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A Level Biology AQA > UNIT 2, Topic 2C - Immune System > Flashcards

UNIT 2, Topic 2C - Immune System Flashcards

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1
Q

What is the cellular immune response (cell-meditated response)?

A

Where T cells (T lymphocytes) are activated by antigen presenting cells and start an immune response.

Important:
Involves T cells, but cell mediated as it’s only responds to antigen presenting cells and not antigens to touched from cells and within body fluids.

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2
Q

Give examples of antigen presenting cells (4)

A

Non-self antigens that are recognised by T cells:
1. Infected body cells present antigens on surface
2. A phagocyte that engulfed and destroyed a pathogen presents its antigens
3. Cells of transplanted organ have different shapes antigens to your own
4. Cancer cells will have abnormal shaped self-cell antigens

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3
Q

What are antigens and what determines their shape?

A

Proteins molecules on cell-surface membrane responsible for self AND non-self cell recognition (so can act as receptors) & for initiating immune response!

The order of amino acids, so primary structure, determines folding in secondary structure; then tertiary structure (forming specific bonds….) creating the antigen binding site.

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4
Q

How do antigens help the immune system?

A

Allow the immune system to easily identify cells that could be potentially harmful and are non-self.

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5
Q

What are pathogens, give an example

A

Disease causing microorganisms: virus or bacteria that cause disease

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6
Q

Examples of abnormal body cells

A

Cancerous cells or ones invaded by a pathogen (infected)

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7
Q

Toxins

A

Produced by pathogens; cause symptoms to make us feel ill

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8
Q

Note

A

Body cells from individuals of same species from a transfusion or organ transplant can stimulate and immune response as the antigens may be recognised as non-self.

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9
Q

Which immune response is non-specific and why?

A

Phagocytosis; the cells involved (phagocytes, a type of WBC) don’t rely on specific shaped complementary receptors to join to the antigens.

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10
Q

7 points to make about the way the humoral response works.

A

check notes on tablet.

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11
Q

Note that both pathogens and phagocytes (that are antigen presenting cells) are engulfed by macrophages when they are grouped together by agglutination.

A

Make this link in your head when agglutination is mentioned.

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12
Q

What is clonal selection?

A

When a foreign antigen enters the body for the first time, the small numbers of B lymphocytes with complementary receptors are stimulated to divide by mitosis
- then go onto clonal expansion (be aware of phrase) where large number of identical B lymphocytes

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13
Q

how do bacteria make you feel ill?

A

Toxins from many bacteria can cause the symptoms of illness by entering the body cells and damaging them (build up can be fatal)

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14
Q

Why dont you suffer symptoms the second time a pathogen enters body?

A

Memory B and T cells produced during the primary response divide very quickly once detecting the antigens complementary to urs receptors: they are able to then flood the blood with millions of antibodies (aka B plasma cells) and also killer T cells (which have come from memory T cells dividing) to kill the cell carrying antigens

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15
Q

What are the differences between cell-meditated and humoral response?

A

T cells where no antibodies produced.
B cells where antibodies can be produced.

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16
Q

meaning of active and passive immunity.

A

Active: where the body makes it’s own antibodies after responding to a pathogen / antigen presenting cells.

Passive: antibodies are given to the body from another organism if you can’t make them yourself.

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17
Q

3 differences each between active and passive immunity.

A

PASSIVE:
1. Exposure to the actual antigen (of pathogen) isn’t required
2. immediate but short-term protection
3. no memory cells

ACTIVE :
1. requires exposure to antigen
2. memory cells produced
3. takes a while (aka secondary response) for protection to develop

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18
Q

Antibody definition

A

A protein molecule which is secreted by B plasma cells in response to non-aelf antigens.

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19
Q

How can you tell antibody is a protein?

A

Disulfide bridges, and 4 polypeptide chains

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20
Q

monomer of antibody

A

amino acud

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21
Q

name for when antibodies and antigens attach

A

antigen-antibody complex

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22
Q

what are the 2 important regions on an antibody?
describe them.

