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AS Biology > Chapter 5: Immunology > Flashcards

Chapter 5: Immunology Flashcards

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1
Q

what is a pathogen? Give three examples

A

disease-causing microorganism

- bacterium, virus, fungus

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2
Q

what is an antigen?

A
  • foreign glycoprotein/protein

- that stimulates an immune response

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3
Q

what is an antibody?

A
  • protein specific to an antigen, b/c of its complementary shape
  • produced by B cells/Secreted by plasma cellls
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4
Q

when a specific antibody encounters the corresponding specific foreign antigen what does it do?

A
  • joins onto this antigen and neutralises, inhibits or destroys it
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5
Q

contrast antibodies and enzymes [2 Marks]

A
  • antibodies have binding sites, enzymes have active sites
  • antibodies bind to antigens, enzymes speed up the rate of a chemical reaction
    OR
  • enzymes are catalysts, whereas antibodies aren’t
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6
Q

give two ways in which pathogens can cause disease

A
  • kills cells/tissues

- release toxins

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7
Q

suggest one advantage of programmed cell death

A
  • prevents replication of virus
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8
Q

Phagocytes and lysosomes are involved in destroying microorganisms. Describe how.

A
  • phagocytes engulf pathogen to form a phagosome
  • phagosome fuses with lysosome, lysosome contains enzymes - lysozymes
  • lysozymes digest pathogen
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9
Q

Describe how B-lymphocytes respond when they are stimulated by antigens

A

divide by mitosis / form clones;
produce plasma cells;
(plasma cells) make antibodies;
(plasma cells) produce memory cells;

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10
Q

Explain why one type of antibody will only detect one type of antigen [3 Marks]

A
  • Antibody’s variable region has very specific AA sequence
  • there a highly specific tertiary structure, tertiary structure of the binding site is complementary to antigen
  • forms antigen-antibody complex
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11
Q

what is a vaccination?

A
  • injection of (dead/inactive) antigens

- that stimulates formation of memory cells

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12
Q

Describe how antibodies are produced in the body following a viral infection [6 Marks]

A
  • virus contains antigens
  • virus engulfed by phagocyte
  • phagocyte presents antigens to B-cells
  • B cells activated (by helper T cells)
  • B cells divide to form clones by mitosis (plasma cells)
  • plasma cells produce antibodies specific/complementary to antigen

explaining:
(in humoral immunity B cell with complementary antibody on surface will bind to antigen, engulf it and present it - clonal selection. Then complementary helper T cell will bind to antigen presented on B cell and it will trigger T cell to divide by mitosis, forming clones which can stimulate B cell with complementary antibody to divide by mitosis and differentiate into plasma cells (which can develop into memory cells) producing more of complementary antibody - clonal expansion)

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13
Q

Describe how a gene could be isolated [4 Marks]

A
  • gene located using gene probe
  • cut using restriction enzymes, at specific base pairs
  • leaving sticky end/unpaired bases
  • cut DNA/vector using same restriction enzyme
  • join using DNA ligase and introduce vector into recombinant DNA in…wherever
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14
Q

People with AIDS die because they are unable to produce an immune response to pathogens. Explain why this leads to death. [3 Marks]

A
  • susceptible to other pathogens (bc of lower helper T cell count)
  • pathogens reproduce/cause disease
  • damage cells/tissues/organs
  • release toxins
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15
Q

how has the human digestive system evolved to defend itself from pathogens? [2 Marks]

A
  • Hydrochloric Acid released in stomach

- lowers pH and destroys pathogens that have entered body from external environment

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16
Q

how has the human respiratory system adapted to defend itself from pathogen invasion? [2 Marks}

A
  • tracheae lined with cilia (small hairs)

- waft foreign objects and trap them in secreted mucus which is then digested/prevented from reaching lungs

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17
Q

When an antigen binds to a receptor on a T cell, the T cell becomes activated and differentiates into different types of T cells. What are these T cells and what are their functions? [6 MARKS]

A

Memory T cells - remain in body from previous infections to enable a faster immune response of the body is re-infected
Cytotoxic/Killer T cells - destroys/kills foreign cells
Helper T cells - stimulate B cells to divide and secrete antibodies

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18
Q

how many polypeptide chains make up an antibody?

A

four

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19
Q

why is the shape of the variable region important?

A

complementary shape to specific antigens

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20
Q

what bonds hold the polypeptide chains together in an antibody?

