Topic 5 - Cell recognition and the immune system Flashcards

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1
Q

Antigen

A

Molecules which, when recognised as non self/foreign by the immune system, can stimulate an immune response and lead to the production of antibodies

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2
Q

The specificity of antigens allows the immune system to identify…

A
  • Pathogens e.g. viruses, fungi, bacteria
  • Cells from other organisms of the same species e.g. organ transplant
  • Abnormal body cells e.g. cancerous cells
  • Toxins released from bacteria
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3
Q

Phagocytosis of pathogens - non specific immune response

A
  1. Phagocyte recognises foreign antigens on the pathogen and binds to the antigen
  2. Phagocyte engulfs pathogen by surrounding it with its cell surface membrane / cytoplasm
  3. Pathogen contained in vacuole/vesicle/phagosome in cytoplasm of phagocyte
  4. Lysosome fuses with phagosome and releases lysosomes (hydrolytic enzymes) into the phagosome
  5. These hydrolyse/digest the pathogen
  6. Phagocyte becomes antigen presenting cell and stimulates specific immune response
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4
Q

Cell mediated response

A
  1. T lymphocytes recognises antigen presenting cells after phagocytosis
  2. Specific T helper cell with receptor complementary to specific antigen binds to it, becoming activated and dividing rapidly by mitosis to form clones which:
    a) Stimulate B cells for the humoral response
    b) Stimulate cytotoxic T cells to kill infected cells by producing perforin
    c) Stimulate phagocytes to engulf pathogens by phagocytosis
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5
Q

The humoral response

A
  1. Clonal selection:
    a) specific B cell binds to antigen presenting cell and is stimulating by helper T cells which releases cytokines
    b) divides rapidly by mitosis to form clones (clonal expansion)
  2. Some become B plasma cells for the primary immune response - secrete large amounts of monoclonal antibody into blood
  3. Some become B memory cells for the secondary immune response
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6
Q

Primary response

A
  • Produces antibodies slower and at a lower concentration because:
  • Not many B cells available that can make the required antibody
  • T helpers need to activate B plasma cells to make antibodies (takes time)
  • So infected individual will express symptoms
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7
Q

Secondary response

A
  • Produces antibodies faster and at a higher concentration because
  • B and T memory cells present
  • B memory cells undergo mitosis quicker / quicker clonal selection
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8
Q

Antibodies

A
  • Quaternary structure protein
  • Secreted by B lymphocytes
  • Binds specifically to antigens forming an antigen-antibody complex
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9
Q

Describe and explain how the structure of an antibody relates to its function

A
  • Primary structure of protein = sequence of amino acids in a polypeptide chain:
  • Determines the folding the secondary structure as R groups interact
  • Determines the specific shape of the tertiary structure and position of hydrogen, ion and disulphide bonds
  • Quaternary structure is comprised of 4 polypeptide chains held together by hydrogen, ionic and disulphide bonds:
  • Enables the specific shaped variable region (binding site) to form which is a complementary shape to a specific antigen
  • Enables antigen-antibody complex to form
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10
Q

How do antibodies work to destroy pathogens e.g. bacterial cells

A
  • Binds to two pathogens at a time (at variable region/binding site) forming an antigen-antibody complex
  • Enables antibodies to clump the pathogens together - agglutination
  • Phagocytes bind to the antibodies and phagocytose many pathogens at once

Note: The hinge region means an antibody can bind to antigens/pathogens different distances apart.

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11
Q

What is a vaccination?

