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AQA A level Biology > Immunity and cell structure > Flashcards

Immunity and cell structure Flashcards

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1
Q

What are the two main immune defence mechanisms?

A

1) cell mediated response (T cells)

2) humoral response (T cells then mainly involves B cells)

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2
Q

Every pathogen will have specific NON-SELF molecules (usually proteins) that can…

A

help our cells to identify them (and distinguish them due to varying tertiary structures)

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3
Q

What do protein molecules on foreign material help our cells to identify?

A
  • pathogens eg. HIV
  • cells from other organisms of the same species
  • toxins produced by pathogens
  • abnormal body cells such as cancer cells
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4
Q

Explain what happens to the immune system during an organ transplant?

A

recognises the tissue/organ as non-self so attempts to destroy it

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5
Q

What can be done to prevent rejection in organ transplants?

A

administer immunosuppressive drugs

transplant from relatives who are genetically similar

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6
Q

Briefly explain the time lag between the body’s expose to a pathogen and its immune response to bring the pathogen under control.

A
  • millions of lymphocytes in blood
  • one lymphocyte has a surface protein that is complimentary to the surface protein on the antigen
  • correct lymphocyte undergoes clonal selection and expansion
  • time lag = time for clonal selection and expansion
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7
Q

Why is infection in the fetus are?

A

protected by the placenta

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8
Q

What happens to lymphocytes that show an immune response to slef natigens/

A

undergo programmed cell death (apoptosis) before they can differentiate into mature lymphocytes

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9
Q

sm random in the textbook

A

X

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10
Q

Name two type of white blood cell

A

phagocytes

lymphocytes

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11
Q

Explain phagocytosis

A
  • chemical products of pathogens or dead/damaged/abnormal cells act as attractants causing phagocytes to move towards the pathogen
  • phagocyte engulfs pathogen to form a vesicle called a phagosome
  • lysosomes inside phagocyte move towards phagosome and fuse with it
  • enzymes within the lysosomes called lysozymes destroy the ingested pathogen (eg. hydrolysis of cell wall)
  • soluble, useful products from breakdown of pathogen are absorbed into the phagocyte’s cytoplasm
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12
Q

Define antigen

A

foreign protein that stimulate immune response and production of antibodies

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13
Q

What type of immune response is phagocytosis?

A

non-specific

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14
Q

Specific immune response (disadv, adv)

A

slower at first

can provide long term immunity

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15
Q

Define B cell

A

cells associated with humoral immunity that mature in the bone marrow and secrete antibodies

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16
Q

Define T cell

A

cells associated with cell-mediated immunity that are originally stem cells in the bone marrow and then migrate to the thymus gland to mature

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17
Q

What do T cells usually only respond to?

A

antigen present on a cell surface rather than antigens floating in the blood

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18
Q

Define antigen presenting cell

A

also called an ‘accessory cell’

cells that present foreign antigens from other foreign cells on their own cell surface membrane

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19
Q

Explain 4 ways T cells distinguish invader cells form normal cells.

(phagocytes, virus, transplant, cancer)

A

1) phagocytes have engulfed and hydrolysed a pathogen to present some of its (pathogen’s) antigens on its own cell surface membrane
2) body cells invaded by a virus present some of the viral antigens on its own cell surface membrane
3) transplanted cells have different antigens on their cell surface membrane
4) cancer cells present antigens on their cell surface membranes

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20
Q

Define cell mediated immunity

A

an immune response that does not involve antibody production.

A response where T cells respond to specific antigens on a cell, in turn activating other immune cells and the release of cytokines.

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21
Q

Response of T cells to infection by pathogen:

A

1) Phagocytes take up pathogen
2) Phagocyte become APC (places antigens from pathogens on its cell surface membrane)
3) T helper cell binds to these specific antigens on the APC to produce activated T helper cell which undergoes clonal expansion by rapid mitosis.
4) Active T helper cell:
- develop into memory cells
- binds to and activates cytotoxic T cell producing activated cytotoxic T cells and cytotoxic memory cells
- B cell becomes APC and active B cell binds to active T cell which caused it clonal expansion that produces memory B cells and plasma cells (these secrete antibdodies)
- stimulate phagocytes to engulf pathogens (phagocytosis)

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22
Q

Explain how cytotoxic T cells kill infected cells?