A

disulfide bridges/bonds

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21
Q

what is meant by the term ‘agglutination’ in reference to antibody action? [3 MARKS]

A
  • each antibody binds to antigens on pathogen
  • pathogens become clumped together
  • phagocytes can easily engulf more pathogens at once
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22
Q

why in a graph will the secondary response be steeper than the primary immune response?

A
  • when body infected again by the same pathogen the response is quicker and stronger
  • memory B cells divide into plasma and produce antibodies
  • memory T cells divide into the correct type of cytotoxic/killer T cells
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23
Q

What cells are identified in the immune system?

A

1 Pathogens eg HIV
2 Cells from other organisms of the same species (eg organ transplants)
3 Abnormal body cells eg Cancer cells
4 Toxins, including those produced by certain pathogens like the bacterium that causes cholera

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24
Q

Explain the role of B-lymphocytes and T-lymphocytes in the defence of the body against a virus infection [6 MARKS]

A
  • B lymphocytes produce antibodies/involved in humoral response;
  • T lymphocytes involved in cell mediated immunity;
  • Phagocytes present antigens;
  • (specific) B lymphocytes recognise/bind to antigen;
    increase in numbers by mitosis;
  • produce plasma cells (which make antibodies);
  • killer T cells kill virus infected cells;
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25
Q

what are self and non-self cells?

A
  • SELF: cells with antigens/proteins on surface of our cells recognised as self-antigens
  • NON-SELF: cells have antigen that doesn’t originate in the body (non-self antigen) so lymphocytes recognize non-self antigens and produce antibodies that bind specifically to each antigen.
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26
Q

describe antigen variability and its effect on disease and disease prevention

A
  • when a pathogen changes their surface antigens due to changes in their genes
  • this means the immune system has to carry out primary response again (no memory cells for this antigen, no complementary antibodies)
  • makes it difficult to produces vaccines
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27
Q

what type of cell is a phagocyte?

A

a white blood cell

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28
Q

what causes antigen variability?

A

1 Random genetic mutation changes DNA base sequence.

  1. Results in different sequence of codons on mRNA
  2. Different primary structure of antigen = H-bonds, ionic bonds & disulfide bridges form in different places in tertiary structure.
  3. Different shape of antigen
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29
Q

Outline the process of Phagocytosis

A
  1. Phagocyte moves towards pathogen via chemotaxis (receptors on phagocyte bind to chemical attractants on surface of pathogen)
  2. Phagocyte engulfs pathogen via endocytosis to form phagosome.
  3. Phagosome fuses with lysosome (phagolysosome).
  4. Lysosome contains enzymes called lysozyme, lysozymes digest pathogen.
  5. Phagocyte absorbs the products from pathogen
    hydrolysis.
    - phagocytes presents some of the pathogen’s antigen on its surface (for B cells to bind to)
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30
Q

Explain the role of antigen-presenting cells (APCs)

A
  • phagocyte displays antigen from pathogen on
    its surface (after hydrolysis in phagocytosis).
  • this enhances recognition by helper T cells, which can’t directly interface with pathogens/ antigens in
    body fluid
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31
Q

give two features and two examples of the specific immune response

A
  • time lag and specific/individual to each pathogen

- e.g. (B and T lymphocytes/Cell-mediated and Humoral immunity)

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32
Q

give two features and two examples of the non-specific immune response

A
  • immediate and same for all pathogens

- e.g. inflammation and phagocytosis

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33
Q

what are t lymphocytes?

A

white blood cells that develop in bone marrow and mature in thymus gland
carry out cell-mediated response

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34
Q

what are b lymphocytes?

A

white blood cells that develop and mature in bone marrow

carry out humoral response

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35
Q

why is it called humoral immunity?

A
  • because it involves substances found in humor or body fluids
36
Q

what is the humoral response?

A
  • immune response involving the transformation of B cells into plasma cells that produce and secrete antibodies to a specific antigen
37
Q

what is the cell-mediated response?

A
  • activation of phagocytes, antigen-specific cytotoxic T cells, and the release of various cytokines in response to an antigen
  • doesn’t involve antibodies
38
Q

Outline the process of humoral immunity

A
  1. Complementary TH lymphocytes bind to foreign antigen on antigen-presenting T cells.
  2. Release cytokines that stimulate clonal expansion (rapid mitosis) of complementary B lymphocytes.
  3. B cells differentiate into plasma cells.
  4. Plasma cells secrete (monoclonal) antibodies with complementary variable region to antigen.
39
Q

Outline the process of the cell-mediated response.