A
  • injection of antigens
  • From attenuated (dead or weakened) pathogens
  • Stimulates the formation of memory cells
  • A vaccine can lead to symptoms because some of the pathogens might be alive therefore, the pathogen could reproduce and release toxins, which can kill cells
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12
Q

The use of vaccines to provide protection for individuals against disease

A
  • Normal immune response but the important part is that memory cells are produced
  • On reinfection / secondary exposure to the same antigen, the secondary response therefore produces antibodies faster and at a higher concentration
  • Leading to the destruction of a pathogen before it can cause harm = immunity
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13
Q

The use of vaccine to provide protection for populations against disease (herd immunity)

A
  • Large proportion but not 100% of population vaccinated against a disease - herd immunity
  • Makes it more difficult for the pathogen to spread through the population because:
  • More people are immune so fewer people in the population carry the pathogen
  • Few susceptible so less likely that a non vaccinated individual will come into contact with an infected person and pass on the disease
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14
Q

Differences between active and passive immunity

A

Active immunity:
- Initial exposure to antigen e.g. vaccine or primary infection
- Memory cells involved
- Antibody is produces and secreted by (B) plasma cells
- Slow; takes time to develop
- Long term immunity –> antibody can be produced un response to specific antigen again

Passive immunity:
- No exposure to anitgen
- No memory cells involved
- Antibody introduced into body from another organism e.g. breast milk/across placenta from mother
- Fast acting
- Short term immunity (antibody broken down)

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15
Q

Ethical issues associated with the use of vaccines

A
  • Tested on animals before use on humans –> animals have a CNS so feel pain
  • Tested on humans –> volunteers may put themselves at unnecessary risk of contracting the disease because they think they’re fully protected e.g. HIV so have unprotected sex
  • Can have side effects
  • Expensive - less money spent on research and treatments of other diseases
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16
Q

Antigen variability is often an explanation for why…

A
  • New vaccines against a disease need to be developed more frequently e.g. influenza
  • Vaccines against a disease may be hard to develop or cant be developed in the first place e.g. HIV
  • May experience a disease more than once e.g. common cold
17
Q

Explain the effect of antigen variability on disease

A
  • Change in antigen shape (due to genetic mutation)
  • Not recognised by B memory cell - no plasma cells/antibodies
  • Not immune
  • must re-undergo primary immune response –> slower/relsease lower concentration of antibodies
  • Disease symptoms felt
18
Q

Explain the effect of antigen variability on disease prevention (vaccines)

A
  • Change in antigen shape (due to genetic mutation
  • Existing antibodies with a specific shape unable to bind to changed antigens / form antigen-antibody complex
  • Immune system i.e. memory cells won’t recognise different antigens (strain)
19
Q

Evaluate methodology, evidence and data relating to the use of vaccinations

A

A successful vaccination programme:
- Produce suitable vaccine:
- Effective - make memory cells
- No major side effects –> side effect discourage individuals from being vaccinated
- Low cost/economically viable
- Provides herd immunity

20
Q

The use of monoclonal antibodies

A
  • Monoclonal antibody = antibody produced from a single group of genetically identical (clones) B cells / plasma cells
  • Identical structure
  • Binds to specific complimentary antigen
  • Have a binding site with a specific tertiary structure
  • Only one complementary antigen will fit
21
Q

Why are monoclonal antibodies useful in medicine

A
  • Only bind to specific target molecules
  • Antibodies have a specific tertiary structure that’s complementary to a specific antigen which can bind/fit to the antibody
22
Q

Monoclonal antibodies: targeting medication to specific cell types by attaching a therapeutic drug to an antibody

A

Example: Cancer cells

  1. Monoclonal antibodies made to be complementary to antigens specific to cancer cells –> cancer cells are abnormal body cells with different antigens (tumour markers)
  2. Anti-cancer drug attached to antibody
  3. Antibody binds / attaches to cancer cells (forming antigen-antibody complex)
  4. Delivers attached anti-cancer drug directly to specific cancer cells so drug accumulates –> fewer side effects e.g. fewer normal body cells killed
23
Q

Exam question example: some cancer cells have a receptor protein in their cell-surface membrane that binds to a hormone called growth factor. This stimulates the cancer cells to divide. Scientists have produced a monoclonal antibody that stops this stimulation. Use your knowledge of monoclonal antibodies to suggest how this antibody stops the growth of a tumour (3 marks)