A

they produce perforin (a protein) that makes holes in cell surface membrane which then becomes freely permeable so the cell dies

Cytotoxic are most effective against killing viruses which are inside body cells as it prevents the virus from multiplying and infecting more cells

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23
Q

Which cells are involved in humoral immunity?

A

B cells

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24
Q

Explain what happens in a humoral response when a B cell responds to an antigen?

A

Millions of different types of B cells in the blood

One B cell has a ANTIBODY specific to the antigen on the pathogen where it’s shape is exactly complimentary

The antigen enters the B cell by endocytosis and gets presented on the surface. (APC)

T helper cells bind to the processed antigens and stimulate the B cell to divide by mitosis to form clones of identical B cells that all produce exactly the same antibody.

This is clonal selection and clonal expansion.

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25
Q

Define monoclonal antibody

A

Antibodies produced by clones of the same (B) cell

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26
Q

After B cell clones have been made what two types of cell do they differentiate into?

A

Memory B cells

Plasma cells

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27
Q

Memory B cells

A
  • responsible for secondary immune response
  • provide long term immunity
  • live a lot longer than plasma cells
  • do NOT produce antibodies directly
  • when the memory B cells encounter the same antigen again they divide rapidly into plasma cells and more memory cells
  • the plasma cells can then produce the antibody specific to the antigen whilst the new memory cells circuits in the blood ready for future infection by the same pathogen.
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28
Q

Explain the primary B cell immune response vs the secondary B cell immune response.

A

Primary immune response:

Millions of B cells in blood, only one has specific antibody to the antigen, bonds and is complimentary. B cell takes up the antigen by endocytosis and presents it on its cell surface membrane. T helper cell binds to processed antigens on the B cell (now an APC) and stimulate it to divide rapidly into plasma cells and memory cells.
Memory cells circulate for next time (what do they do next time?)

Secondary:

Memory cells encounter same antigen and divide rapidly to produce plasma cells (that produce the correct antibody) and more memory cells.
So faster response because memory cell bind to antigen? And immediately stimulate correct plasma cells with correct antibodies?

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29
Q

What do memory cells mean happens in the secondary immune response?

A

An increased quantity of the correct antibodies is secreted at a faster rate that the primary immune response

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30
Q

Summarise the role of B cells in humoral immunity. (6)

A

1) the surface antigens of the invading pathogen are taken up by a B cell
2) the B cell processes the antigen and presents it on its cell surface membrane
3) T helper cells bind to the processed antigens on the B cell and activate the B cell
4) this stimulate sin to divide rapidly by mitosis to produce clones (clonal selection and expansion) which are either memory B cells or plasma cells.
5) the plasma cells secrete the antibody specific to the antigen on the pathogen’s cell surface and kill the pathogen
6) the memory B cells circuit in the blood so next time the same pathogen invades they can divide rapidly into more memory B cells and plasma cells (which secrete the correct specific antibody)

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31
Q

Define antibody

A

Proteins with binding sites specific to a particular antigen that are serve test by plasma cells which have differentiated form B cells

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32
Q

Describe the structure of an antibody

A
  • 4 polypeptide chains
  • 2 heavy chains
  • 2 light chains
  • TWO antigen binding sites
  • one receptor binding site
  • forms antigen-antibody complexes
  • binding site is different on each antibody - ‘variable region’
  • ## rest of antibody is the same - ‘constant region’
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33
Q

What to talk about when reference antibody binding sites?

A
  • specific tertiary structure of the protein
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34
Q

How do antibodies assist destruction of a pathogen?

A
  • could cause AGGLUTINATION of bacterial cells… clumps of bacterial cells form making them easier for phagocytes to identify them
  • stimulates phagocytes to engulf the bacterial cells the antibodies are attached to
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35
Q

How does agglutination work?

