Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

A level biology > immunity P1 > Flashcards

immunity P1 Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

what is an antigen? [2]

A

a foreign protein that stimulates an immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are antibodies?

A

a protein produced by B/plasma cells in response to a non self substance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is a monoclonal antibody?

A

antibodies with the same tertiary structure
OR
antibodies produced from identical B-cells/plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe phagocytosis

A
  • the phagocyte recognises the foreign antigens on a pathogen
  • phagocyte engulfs pathogen
  • the pathogen is now contained in a phagosome in the cytoplasm of the phagocyte
  • a lysosome fuses with the phagosome, and the lysozymes break down the bacterial cell wall.
  • the phagocyte then presents the pathogens antigens in their own cell surface - APC and also components of the pathogen are absorbed in the cytoplasm of phagocyte.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe how a phagocyte destroys a pathogen present in the blood [3]

A

engulfs it
forming a phagosome which fuses with lysosome
lysozyme digests it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe the cell mediated response

A
  • helper T-cells have receptors on their surface which bind to the complementary antigens on an antigen presenting cell.
  • this activates the helper T-cell to divide by mitosis and make a large number of clones
  • some remain as T-helper cells and activate B-cells
  • some turn into memory cells
  • some turn into cytotoxic (killer) T-cells, which release perforin which forms pores in the bacterial cell membrane, destroying it as they can no longer maintain their internal environment.
  • they also stimulate more phagocytosis to occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe the humoral response

A
  • when a B-cell encounters a pathogen with a complementary antigen, the surface antibody will bind to it.
  • the B-cell engulfs the pathogen via endocytosis, and presents the pathogens antigens on its own surface membrane
  • helper T -cells bind to the presented antigens and stimulate the B-cells to divide by mitosis to produce plasma cells.
  • plasma cells secrete antibodies
  • some of the B-cells form memory cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what do helper T-cells do?

A

release chemical signals that activate and stimulate phagocytes to digest more pathogens, cytotoxic T-cells, B-cells (to secrete antibodies) and memory cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is clonal selection?

A

the activation of a B-cell by a specific antigen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is clonal expansion?

A

when the activated B-cells divided repeatedly by mitosis to produce plasma cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what do activated B-cells divide into, and what do these secrete?

A

plasma cells - monoclonal antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe how B cells would respond to a vaccination against a virus [3]

A

B cell antibody binds to viral antigen.
B cell divides by mitosis and forms clones.
Plasma cells produce monoclonal antibodies against the virus.
B/plasma cells develop memory cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe the structure of antibodies

A
  • made up of 4 polypeptide chains - 2 light chains and 2 heavy chains held together by disulphide bridges.
  • has 2 antigen binding sites and one receptor binding sites
  • has a variable region which it’s specificity depends on (different in all antibodies)
  • has a constant region (same in all antibodies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe how having 2 antigen binding sites helps antibodies destroy pathogens

A
  • with 2 antigen binding sites, it can clump together bacterial cells making it easier for phagocytes to engulf large quantities and faster.

this is called agglutination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe how antibodies destroy pathogens other than agglutination

A

markers for phagocytes - they stimulate phagocytes to engulf bacterial cells that they are attached to via the receptor binding site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where are B -cells made and matured?

A

Bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where are T-cells made and matured?

A

made - bone marrow
matured - thymus gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe and explain the role of antibodies in stimulating phagocytosis

A

bind to antigen
which causes agglutination

or
are markers
which attracts phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe how presentation of a virus antigen leads to the secretion of an antibody against the virus antigen [3]

A

helper T cells bind to the antigen which stimulates a specific B cell
B cell divides lots by mitosis and forms clones (plasma cells)
plasma cells secrete antibodies

20
Q

When a vaccine is given to a person, it leads to the production of antibodies against a disease causing organism - explain how [6]

A
  • vaccine contains antigen from pathogen
  • phagocyte presents antigen on its surface
  • T cell with complementary receptor protein binds to antigen
  • T cell stimulates B cell to divide by mitosis and form clones (plasma cells)
  • plasma cells secrete large amounts of antibody
  • some B cells become memory cells which produce antibodies faster
21
Q

what is active immunity

A

when the immune system makes its own antibodies.

22
Q

what’s passive immunity?

A

when you become immune after being given antibodies made by a different organism - immune system doesn’t make its own antibodies

23
Q

describe the differences between active and passive immunity [5]

A
  • active involves memory cells, passive doesn’t
  • active involves production of antibody by plasma, whereas passive involves antibody introduced into body from outside
  • active can take time to work, whereas passive is fast acting
  • active is long-term due to antibody being produced in response to antigen, whereas passive is short-term as the antibody given is broken down
24
Q

what’s herd immunity?

A

when a large proportion of a population are vaccinated against a disease, it prevents the spread of disease to unvaccinated individuals.

25
Q

describe the structure of a HIV molecule

A

have attachment proteins on surface - lipid membrane.
capsid which contains RNA and reverse transcriptase.