A

1 Pathogens invade body cells or are taken in by phagocytes
2 The phagocyte places antigens from the pathogen on its cell-surface membrane.
3 Receptors on a specific helper T cell fit exactly onto these antigens.
4 This attachment activates the T cell to divide rapidly by mitosis and form clone of genetically identical cells..
5 The cloned T cells:
a develop into memory cells that enable a rapid response to future infections by the same pathogen
b stimulate phagoctyes to engulf pathogens by phagocytosis
c stimulate B cells to divide and secrete their antibody
d activate cytotoxic T cells

40
Q

describe the structure of an antibody

A

Quaternary structure: 2 ‘light chains’ held together by
disulfide bridges, 2 longer ‘heavy chains’.

  • binding sites on variable region of light chains have
    specific tertiary structure complementary to an antigen.
    -rest of the molecule is known as the constant region
41
Q

How do antibodies lead to the destruction of a pathogen?

A

Formation of antigen-antibody
complex results in agglutination, which
enhances phagocytosis (makes it easier to locate and engulf)

42
Q

what are monoclonal antibodies?

A
  • identical antibodies specific to an antigen from one type of plasma cell
43
Q

what are memory cells?

A
  • specialised T helper/ B cells produced from primary immune response
  • remain in low levels in the blood
  • divide very rapidly by mitosis if
    organism encounters the same pathogen
    again, resulting in a more efficient and rapid response
44
Q

Contrast the primary and secondary immune response

A

secondary response:
● Faster rate of antibody production.
● Shorter time lag between exposure & antibody production.
● Higher concentration of antibodies.
● Antibody level remains higher after the secondary response.
● Pathogen usually destroyed before any symptoms

45
Q

Explain how antigen variability affects the incidence of disease

A

● Memory cells no longer complementary to antigen = individual not immune = can catch the disease more than once.
● Many varieties of a pathogen = difficult to develop vaccine containing all antigen types

46
Q

Compare passive and active immunity

A

● both involve antibodies

● can both be natural or artificial

47
Q

what is passive immunity? give examples of both types

A
  • the short-term immunity which results from the introduction of antibodies from another person or animal
    passive artificial: injection of antibodies
    passive natural: antibodies in breastmilk/ across placenta
48
Q

what is active immunity? give examples of both types

A
  • long-term immunity when antibodies develop in a person’s own immune system (i.e. from their own b cells)
    active artifical: vaccine
    active natural: humoral response to infection
49
Q

contrast passive and active immunity

A 
Passive 
- no memory cells & short term b/c antibodies not
replaced when broken down =
short-term
- immediate 
- antibodies from external source 
- direct contact with antigen not
necessary
ACTIVE:
- memory cells produced = long-term
- time lag
- antibodies produced by plasma cells 
- direct contact with antigen
necessary
50
Q

Explain the principles of vaccination

A
  1. Vaccine contains dead/ inactive form of a pathogen
    or antigen.
  2. Triggers primary immune response.
  3. Memory cells are produced and remain in the
    bloodstream, so secondary response is rapid &
    produces higher concentration of antibodies.
  4. Pathogen is destroyed before it causes symptoms
51
Q

What is herd immunity?

A
  • vaccinating large proportion of population
    reduces available carriers of the pathogen.
  • protects individuals who have not been
    vaccinated e.g. those with a weak immune
    system
52
Q

suggest some ethical issues surrounding the use of

vaccines

A

● production may involve use of animals
● potentially dangerous side-effects
● clinical tests may be fatal
● compulsory vs opt-out

53
Q

describe clonal selection

A

1 antibody attaches to complementary antigen on B cell
2 antigen enters the B cell by endocytosis and gets presented on its surface.
3 Helper T-cells bind to these complementary antigens and stimulate B cells (this together w substances released from helper T-cells) to divide by mitosis into plasma cells all of which produce the antibody that is specific to the foreign antigen - clonal selection

54
Q

Are B cells with appropriate antibody produced in response to pathogens?

A
  • no

- they are present from birth. Being present, they simply MULTIPLY in response to the pathogen.

55
Q

explain how cytotoxic t cells kill infected cells?