A

Each antibody binds to two pathogenic cells causing them to clump together

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36
Q

Explain direct monoclonal antibody therapy in cancer treatment.

A
  • monoclonal antibodies that are specific to antigens on cancer cells are produced
  • these antibodies are given to a patient; they bind to the antigens on the cancer cells
  • by binding they block chemical signals that stimulate uncontrolled growth
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37
Q

Example of a monoclonal antibody used in cancer treatment?

A

Herceptin

Breast cancer monoclonal antibody

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38
Q

Advantage of direct monoclonal antibody therapy?

A

Since antibodies are not toxic and they are highly specific, they lead to fewer side effects that other forms of therapy

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39
Q

Explain indirect monoclonal antibody therapy in cancer treatment

A
  • involves attaching a radioactive or cytotoxic drug to the monoclonal antibody
  • when the antibody binds to the antigen on the cancer cell it kills them
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40
Q

Advantages of indirect monoclonal antibody therapy?

A
  • can be used in small doses (why?)

- using in small does is cheaper and means less side effects

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41
Q

Name four disease that monoclonal antibodies are used in diagnosis for?

A

Influenza
Hepatitis
Chlamydia
Certain cancers

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42
Q

How are monoclonal antibodies used in identification of tumors?

A

They bind to specific antigens on cancer cells causing them to clump together which makes it easier to identify a cancerous tumor that can then be treated or removed

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43
Q

How can monoclonal antibodies be used to diagnose prostrate cancer?

XXX

A

Men with prostate cancer produce more prostate specific antigen (PSA) leading to unusually high levels in the blood

Using a monoclonal antibody which interacts with this antigen means you can obtain a measure of how much PSA is in the blood (depending on how much monoclonal antibody binds?/clumping?)

Above normal level of PSA suggests disease so gives early warning

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44
Q

How are monoclonal antibodies used in pregnancy testing?

A

Used for early detection of pregnancy

Placenta produces human chorionic gonadatrophin (hCG) that is found in mother’s urine.

Monoclonal antibodies linked to colored particles; if they bind to the hCG present in urine,

hCG-antibody-colour complex moves along strip until it is trapped by a different type of antibody which creates a colored line.

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45
Q

Two disadvantages (ethics) of monoclonal antibodies

A
  • production of monoclonal antibodies involves use of mice. (Tumour induced in mice so can get tumour cells and specific antibodies which mice produce in response)
  • issues about conduct of drug trials: March 2006, six healthy volunteers involved in trial of new monoclonal antibody (TGN1412) in London. All six suffered multiple organ failure as a result of T cells overproducing chemicals that stimulate an immune response or attacking body tissue. All survived but highlights dangers of testing for safety of new drugs.
46
Q

Ethical use of monoclonal antibodies

On informed consent and success

A

Used to successfully treat number of diseases including cancer and diabetes

Informed consent required (patients should have full knowledge of the risks and benefits of the drugs)

47
Q

Explain how monoclonal antibodies are produced?

A

X

48
Q

Link AIDS and HIV

A

HIV (human immunodeficiency virus) causes AIDS (acquires immune deficiency syndrome) which then means a weakened immune system so more susceptible to diseases

49
Q

Describe the structure of HIV (3)

A
  • lipid envelope embedded with attachment proteins
  • protein layer - capsid - encloses two single strands of RNA (and some enzymes including reverse transcriptase)
  • matrix
50
Q

HIV is a

A

Retrovirus

51
Q

What are retroviruses?

A

Type of virus that uses special enzyme

Reverse transcriptase

To translate it’s genetic information into DNA. The DNA then integrates into the host cell’s DNA. And once integrated the virus can use components in the host cell to make reproduce.

52
Q

Describe the role of reverse transcriptase?

A

Transcribes single stranded RNA into DNA.

(Transcribes into one single stranded DNA and then is also able to synthesise DNA double helix once RNA has been reverse transcribed in the first step)

53
Q

HIV can…

A

Lie dormant in a person’s body for many years

54
Q

Summarise how HIV replicates.