A
  • Antibody has specific tertiary structure / binding site / variable region
  • Complementary (shape / fit) to receptor protein / GF / binds to receptor protein
  • Prevents GF binding (to receptor)
24
Q

Monoclonal antibodies: medical diagnosis

A

Example: pregnancy test

  • Pregnant women have the hormone hCG in their urine
  • Urine test strip has 3 parts with 3 different antibodies:
  • Application area, position 1: antibodies complementary to hCG (bound to a blue coloured bead)
  • Middle, position 2: antibodies complementary to hCG-antibody complex
  • End position 3: antibodies complementary to antibody without hCG attached
  • If pregnant:
  • hCG binds to antibodies in application area = hCG antibody complex
  • Travels up test strip, binds to antibodies at position 2 = blue line

If not pregnant:
- No hCG in urine so hCG doesn’t bind to antibodies in application area so doesn’t bind to antibodies in position 2 = no blue line
- Bind to antibodies at position 3 –> blue line = control

25
Q

The use of antibodies in ELISA (enzyme linked immunosorbent assay) test

A

Can determine if a patient has:
a) antibodies to a certain antigen
b) antigen to a certain antibody
- used to diagnose diseases or allergies (e.g. lactose intolerance)

26
Q

Why use controls when performing the ELISA test?

A
  • Controls enable a comparison with the test
  • To show that:
  • Only the enzyme and nothing else causes colour change
  • Washing is effective and all unbound antibody is washed away
27
Q

Explain why the secondary and detection antibody must be washed away during ELISA?

A
  • Enzyme attached to antibody react with substrate turning the solution a different colour; indicates a positive result
  • Not washed out –> enzymes will react with the substrate
  • Therefore give a positive result even if no antigen present (false positive)
28
Q

Ethical issues associated with the use of monoclonal antibodies

A
  • Animals are involved in the production of monoclonal antibodies i.e. by producing cancer in mice who have a CNS so feel pain, and it is unfair to give them a disease
  • Although effective treatment for cancer and diabetes has caused deaths when used in treatment of Multiple Sclerosis:
  • Patients need to be informed of risk and benefits before treatment so they can make informed decisions
29
Q

The structure of HIV - human immunodeficiency virus

A
30
Q

The replication of HIV in helper T cells

A
  1. HIV infects T helper cells (host cell)
  2. Virus lipid envelope fuses with cell surface membrane and capsid released into cell which uncoats, releasing RNA and reverse transcriptase into cytoplasm.
  3. Viral DNA is made from viral RNA
    - Reverse transcriptase produces a complementary viral DNA strand from viral RNA template
    - Double stranded DNA is made from this (DNA polymerase)
  4. Viral DNA integrated into hosts cell’s DNA (by enzyme integrase)
  5. This remains latent for a long time in host cell until activated
  6. Host cell enzymes used to make viral RNA to make a new virus
  7. New virus bud from cell (taking some of cell surface membrane as envelope)
  8. Eventually kills helper T cells
  9. Most host cells are infected and process repeat
31
Q

How HIV cause the symptoms of AIDS

A
  • Infects and kills helper T cells (host cell) as it multiplies rapidly
  • T helper cells then cant stimulate cytotoxic T cells, B cells and phagocytes –> imparted immune response
    e.g. B plasma cells can’t secrete antibodies from agglutination and destruction of pathogens by phagocytosis

-Immune system deteriorates:
-More susceptible to infections
- Diseases that wouldn’t cause serious problems in healthy immune system are deadly (opportunistic infections) e.g. pneumonia

32
Q

Why antibiotics are ineffective against viruses

A
  • Antibiotics cant enter human cells - but viruses exist in its host cell (acellular)
  • Viruses don’t have their own metabolic reactions e.g. ribosomes (use of host cell’s) which antibiotics target
  • If we did use them … act as a selection pressure + gene mutation = resistant strain of bacteria via natural selection –> reducing effectiveness of antibiotics and waste money