A
  • produce protein called perforin that makes holes in the cell surface membrane
  • these holes mean cell membrane is freely permeable to all substances and the cell dies as a result
56
Q

explain how the humoral immunity and cell-mediated immunity work in the body together

A
  • both types of responses needed to remove pathogen
  • responses interact with each other, e.g. T-cells help to activate B-cells, and antibodies coat pathogens making it easier for phagocytes to engulf them
57
Q

describe the function of monoclonal antibodies

A

bind to the antigens on the surface of the pathogen to form lots of antigen-antibody complexes (agglutinations as pathogens clump together)
(enhance phagocytosis by making pathogens easier to locate and engluf)

58
Q

Describe Direct Monoclonal Antibody Therapy for Cancer Cells

A
  • mAb designed w binding site complementary to antigens on cancer cells (tumour markers)
  • these mAb given to a patient and attach themselves to the tumour markers, blocking the chemical signals that bind and stimulate their uncontrolled growth
  • designed to bind only to cancer cells so don’t harm other cells and mAb prevent cancer cell growing
59
Q

Advantage of direct monoclonal antibody therapy

A
  • antibodies aren’t toxic and are highly specific, they lead to fewer side effects than other forms of therapy.
60
Q

Describe Indirect Monoclonal Antibody Therapy

A
  • involves attaching a radioactive or cytotoxic drug (drug that kills cells) to the complementary mAb
  • when the antibody attaches to the cancer cells, it kills them
61
Q

Advantages of Indirect Monoclonal Antibody Therapy

A

can be used in smaller doses so:

  1. cheaper
  2. reduces any side effects the drug might have (because only accumulates near specific cells)
62
Q

uses of mAbs

A
  • mAb can be used to test for influenza, pregnancy etc.

- works via the ELISA test

63
Q

why are antibiotics ineffective 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 = difficult to
    destroy them without damaging normal body
    cells
64
Q

suggest the clinical applications of monoclonal

antibodies

A

● Pregnancy tests by detecting HCG hormones in urine.
● Diagnostic procedures e.g. ELISA test
● Targeted treatment by attaching drug to antibody so that it only binds to cells with abnormal antigen e.g. cancer cells due to specificity of tertiary structure of binding site.

65
Q

What is Apoptosis?

A
  • programmed cell death that occurs when lymphocytes show an immune response to self-cells,
  • occurs before lymphocytes mature
66
Q

describe the primary immune response

A
  • pathogen enters the body for the first time
  • primary response is slow b/c there aren’t enough B-cells to make complementary antibodies needed to bind to the antigens.
  • will show symptoms
  • after being exposed to the antigen, memory t-cells (which remember the antigen and will recognise it) and memory b-cells (which remember the antibodies and will make them quicker) are produced, making the person immune
67
Q

describe the secondary immune response

A
  • same pathogen enters the body again, the immune system will produce a quicker, stronger immune response.
  • clonal selection happens faster and complementary antibodies are released sooner
  • won’t show symptoms
68
Q

Explain the principle of the ELISA

test

A
  • detects presence of a specific antigen
  1. add test sample from patient to base of beaker (e.g. blood/urine) and wash (to remove any unbound test sample)
  2. add mAb complementary in shape to antigen you’re testing for, wash to remove any unbound antibodies
  3. add second antibody complementary in shape to first antibody. this second antibody has an enzyme attached
    4 substrate for enzyme (colourless) added, substrate produces coloured product when binds to enzyme
    5 presence of colour indicates presence of antigen in test sample and intensity of colour indicates quantity present
69
Q

describe the methodology of pregnancy tests (ELISA test)

A

1 application area contains mobile complementary mAb for hCG bound to coloured bead/dye
2 when urine applied to application area any hCG will bind to antibody on beads, forming an antigen-antibody complex
3 urine moves up stick to test strip, carrying any beads w/ it
4 test strip contains immoblised antibodies complementary to hCG, if hCG present test strip turns blue b/c immoblised antibody binds to any hCG

  • w/o hCG beads will pass through test area w/o binding to anything, so it won’t go coloured
70
Q

discuss ethical issues of using mAb in medical diagnoses

A
  • creating mAb requires using animals (mice) to produce antibodies and tumour cells
  • leads to debate whether to use animals is justified to enable treatment of cancer in humans and detect disease

THE GOOD:

  1. target specific
  2. cancer therapy
  3. diagnose disease

THE BAD:

  1. expensive and time-consuming
  2. side effects
  3. too specific
71
Q

describe the structure of HIV

A
  • outside is a lipid envelope, embedded in them are attachment proteins (peg like shapes).
  • inside envelope is protein layer called capsid that encloses two single strands of RNA and some enzymes
  • one of these enzymes is reverse transcriptase
72
Q

Role of reverse transcriptase

A
  • able to synthesize a double helix DNA once the RNA has been reverse transcribed in a first step into a single-strand DNA.
73
Q

Why is HIV a retrovirus?