A

1) HIV enters blood stream and circulates around the body
2) protein on HIV binds to CD4 on T helper cells
3) protein capsid fuses with the cell-surface membrane. The RNA and enzymes of HIV enter the T helper cell.
4) HIV reverse transcriptase converts the virus’s RNA into DNA
5) this DNA integrates into the T helper cell’s DNA in the nucleus
6) HIV DNA creates mRNA using cell’s enzymes. (This mRNA codes for new viral proteins and viral RNA that once made can be inserted into new viral particles)
7) mRNA passes out of nucleus through nuclear pore and uses cell’s protein synthesis mechanisms to make new HIV particles
8) HIV particles are exocytosed from T helper cell, as a vesicle ??¿

55
Q

How does HIV cause an inadequate immune response?

A
  • HIV attacks T helper cells and thus interferes with how they normally function

(Uninfected person = 800-1200 T helper cells in each mm^3 blood, infected = 200mm^3)

Without a sufficient number of T helper cells:

T helper cells cannot bind and activate B cells to divide to produce plasma cells (produce antibodies) or memory B cells

T helper cells cannot bind to processed antigens on APC (after phagocyte has taken up pathogen)

Active T helper cells cannot become memory cells

T helper cells cannot bind to and active cytotoxic T cells

All of this means the body can’t produce an adequate immune response so it becomes susceptible to other infections.

56
Q

What are typical symptoms of AIDS sufferers?

A

Infections of lungs, intestines, brain and eyes.

Weight loss, diarrhoea

57
Q

How does HIV cause death?

A

It doesn’t!

It causes AIDS which makes you more susceptible to disease

These SECONDARY disease cause death

58
Q

What does the ELISA test stand for?

A

Enzyme
Linked
Immunosorbant
Assay

59
Q

Summarise what the ELISA test does?

A

Detects the presence and quantity of a particular protein (often an antigen) [not wha it is, we need to know what we are looking for] in the body

60
Q

Describe the procedure of the ELISA test. (7)

A

1) apply the sample to a surface (eg. A slide) to which all antigens on the sample can attach to
2) wash surface several times to remove any unattached antigens
3) add the antibody specific to the antigen we are trying to detect and leave it to bind to it
4) wash the surface again to remove any excess antibody
5) add a second antibody (with an enzyme attached to it) that binds with the first antibody and allow time for binding
6) add colourless substrate of the enzyme. The enzyme acts on the substrate and changes it to a coloured product.
7) intensity of colour = amount of antigen present present

61
Q

How does the ELISA test actually work?

A

Eg.

5 antigens, bind to 5 antibodies, 5 antibodies with enzyme bind to the 5 antibodies that are bound to the antigen.

Adding substrate of enzyme means 5 lots of substrate will be used up but the 5 antibodies attached to the 5 antigens so little bit of colour so know little bit of antigen

62
Q

Uses of the ELISA test?

A

Detects HIV

pregnancy tests

cytokines or soluble receptors present in cell supernatant serum

Drug and allergen tests

63
Q

Why are antibiotics ineffective against viral disease like AIDS?

A

Viruses have a protein coat so no cell wall that antibiotics could target

When viruses are within an organisms own cells antibiotics cannot reach them

Viruses lack their own cell structures or metabolic pathways so no try obj for antibiotics to target (without damaging own cells?)

64
Q

What do antibiotics often target?

A

Hydrolyse cell wall

Or targets enzymes for cell wall synthesis

Eg. Penicillin - inhibits enzymes required for synthesis and assembly of the peptide cross -linkages in bacterial cell walls.

This means as water enters by osmosis the cell bursts

65
Q

Passive immunity

A

Introduction of antibodies into individuals from outside source

(No direct contact with pathogen or its antigen required to induce an immune response)

66
Q

Examples of passive immunity (2)

A

Antibodies acquired by fetid from mother as they pass across the placenta

Anti-venom given to the victims of snake bites

67
Q

Disadvantage of passive immunity

A

Antibodies not produced when they are broken down

No memory cells form so no lasting immunity

68
Q

Active immunity

A

Direct contact with pathogen or its antigen stimulate a production of antibodies by individuals own immune system

Generally long lasting

69
Q

Two types of active immunity

A

Natural active immunity

Artificial active immunity

70
Q

Natural active immunity

A

Occurs when an individual is infected with a disease in normal circumstances (body produced antibodies itself)

71
Q

Artificial active immunity

A

Induced the immune response but they don’t suffer the disease

(Forms basis of vaccination)

72
Q

How does a vaccine work?