A

variable region (tertiary sturcture) - different for each antibody complementary to different pathogens.
constant region - the same polypeptide chain for every antobody

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23
Q

why might it be useful to have 2 attachment sites on the antibody?

A

For agglutination: pathogens carrying this same antigen are identified, engulfed and hydrolysed. Allows for one antibody to bind to 2 antigens at once from different pathogens.

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24
Q

Briefly explain how vaccines work to give you immunity (mention immunity cells)

A

Vaccines contains antigens/ DNA of a particular pathogen. Antigens can be detected and trigger an immune response > (plasma) memory cells are made of these antigens meaning that upon reinfection, the pathogen will be recognise and destroyed very quickly, a stronger secondary response; you won’t show symptoms.

They produce long term immunity due to the cells created.

25
Q

Why won’t vaccines make us ill?

A

They’re harmless by:

  1. killing pathogens, leaving the antigen unaffected - inactive
  2. (live vaccine) weakening pathogen
  3. removing the antigens and then injecting them
  4. only injecting the DNA/RNA of microbe
26
Q

What’s herd immunity?

A

It arises when a large amount of population are vaccinated and immune; it’s harder for pathogens to spread.
And, for those who aren’t immunised are protected and unlikely to contract as levels of disease are low.

  • proportion of population that needs to be vaccinated varies for each disease, if not enough- herd immunity can break down AND MORE CHANCE OF BEING IN CONTACT WITH INFECTED.
27
Q

name a few ethical issues associated with vaccines

A

should they be compulsory?
should expensive vaccine programmes continue when disease almost eradicated?
achieving a balance between individual health risks due to vaccines vs protecting population?
acceptable to trial new vaccines with unknown health risks? - volunteers may put themselves at risk if they think they’re fully protected

animal testing?
Difficult to decide who should be the first to receive vaccines.

28
Q

some considerations to make if you were in charge of a vaccine prgramme.

A
  • shelf life
  • few side effects
  • number of doses for effective
  • ease of administration
  • affordable and available to population (including transportation of it)
29
Q

Why would vaccines fail to eliminate a disease?

A
  1. mutations (new strains)
  2. people with compromised immune systems more likely to develop it and die despite vaccination
  3. herd immunity reduced; not having vaccine due to religious/ ethical grounds or personal concerns
30
Q

why do we get the glue from the same pathogen multiple times?

A

Antigenic variation.
Virus, e.g, develops different surface antigens causing a new primary response to occur to develop new complementary antibodies: this doesn’t happen quickly enough to kill the pathogen/ toxins so you suffer symptoms.
- no previous memory B cells for it.

31
Q

Why does getting sick from the same pathogen (considering antigenic variation) cause issues for vaccine development?

A
  • may not be able to keep up every year
    New vacc made everytime increases expenses and is time consuming
32
Q

HIV (human immunodeficiency virus) can lead to what?

A

AIDS

33
Q

Why are people with AIDS vulnerable to infection?

A

Because the helper T cells, which the HIV (viruses) attack and replicate in as the host cell, reach a critically number.

  • noting that T cells are responsible for sending chemical signals that activate phagocytes, cytotoxic T cells and B cells
34
Q

why might a person with HIV not develop AIDS immediately?

A

Latency periods mean replication levels of the virus drops and no symptoms are experienced.

35
Q

what causes death usually when you have AIDS?

A

At the late stages, serious infections kill patients due to low number of immune cells (T helper cells specifically)

36
Q

Name 4 factors that can affect how long until someone develops AIDS

A
  1. existing infections
  2. strain of HIV infected with
  3. age of person (^ vulnerability)
  4. lifestyle (access to healthcare even)
37
Q

what’s the name of the receptor that the HIV attachment protein attaches to on the membrane of the T helper cell?

A

CD4

38
Q

why antibiotics aren’t effective against HIV?

A

These drugs kill bacteria by interfering with their enzymes and ribosomes in their reactions, which are different to human ones and so won’t be damaged.
Viruses use the organelles of the host cells and antibiotics cant inhibit them because they dont target human processes (antiviral drugs should be used instead, targeting virus specific enzymes).

