells that mature in the bone marrow, they are associated with humoral immunity - they produce antibodies

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9
Q

What are memory cells?

A

They remain in the body after infection and live much longer than other immune cells. They respond quickly if the same pathogen is encountered again

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10
Q

Describe the process of phagocytosis.

A
  1. Phagocyte recognises the foreign antigens on a pathogen
  2. Cytoplasm of phagocyte moves around the pathogen, engulfing it
  3. Pathogen is now contained in a phagosome (phagocytic vacuole) in the cytoplasm
  4. Lysosome fuses with phagosome, forming phagolysosome, lysozymes (hydrolytic enzymes) now fuses towards the pathogen
  5. Pathogen is hydrolysed by lysozymes, it now presents the pathogen’s antigens by sticking them on its surface to activate other immune system cells
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11
Q

What are lymphocytes activated by?

A

Antigen-presenting phagocytes, virally infected cells, cancer cells, transplanted cells

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12
Q

What happens to Helper T lymphocytes when they meet an antigen-presenting phagocyte.

A

If they have complementary receptors to antigens, clonal expansion is triggered and they start dividing by mitosis

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13
Q

What are the roles of newly divided Helper T lymphocytes.

A

Activate B lymphocytes

Activate cytotoxic T lymphocytes

Enhance phagocytosis

Become memory T lymphocytes

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14
Q

What do cytotoxic T lymphocytes do?

A

They release perforin which put holes in the pathogen, damaging the integrity of cell membrane, allowing substances to enter and exit - killing pathogen

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15
Q

What happen to B lymphocytes when they meet an antigen presenting phagocyte?

A

If they have complementary antibodies to antigens, they will bind to them, they will then be activated by Helper T lymphocytes, triggering clonal expansion

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16
Q

What are the roles of newly divided B lymphocytes?

A

Most:
Plasma cells - release antibodies

Some:
Memory B lymphocytes

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17
Q

Where do T and B lymphocytes mature at?

A

T: Thymus
B: Bone marrow

18
Q

How are antibodies released from B lymphocytes when faced with pathogen?

A
  1. Pathogens have antigens on its surface
  2. Phagocytes present antigens on their surface
  3. Helper T lymphocytes with the complementary receptors bonds to the antigens
  4. This activates B lymphocytes with the complementary antibodies
  5. B lymphocytes divide by mitosis/ go through clonal expansion
  6. Some become plasma cells which all releases the same antibodies
19
Q

What are monoclonal antibodies?

A

Antibodies that are all identical in structure, produced from a single group of genetically identical B cells

20
Q

How many polypeptide chains make up an antibody?

A

4
2 heavy chains
2 light chains (shorter on the outside)

21
Q

How are the antigen binding-sites of antibodies specific?

A

Binding sites are located in variable regions on antibodies

Antibodies are proteins - their tertiary structures are unique

22
Q

What bond joins the two heavy chains of antibodies together?

A

Disulphide bond

23
Q

What is agglutination of antibodies?

A

As each antibody have 2 binding sites, by binding two different antigens to the same antibody, pathogens are clumped together

24
Q

What is the benefit of agglutination?

A

More pathogens are clumped closely together, more could be engulfed by phagocytes - enhance phagocytosis

25
Q

What is an ELISA test and what is it used for?

A

Test for pathogenic infections/allergies/ (anything you can make an antibody for)

It shows whether or not the patient has any antibodies to a certain antigen or vice versa.

26
Q

How does an ELISA test work?

A
  1. Blood sample is added to a well with fixed antibodies at the bottom

(stir + incubate + wash off)

  1. Primary Ab is added and will bind with antigen (if present)

(stir + incubate + wash off)

  1. Secondary Ab is added and will bind with primary Ab (if present as its complementary)

Enzyme which catalyses colour changing reaction is attached to secondary Ab

(stir + incubate + wash off)

  1. Substrates to enzyme are added , enzyme-substrate complex will form if enzymes are present - colour change
27
Q

Why are secondary Ab used?

A

To amplify signal

28
Q

Why is the well washed off between each step?

A

To get rid of anything that is not bound to something

29
Q

What is targeted therapy?

A

Drugs that find and attack cancer cells

30
Q

What are the two ways targeted therapies can slow down the growth of cancer cells?

A
  1. Antibodies which are complementary to cancer’s unique receptor is bound to a drug

Antibody will bring drug to cancer cells - only a small dose is needed as most will bind to cancer cells

  1. Antibodies which are complementary to cancer’s unique receptor will bind to receptors instead of growth factors

Growth factors that tell cells to divide will no longer be able to bind to receptors - blocked

31
Q

What is the similarity between passive and active immunity?

A

Both could be stimulated naturally and artificially

32
Q

What is active immunity?

A

The immunity you get when your immune system makes its own antibodies after being stimulated by an antigen

33
Q

What is passive immunity?

A

The immunity you get from being given antibodies made by a different organism (your immune system doesn’t produce any antibodies of its own)

34
Q

What are the differences between passive and active immunity?

A

P: doesn’t require exposure to antigen
A: requires exposure to antigen

P: gives immediate protection
A: takes a while for protection to develop (produce antibodies)

P: doesn’t produce memory cells
A: produce memory cells

P: provides short term immunity
A: provides long term immunity

P: couldn’t result in herd immunity
A: could result in herd immunity

35
Q

What is passive immunity caused by?

A

Natural: Baby acquiring antibodies from its mother through breast milk and placenta

Artificial: Injection with antibodies

36
Q

What is active immunity caused by?

A

Natural: Becoming immune after catching a disease

Artificial: Becoming immune after given a vaccination

37
Q

What is HIV and what could it cause?

A

Human immunodeficiency virus
Causes AIDS - Acquired immunodeficiency syndrome

38
Q

What does a virus consists of?

A

Antigens on surface

Genetic material (DNA/RNA) inside a capsid - layer of proteins

Surrounded by a matrix (inner) and lipid envelope (optional) - phosolipid bilayer

39
Q

What are found specifically in HIV?

A

Enzyme - reverse transcriptase in capsid

RNA as genetic material

40
Q

Why is HIV able to modify DNA of Helper T lymphocytes

A

They have receptors that are complementary to antigens of HIV - CD4

41
Q

How does HIV replicate inside the cells of organism

A
  1. Helper T lymphocyte binds to HIV
  2. Capsid of HIV is released into Helper T lymphocyte, uncoats and releases RNA and RT into cytoplasm
  3. Inside cell, RT is used to make a complementary strand of DNA from viral RNA strand
  4. Viral DNA is added to cell’s DNA found in nucleus
  5. Viral DNA now codes for viral proteins and when released from cell, will infect other cells
42
Q

How does HIV kill its host?

A

As immune system is weakened (Helper T lymphocytes is virally infected), B lymphocytes can’t be activated - no antibodies produced - opportunistic/secondary infections will then be able to attack cells and kill the host