A

Introduction of (small amount of) antigens from the pathogen

Stimulates immune response

Produces memory cells that remain in the blood and can rapidly divide to produce memory cells and more plasma cells (which then produces the antibodies)

73
Q

Features of a successful vaccination programme

A
  • must be economically available in large quantities
  • few side effects (unpleasant side effects could discourage people taking the vaccine)
  • means of production
  • means of transport (usually refrigerated as well)
  • means of storage (refrigerated, large space, hygienic conditions)
  • means of administering vaccine (need to train staff to have appropriate skills)
  • need centres to administer the vaccine
  • vaccine administration must be quick
  • must be possible to vaccinate majority of population to establish herd immunity
74
Q

How does hers immunity arise?

A

Arises when a sufficiently large proportion of population has been vaccinated making it difficult for the pathogen to spread within the population

75
Q

What does herd immunity mean for susceptible individuals?

A

It is unlikely that a susceptible individual will come into contact with an infected individual

76
Q

Why is herd immunity important?

A

Protects those who cannot be vaccinated

Eg. Babies and young children who’s immune systems haven’t fully developed yet

Those who are ill/ immune systems are compromised

77
Q

What is different about herd immunity for each disease?

A

The percentage of population to be vaccinate d to achieve herd immunity is different

78
Q

To achieve herd immunity when is vaccination best carried out?

A

At one time

79
Q

Reasons for why vaccination may not eliminate a disease? (6)

A

1) vaccination fails to induce immunity in people with defective immune systems

2) individuals might develop disease straight after vaccination before immune response from vaccination has occurred so they still don’t have enough antibodies or memory cells
( these individuals can infect others)

3) pathogen may mutate so it’s antigens change. Vaccines become ineffective because the antibodies that the memory cells produce are no longer complimentary or the new antigen
4) so many varieties of a pathogen that impossible to develop vaccine effective for them all (eg. Common cold you get infected by a different virus each time)
5) certain pathogens conceal themselves from the immune system (inside cells, in place spit of reach like the intestines) (eg. Cholera pathogen - vibrio cholerae)
6) individuals may not want to take vaccinations (religious, ethical, medical reasons) (eg. MMR Andrew Wakefield autism study)

80
Q

What’s a virus which antigenic variability?

A

Influenza

Constantly mutating

Changes in antigen mean new vaccines must be administered to individuals

(Immunity for influenza can be short lived)

81
Q

Ethics of vaccines

Disadvantages
+ what needs to be balanced

A
  • production involves animal use
  • side effects causing long term harm need to be balanced with harm disease could cause
  • unknown long term effects
82
Q

Questions on the ethics of vaccines (3)

A
  • who should vaccines be tested on, how should the trials be carried out and to what extent should individuals be asked to accept risks in the interests of public health
  • should vaccines be compulsory?
  • should expensive vaccine programmes continue if a disease is nearly eradicate seven of it means less money for treatment of other diseases?
83
Q

MMR vaccine

A

X

84
Q

Immunity

A

X

85
Q

X

A

X

86
Q

X

A

X

87
Q

X

A

X

88
Q

X

A

X

89
Q

Explain how proteins are made in a eukaryotic cell

A

In the nucleus is DNA

Ribosomes are made in the nucleolus

Ribosomes exit through nuclear pores and some float freely in cytoplasm whilst some attach to the rough ER.

Proteins synthesised by the ribosomes in the rough ER exit in vesicles and enter the golgi where they are further modified

90
Q

Where do we find eukaryotic cells?

A

Plants, animals and fungi

91
Q

What type of organelles do eukaryotic cells have versus prokaryotic cells?