A
  • presence of reverse transcriptase

- and so its ability to make DNA from RNA

74
Q

describe the replication of Human Immunodeficiency Virus (HIV)

A

1 attachment protein attaches to a receptor molecule on the cell membrane of the host helper T cell.
2 capsid is released into the cell, where it uncoats and releases RNA (genetic material) into helper T cell’s cytoplasm.
3 inside cell, reverse transcriptase is used to make a complementary strand of DNA from the viral RNA.
4 newly-made double-stranded DNA is moved into helper T cell’s nucleus where it’s inserted into the cell’s DNA.
5 viral protein is produced in protein synthesis
6 the viral proteins are assembled into new viruses, which bud from the cell and go and infect other cells.

75
Q

How does the destruction of T-cells (i.e. a low T-cell count) lead to the death of an infected person?

A
  • not enough T-cells to activate B cells so cannot make antibodies and activate immune system.
  • person unable to fight infection and leads to death
76
Q

How does HIV result in the symptoms of AIDS?

A
  1. Attachment proteins bind to complementary CD4
    receptor on TH cells.
  2. HIV particles replicate inside TH cells, killing or damaging them.
  3. AIDS develops when there are too few TH cells for the immune system to function.
  4. Individuals cannot destroy other pathogens & suffer from secondary diseases/ infections.
77
Q

When does HIV become AIDS?

A
  • when symptoms of their failing immune system start to appear
  • helper T cell count is below a certain level
78
Q

Symptoms of AIDS

A
  • unexplained weight loss, rare forms of pneumonia, rare cancers and infections not found in healthy human populations
79
Q

Why is the ELISA test useful?

A

especially useful where quantity of an antigen needs to be measured
- it’s very sensitive

80
Q

When a vaccine is given to a person, it leads to the introduction of antibodies against a disease-causing organism. Describe how. (5)

A

1 Vaccine contains antigen from pathogen
2 Macrophage presents antigen on its surface
3 T cells w/ complementary receptor protein bind to antigen
4 T cell stimulates B cell
5 (With) complementary antibody on its surface
6 B cells secretes large amounts of antibody
7 B cell divides to form clone all secreting same antibody

81
Q

not this topic but: define non-coding base sequences and describe where the non-coding multiple repeats are positioned in the genome

A
  • base triplets/DNA nucleotide bases that don’t code for an amino acid in a polypeptide
  • positioned between genes
82
Q

not this topic but: describe how mRNA is formed by transcription in eukaryotes [5 MARKS]

A
  • H bonds between DNA bases break
  • one DNA strand acts as template
  • free RNA nucleotides align by complementary base pairing
  • in RNA uracil base pairs with adenine
  • RNA polymerase joins adjacent RNA nucleotides
  • by phosphodiester bonds (between adjacent RNA nucleotides)
  • pre-mRNA spliced to form mRNA
83
Q

not this topic but: describe how a polypeptide is formed by translation of mRNA [6 MARKS]

A
  1. mRNA attaches to ribosomes
  2. tRNA anticodons bind to complementary mRNA codons
  3. tRNA brings a specific amino acid
  4. amino acids join by peptide bonds
  5. amino acids join together with use of ATP
  6. tRNA released (after AA joined to polypeptide)
  7. ribosome moves along mRNA to form polypeptide
84
Q

A vaccine can be used to produce immunity to HPV. Describe how memory cells are important in thus process

A
  • memory cells produced from previous infection
  • when individuals come in contact with virus/antigen (again)
  • rapid/secondary/greater response
  • destroys virus
  • no symptoms experienced/felt
85
Q

difference between clonal selection and clonal expansion

A
  • Clonal selection is the theory that specific antigen receptors exist on B cells before they’re presented with an antigen due to random mutations
  • After antigen presentation, selected B cells undergo clonal expansion because they have the needed antigen receptor (i.e. divide by mitosis to produce plasma cells)

AS Biology (9 decks)

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