  • virus inside cell and antibiotic in blood can’t access it.
39
Q

what are monoclonal antibodies?

A

Plasma cells (identical to B cells) secrete loads of antibodies for a specific antigen. these are the monoclonal antibodies that then form antigen-antibody complexes.
- they will only bind with these target molecules.

40
Q

How can monoclonal antibodies be used to treat cancer?

A

They bind to complementary antigens (tumour markers) on cancer cells and deliver the drug that’s attached to them, this destroys the cancer and prevents it from further uncontrolled cell division and further tumour growth.

41
Q

Advantage of using monoclonal antibodies to treat cancer?

A

Only targets cancer cells and so fewer side effects as less healthy cells are killed.

42
Q

name of hormone present in urine of pregnant women

A

hCG

43
Q

What is the ELISA (enzyme linked immunosorbant assay) test used for?
And, what is the direct ELISA used for?

A

to identify the presence of certain antigens or antibodies in the blood plasma.
- direct: useful for medical diagnosis of infections. used if you want to find out if patients blood has antigens to a certain antibody OR antibodies to a certain antigen (indicating B plasma cells have been activated)

44
Q

how does direct ELISA test work?

A

See drawn notes on tablet.
- important to note the antigens from sample blood become fixed onto the well plate and then antibodies with enzymes are added.

45
Q

ELISA tests only tell us if antibody or antigen is present, not its concentration - aka the intensity of the colour change. What could you use to measure this?

A

colourimeter to compare the % of light absorption of unknown concentration
OR
serial dilution of a known concentration (of said antigen / antibody / banned drug) and compare with patient blood sample.

46
Q

ELISA tests only tell us if antibody or antigen is present, not its concentration - aka the intensity of the colour change. What could you use to measure this?

A

colourimeter to compare the % of light absorption of unknown concentration
OR
serial dilution of a known concentration (of said antigen / antibody / banned drug) and compare with patient blood sample.

47
Q

Why is it necessary to look for antibodies and not antigens when testing for HIV?

A

HIVs antigens (attachment proteins) enter and replicate inside T helper cells so wouldn’t usually be detected in blood plasma - which is the sample that must be used in (indirect) ELISA tests

48
Q

Why are the side effects usually lower with anti-body based drugs for treating cancer?

A

the drug will only accumulate near specific (cancer) cells.

49
Q

Ethical issues with monoclonal antibodies?

A

✓ Good that we have resources to treat diseases, may not even have to test on humans.

  • for antibodies to be made from tumour cells, mice induced w/ cancer (✓ guidlines to decrease suffering)
  • deaths may occur from use : informed consent from patient needed of risks and benefits
  • issues about conduct of drug trials, unknown side effects in healthy volunteers
50
Q

Uncommon reasons to repeat test

A

Make it more representative and reduce random error

51
Q

Reasons to use a control test

A

Highlight anomalies to remove them from mean calculations ; for a more reliable mean.
To ensure that the variable that’s changed is the only reason you’re getting the results.

52
Q

how do cytotoxic cells kill?

A

They release perforin.
Makes holes in the infected cells, and dies by osmosislysis

53
Q

endocytosis

A

where substances are brought into cells

54
Q

How does a small sample size affect results

A

^ probability correlations may have been due to chance, not representative
- bias?
- may be misinformation, dangerous to make further decisions off of this.

55
Q

How to respond to a Q that asks to draw conclusions from the graph

A

Think of correlation, is there any link between the variables?

56
Q

What’s the latency period?

A

Where after the initial replication of HIV takes place, the replication levels then drop (this could last for years), and during this period no symptoms will be experienced

57
Q

antibodies…

A

inhibit the function of foreign cells with specific antigen

58
Q

T helper cells activate…

A

phagocytes, cytotoxic T cells and B cells
- phagocytosis might come first though

59
Q

Why is there no effective vaccine against HIV

A

HIV decreases amounts of T helper cells, and so the immune response to the vaccine doesn’t happen (may be unsafe to do so or not feasible)

A Level Biology AQA (6 decks)

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