A

Eukaryotic - membrane bound organelles

Prokaryotic - not membrane bound organelles

92
Q

State structures of the nucleus (5)

A 
> DNA wrapped in histone proteins 
> nuclear envelope
> nuclear pores
> nucleolus
> nucleoplasm
93
Q

Chromatin

A

Substance within chromosome consisting of DNA and protein (usually histones)

94
Q

Why is DNA in eukaryotic cells wrapped around histone proteins?

A

Support for DNA and makes DNA more compact, called ‘chromatin’

95
Q

Nuclear envelope

A
  • double membrane (two lipid bilayers) that protects everything in the nucleus
  • has nuclear pores
96
Q

Nuclear pores

A
  • within nuclear envelope and allow small molecules (eg. mRNA and ribosomes) so leave or enter.
  • too small for DNA to pass through
97
Q

Nucleolus

A
  • contains densely packed DNA and protein
  • can be more than one nucleolus

Functions:

  • produces mRNA and ?tRNA?
  • where ribosomes are assembled
98
Q

Nucleoplasm

A
  • contains DNA, chromatin, nucleotides, enzymes
99
Q

Ribosomes

A
  • site of protein synthesis
  • some attach to rough ER, others float around in cytoplasm
  • 80S in eukaryotic, 70S in prokaryotic
100
Q

Endoplasmic Reticulum (6 things)

A
  • interlinked membranes in the cytoplasm that form elongated sacks called cisternae
  • rough ER - has ribosomes attached (makes proteins)
  • smooth ER - NO ribosomes attached (makes lipids/carbohydrates)
  • found throughout cell but higher density near nucleus
  • can extend form the nuclear envelope
  • stores lipids, carbohydrates and proteins before they go to the golgi apparatus
101
Q

Golgi Apparatus (3 things)

A
  • series of flattened sacs (cisternae) and vesicles located by the ER
  • receives proteins and lipids from the rough ER,modifies and processes them so they leave in a golgi vesicle and move to different locations in the cell
  • modifies lipids, produces lysosomes, adds carbohydrates to proteins to form glycoproteins
102
Q

Lysosomes

A
  • type of golgi vesicle containing digestive enzymes
  • releases digestive enzymes that break down a cell after it has died or break down old organelles to recycle useful materials
103
Q

Describe the features of a mitochondria (4 things)

A

cristae - inner membrane folds into cristae ( layered structures that increase surface area so more enzymes and proteins can attach to it)

double membrane - outer membrane and inner membrane (which folds into the cristae)

matrix - fluid in inner membrane (contains proteins, enzymes, ribosomes)

oval shape

104
Q

State the features of a chloroplast

A

double membrane (inner + outer)
thylakoids
stroma

105
Q

thylakoid

A

dics - large surface area

contains chlorophyll

stack of thylakoids is a granum

surrounded by fluid stroma

106
Q

chloroplast stroma

A

contains single stranded DNA (so proteins can be made for photosynthesis), starch grains and enzymes needed to synthesis sugars

107
Q

Vacuole

A
  • surrounded by membrane called the tonoplast
  • contains cell sap (sugar, water, minerals)
  • supports plants making them turgid
  • sugar and amino acids inside can be a temporary food source
  • pigments can colour plants, attracting pollinating insects
108
Q

cell membrane functions

A
  • semi-permeable lipid bilayer so selected molecules can diffuse across the membrane
  • maintains cell’s chemical climate
  • cell membrane interacts with cell membrane of adjacent cells to form tissues
  • protects cell from surroundings
109
Q

Are prokaryotic cells smaller or larger than eukaryotic cells?

A

smaller

110
Q

Prokaryotic cells can be found in

A

bacteria

111
Q

What do prokaryotic cells NOT have?

A

no membrane bound organelles:

1) no nucleus
2) no mitochondria
3) no endoplasmic reticulum
4) no golgi apparatus
5) no vacuole
6) no lysosomes (these are membrane bound as well)
7) no chloroplasts

AQA A level Biology (36 decks)

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