26
Q

describe HIV replication

A
  • attachment proteins attach to CD4 receptors on helper T cell
  • RNA and reverse transcriptase enters the cell
  • reverse transcriptase converts RNA to DNA
  • viral DNA inserted into helper T cell DNA
  • DNA transcribed into HIV mRNA
  • viral proteins produced
  • virus assembled and released from cell
27
Q

describe how monoclonal antibodies are used to target drugs to cancer cells

A
  • cancer cells have antigens called tumour markers that aren’t found on normal body cells (specific tertiary structure)
  • monoclonal antibodies with anti-cancer drugs attached can be made that will bind to these
  • when the antibodies come into contact with the cancer cells, they will bind to the tumour markers.
  • this means the drug will only accumulate in the body where there are cancer cells
  • this also means that the side effects of an antibody-based drug are lower than other drugs as they accumulate near specific cells.
28
Q

describe pregnancy testing

A
  • the application area contains antibodies for hCG bound to a coloured blue bead.
  • when urine is applied to the application area, any hCG will bind to the antibody on the beads, forming an antigen-antibody complex.
  • the urine moves up the stuck to the test strip, carrying ant beads with it.
  • the test strip contains antibodies to hCG that are immobilised
  • if there is hCG present, the test strip turns blue as the immobilised antibody binds to any hCG and if no hCG is present, the beads will pass through the test area without binding to anything, so it won’t go blue.
29
Q

explain how you use an ELISA test as a HIV test. (indirect ELISA)

A
  • HIV antigen is bound to the bottom of a well in a well plate
  • a sample of the patients blood plasma is added to the well. if there are any HIV-specific antibodies they will bind to the HIV antigens
  • well washed out to remove any unbound antibodies
  • a secondary antibody with specific enzyme attached to it is added
  • this can bind to the first antibody
  • well is washed out again to remove any unbound secondary antibody
  • substrate is added and if solution changes colour, pos result
30
Q

describe the role of antibodies in producing a positive result in an ELISA test [4]

A

first antibody binds to antigen
second antibody with enzyme attached is added
second antibody attaches to first antibody
substrate is added and colour changes

31
Q

describe ethical issues surrounding vaccines.

A
  • use of animals
  • potentially dangerous side effects
  • clinical tests may be fatal
32
Q

how does HIV cause the symptoms of AIDS?

A

attachment proteins bind to complementary CD4 recepor on helper T cells

HIV particles replicate inside helper T cells, killing or damaging them

AIDS develops where there are too few helper T cells for the immune system to function

individuals cannot destroy other pathogens and suffer from secondary infections/ diseases

33
Q

what happens as AIDS progresses

A

during the late stages of AIDS, patients have a very low number of T helper cells and can develop a range of serious infections.

it is these serious infections that kill AIDS patients, not HIV itself

34
Q

explain how HIV effected the production of antibodies when AIDS develops in a person [3]

A

less/no antibody produced
because HIV destroys helper T cells
so few/ no B cells form plasma cells

35
Q

why don’t antibiotics work against viruses?

A

antibiotics often work by damaging murein cell walls to cause osmotic lysis. viruses have no cell wall.

viruses replicate inside host cells so would be difficult to destroy them without damaging normal body cells

36
Q

how is HIV spread?

A

unprotected sexual inter course, infected bodily fluids, from HIV-positive mother to her foetus.

37
Q

describe the role of one named organelle in digesting bacteria in the cytoplasm

A

lysosomes
fuse with phagosome/ vesicle
and release lysozymes

38
Q

describe how mice injected with human EPO produce anti-human EPO antibody

A

human EPO antigen displayed on antigen-presenting cells/ phagocytes (in mice)

specific helper T cell stimulates B cell to divide

plasma cells secrete antibody

39
Q

a drug is initially tested on mice. suggest and explain 2 further investigations that should be done before it’s tested on human patients.

A
  • test on healthy humans to check for safety/ side effects
  • investigate different concentrations to find suitable/ safe dosage

(or test in other mammals to check for safety/side effects)

40
Q

name types of cell, other than pathogens, that can stimulate an immune response

A
  • cells from other organisms
  • non-self cells
  • cancer/ tumour cells
  • cells infected by virus
41
Q

suggest and explain how a virus becomes able to effect different species [2]

A

mutation in the viral DNA
altered tertiary structure of the antigen
allows virus to bind to receptors of other species

42
Q

determining the genome of the viruses could allow scientists to develop a vaccine. Explain how [2]

A

the scientists could identify the proteome
they could then identify potential antigens to use in the vaccine

43
Q

what causes antigen variability?

A

random genetic mutation changes DNA base sequence

results in different sequence of codons on MRNA

different primary structure of antigen - H-bonds, ionic bonds and disulphide bridges form in different places in tertiary structure

different shape of antigen

44
Q

how does antigen variation affect immunity?

A

memory cells are no longer complementary to antigen - so individual not immune and can catch the disease more than once

due to their being many varieties of a pathogenic it’s difficult to develop a vaccine containing all antigen types

45
Q

what is the proteome of the cell?

A

the full range of different proteins that the DNA is able to code for

A level biology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions