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A-Level Bio > 3.2 Immunity > Flashcards

3.2 Immunity Flashcards

1
Q

what are antigens?

A

proteins on the surface of all cells.

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2
Q

what are foreign antigens?

A

antigens which are not normally found on the surface of cells.

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3
Q

what do antigens allow the body to recognise?

A

pathogens, abnormal body cells, toxins and cells from other individuals of the same species.

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4
Q

what do phagocytes do?

A

they recognise a foreign antigen on a pathogen, they surround it (engulfing it), the pathogen is then contained in a phagocyte vacuole. a lysosome fuses with the vacuole and releases lysozymes. the phagocyte then presents the antigens which activates other immune system cells to respond.

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5
Q

what do lysozymes do?

A

they destroy the pathogen by hydrolysis.

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6
Q

what are lymphocytes made from?

A

stem cells in the bone marrow.

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7
Q

where do t cells mature and what do they have on their surface?

A

mature in the thymus and they have receptor proteins on the surface that bind to complementary antigens presented to them by phagocytes.

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8
Q

what do helper t cells do?

A

they release chemical signals which activate phagocytes, they also activate b cells which secrete antibodies.

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9
Q

what do cytotoxic t cells do?

A

they kill virally infected cells/tumours and produce a protein called perforin which makes holes on the surface membrane.

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10
Q

what does perforin do?

A

makes the cell permeable to all substances by producing holes in the surface membrane so the pathogen dies.

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11
Q

why are lymphocytes stimulated to divide when responding?

A

because there are only a few of each type.

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12
Q

what are b cells?

A

lymphocytes which mature in the bone marrow and are covered in antibodies.

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13
Q

what are antibodies?

A

proteins produced by b lymphocytes in response to the presence of a specific antigen, they will bind to form an antigen-antibody complex.

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14
Q

what does each b cell have that is different?

A

a different shaped antibody in the surface membrane so different b cells bind to different antigens.

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15
Q

what happens when an antibody meets a complementary antigen?

A

the antibody binds to the antigen and the antigen enters the b cell by endocytosis. they are presented on the surface so helper t cells can bind to them.

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16
Q

once the helper t cells are bound to the antigens presented on the b cell, what do the t cells do?

A

they activate the b cell to reproduce by mitosis. the b cell starts to clone itself into plasma cells.

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17
Q

what does an antibody have 2 of?

A

binding sites, it can bind to 2 pathogens at the same time and the pathogens bind together (agglutination.)

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18
Q

what are antibodies made of?

A

proteins made of long chains of amino acids.

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19
Q

what are AB soluble in?

A

blood/tissue fluid.

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20
Q

why does each AB’s variable site have a unique structure?

A

because of the different amino acid sequence.

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21
Q

what is the cellular immune response?

A

the t cells and other cells which interact with phagocytes.

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22
Q

what is the humoral immune response?

A

the response of B lymphocytes to a foreign antigen, clinal selection and the release of monoclonal antibodies.

23
Q

what is the primary response?

A

the first time a pathogen enters the body and activates the immune system, the response is slow because there aren’t many b cells which can make the antibody needed to bind. while enough of the correct antibody is being made to overcome the pathogen, the body will show symptoms of the disease.

24
Q

when do memory cells form and what do they do?

A

after an infection, both t and b cells will make them, they remain in the body for decades.
they don’t make ABs directly but circulate through the blood/tissues.

25
Q

what will memory t cells do?

A

they will remember the antigen.

26
Q

what will memory b cells do?

A

they will remember the specific antibodies needed.

27
Q

what is the secondary response?

A

if the pathogen enters the body again it will be able to quickly respond. memory b cells divide into plasma cells quicker to produce the correct type of AB for the antigen. memory t cells divide into the correct type of t cells to kill the pathogen with the antigen.

28
Q

what are tumour markers?

A

the different antigens on cancer cells

29
Q

what do MCAs do to cancer cells?

A

the anti-cancer drugs can be attached to the antibody so when they come into contact with the cancer cells they’ll bind to the tumour makers.

30
Q

what is the advantage of monoclonal antibodies?

A

the anti cancer drugs will only build up where the cancer is found so there are less side effects as the drugs are only in specific cells

31
Q

how are monoclonal antibodies used in pregnancy tests?

A

-application window contains MCAs that attach to the hCG with blue beads attached.
-once urinated on, any hCG present will bind to the antibodies and will move along the strip.
-further up are a second set of antibodies which all bind to the hormone but are immobilised.
-as the 1st antibodies with the beads and bound to hCG pass over the immobilised MCA, the hCG also binds to the immobilised antibodies.
-a blue line is seen.
-any antibodies from the application window that aren’t bound to hCG continue to move and bind to a different set of antibodies (test window)

32
Q

how does the secondary immune response differ to the primary immune response?

A

plasma cells and antibodies are produced at higher speed and concentration as a result of memory cells being produced during the primary immune response.

33
Q

what are monoclonal antibodies?

A

antibodies with the same tertiary structure, produced from cloned b lymphocytes.

34
Q

what is the term used to define the response of T cells to a foreign antigen?

A

cell-mediated immunity

35
Q

what is active immunity?

A

resistance that arises due to exposure to an antigen which causes b lymphocytes to produce antibodies

36
Q

what is passive immunity?

A

resistance that arises when antibodies are introduced into the body (either via injection or breastfeeding) bind to and destroy specific toxins/venoms/antigens.

37
Q

what is herd immunity?

A

when more people are immune, fewer people carry the pathogen, so unvaccinated people are less likely to make contact with infected people.

38
Q

describe the steps of phagocytosis

A

phagocytes move towards the pathogen
receptors on their CSM recognise/attach to chemicals on the surface of the pathogen
engulf the pathogen to form a phagosome
lysosomes move towards and fuse to the vacuole
lysozymes then destroy ingested bacteria
the soluble products are absorbed into the cytoplasm of the phagocyte

39
Q

how can t lymphocytes distinguish invader cells from normal cells

A
  • phagocytes present some of the pathogen’s antigens on their own CSM
  • body cells invaded by a virus present some of the viral antigens on their own CSM
  • transplanted cells from individuals of the same species have different antigens on their own CSM
  • cancer cells present antigens on their CSM
40
Q

define antigen-presenting cells

A

cells that display foreign antigens on their surface

41
Q

define plasma cells

A

cells which secrete antibodies usually into the plasma
memory cells circulate in blood/tissue fluid until they later encounter the same antigen and then divide rapidly into plasma cells or more memory cells

42
Q

describe the structure of an antibody

A

4 polypeptide chains, one pair of the chains are longer and known as ‘heavy chains’ and the second are shorter and known as ‘light chains.’
the variable region is the binding site that differs on different antibodies
the constant region is the rest of the antibody

43
Q

describe how antibodies lead to destruction

A

they cause agglutination of bacterial cells so it is easier for phagocytes to locate them
they serve as markers that stimulate phagocytes to engulf the bacterial cells to which they are attached

44
Q

describe the uses of monoclonal antibodies in medicine

A
  • monoclonal antibodies are produced which are specific to antigens on cancer cells
  • these antibodies attach to receptors on the cancer cells
  • they block the chemical signals which stimulate their uncontrolled growth
45
Q

what are the benefits of monoclonal antibodies

A

they can be used in smaller doses because they are so specific
they are cheaper and reduce side effects

46
Q

explain Indirect Monoclonal Antibody Therapy

A

the process of attaching radioactive/cytotoxic drugs to the monoclonal antibodies so that upon attachement, the MCA kills the cancer cell

47
Q

what are the ethical issues with monoclonal antibodies

A

use of mice
deaths associated so informed consent necessary
testing with small groups for safety poses dangers

48
Q

describe the features of a successful vaccination programme

A
  • need to be economically available in sufficient quantities for the population
  • minimum side effects so as not to discourage takers
  • available means of production, storage + transportation
  • a means of administering at an appropriate time (staff trained etc)
  • possible to vaccinate the majority of the vulnerable population
49
Q

define herd immunity

A

when the vast majority of a population is immune so it is highly improbable that a vulnerable individual will come into contact with the infection so those not immune are somewhat protected

50
Q

why might a vaccination programme not eliminate disease

A

it might not be effective if people have defective immune systems
they may develop the disease after being vaccinated but before they have high enough immunity levels so they reinfect other people
antigenic variability means one type of vaccine will not eradicate it
if there are too many varieties of a pathogen so it is impossible to act against all of them

51
Q

explain the replication of HIV

A

a protein of HIV binds to a protein (CD4) and will attach to helper T cells
the protein capsid fuses with the CSM so that RNA and enzymes of HIV can enter the T cell
HIV reverse transcriptase converts the virus’ RNA into DNA
the DNA is moved into the T nucleus and is inserted into the cell’s DNA
HIV DNA creates mRNA containing instructions for making new viral proteins + RNA for the new HIV
the mRNA passes out the nucleus through a nuclear pore and new HIV particles are synthesised
these break away from the helper T cell with a piece of the CSM attached which form their own lipid envelope.

52
Q

how does HIV cause aids

A

it interferes or kills the normal functioning of a Th and without enough helper T cells, the immune system cannot stimulate B cells to produce antibiotics or cytotoxic T cells. memory cells may also be affected or destroyed.
people die from infections that they cannot be protected against

53
Q

explain how an ELISA test works

A

apply the sample to a well so that the antigens bind to the bottom
antigens will attach and the sample is washed in order to remove unattached antigens
add the specific antibody that is complementary to the wanted antigen and leave them to bind
wash the well to remove excess antibodies
add a second antibody that binds with the first and has an enzyme attached
add the colourless substrate to the enzyme so that the enzyme acts on it to change it into a coloured product

54
Q

why are antibiotics ineffective against viruses

A

because antibiotics inhibit enzymes needed for the synthesis of peptide cross linkages in bacterial cell walls in order to make them unable to withstand osmotic pressure so they burst and die. however viruses have no cell structures or metabolic pathways for the antibiotics to disrupt.
viruses also have protein coats in place of murein , no sites for antibiotics to work and if the virus is already in a host cell, the antibiotics cannot reach them.

A-Level Bio (21 decks)

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