Topic 2 : 2.4 Cell recognition and the immune system Flashcards

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1
Q

What is an antigen?

A

● Foreign molecule / protein / glycoprotein / glycolipid
● That stimulates an immune response leading to production of antibody

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2
Q

How are cells identified by the immune system?

A

● Each type of cell has specific molecules on its surface (cell-surface membrane / cell wall) that identify it
● Often proteins → have a specific tertiary structure (or glycoproteins / glycolipids)

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3
Q

What types of cells and molecules can the immune system identify?

A
  1. Pathogens (disease causing microorganisms) eg. viruses, fungi, bacteria
  2. Cells from other organisms of the same species (eg. organ transplants)
  3. Abnormal body cells eg. tumour cells or virus-infected cells
  4. Toxins (poisons) released by some bacteria
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4
Q

Describe phagocytosis of pathogens (non-specific immune response)

A

Phagocyte detects chemicals/antigens on pathogen.
Phagocyte engulfs pathogen with its membrane.
Pathogen forms a vesicle (phagosome) in the cytoplasm.
Lysosome fuses with phagosome, releasing lysozymes.
Lysozymes digest the pathogen.

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5
Q

Describe the response of T lymphocytes to a foreign antigen (the cellular
response)

A

Specific helper T cells with complementary receptors (on cell surface) bind to antigen on
antigen-presenting cell → activated and divide by mitosis to form clones which stimulate:
● Cytotoxic T cells → kill infected cells / tumour cells (by producing perforin)
● Specific B cells (humoral response - see below)
● Phagocytes → engulf pathogens by phagocytosis

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6
Q

Describe the response of B lymphocytes to a foreign antigen (the humoral
response)

A
  1. Clonal selection:
    ○ Specific B lymphocyte with complementary receptor (antibody on cell surface) binds to antigen
    ○ This is then stimulated by helper T cells (which releases cytokines)
    ○ So divides (rapidly) by mitosis to form clones
  2. Some differentiate into B plasma cells → secrete large amounts of (monoclonal) antibody
  3. Some differentiate into B memory cells → remain in blood for secondary immune response
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7
Q

What are antibodies?

A

● Quaternary structure proteins (4 polypeptide chains)
● Secreted by B lymphocytes eg. plasma cells in response to specific antigens
● Bind specifically to antigens forming antigen-antibody complexes

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8
Q

Describe the structure of an antibody

A

on email

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9
Q

Explain how antibodies lead to the destruction of pathogens

A

● Antibodies bind to antigens on pathogens forming an antigen-antibody complex
○ Specific tertiary structure so binding site / variable region binds to complementary antigen
● Each antibody binds to 2 pathogens at a time causing agglutination (clumping) of pathogens
● Antibodies attract phagocytes
● Phagocytes bind to the antibodies and phagocytose many pathogens at once

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10
Q

Explain the differences between the primary & secondary immune response

A

● Primary - first exposure to antigen
○ Antibodies produced slowly & at a lower conc.
○ Takes time for specific B plasma cells to be
stimulated to produce specific antibodies
○ Memory cells produced
● Secondary - second exposure to antigen
○ Antibodies produced faster & at a higher conc.
○ B memory cells rapidly undergo mitosis to
produce many plasma cells which produce
specific antibodies

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11
Q

What is a vaccine?

A

● Injection of antigens from attenuated (dead or weakened) pathogens
● Stimulating formation of memory cells

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12
Q

Explain how vaccines provide protection to individuals against disease

A
  1. Specific B lymphocyte with complementary receptor binds to antigen
  2. Specific T helper cell binds to antigen-presenting cell and stimulates B cell
  3. B lymphocyte divides by mitosis to form clones
  4. Some differentiate into B plasma cells which release antibodies
  5. Some differentiate into B memory cells
  6. On secondary exposure to antigen, B memory cells rapidly divide by mitosis to produce B plasma cells
  7. These release antibodies faster and at a higher concentration
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13
Q

Explain how vaccines provide protections for populations against disease

A

● Herd immunity - large proportion of population vaccinated, reducing spread of pathogen
○ Large proportion of population immune so do not become ill from infection
○ Fewer infected people to pass pathogen on / unvaccinated people less likely to come in contact
with someone with disease

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14
Q

Describe the differences between active and passive immunity

A

Active immunity
Initial exposure to antigen eg.
vaccine or primary infection

Memory cells involved

Antibody produced and secreted
by B plasma cells

Slow; takes longer to develop

Long term immunity as antibody can be produced
in response to a specific antigen again

Passive :

No exposure to antigen

No memory cells involved

Antibody introduced from another organism eg.
breast milk / across placenta from mother

Faster acting

Short term immunity as

antibody hydrolysed

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15
Q

Explain the effect of antigen variability on disease and disease prevention

A

● Antigens on pathogens change shape / tertiary structure due to gene mutations (creating new strains)
● So no longer immune (from vaccine or prior infection)
○ B memory cell receptors cannot bind to / recognise changed antigen on secondary exposure
○ Specific antibodies not complementary / cannot bind to changed antigen

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16
Q

Describe the structure of a HIV particle

A

check email

17
Q

Describe the replication of HIV in helper T cells

A
  1. HIV attachment proteins bind to receptors on helper T cells.
    2 lipid envelope fuses with the cell membrane, releasing the capsid.
  2. capsid uncoats, releasing RNA and reverse transcriptase.
  3. Reverse transcriptase converts viral RNA to DNA.
  4. Viral DNA integrates into the helper T cell DNA (may remain latent).
  5. Viral proteins are produced:
    a. DNA transcribed into HIV mRNA.
    b. HIV mRNA translated into new proteins.
  6. Virus particles are assembled and released via budding.
18
Q

Explain how HIV causes the symptoms of acquired immune deficiency
syndrome (AIDS)

A
  1. HIV infects and kills helper T cells, impairing immune response.
  2. Cytotoxic T cells, B cells, and phagocytes can’t be properly stimulated, reducing antibody production.
  3. The immune system weakens, increasing susceptibility to opportunistic infections.
  4. Pathogens reproduce, release toxins, and damage cells.
19
Q

Explain why antibiotics are ineffective against viruses

A

● Viruses do not have metabolic processes (eg. do not make protein) / ribosomes
● Viruses do not have bacterial enzymes / murein cell wall

20
Q

What is a monoclonal antibody?

A

● Antibody produced from genetically identical / cloned B lymphocytes / plasma cells
● So have same tertiary structure

21
Q

Explain how monoclonal antibodies can be used in medical treatments

A

● Monoclonal antibody has a specific tertiary structure / binding site / variable region
● Complementary to receptor / protein / antigen found only on a specific cell type (eg. cancer cell)
● Therapeutic drug attached to antibody
● Antibody binds to specific cell, forming antigen-antibody complex, delivering drug

22
Q

Explain how monoclonal antibodies can be used in medical diagnosis

A

● Monoclonal antibody has a specific tertiary structure / binding site / variable region
● Complementary to specific receptor / protein / antigen associated with diagnosis
● Dye / stain / fluorescent marker attached to antibody
● Antibody binds to receptor / protein / antigen, forming antigen-antibody complex

23
Q

Explain the use of antibodies in the ELISA (enzyme-linked immunosorbent
assay) test to detect antigens

A
  1. Attach sample with potential antigens to well
  2. Add complementary monoclonal antibodies with enzymes attached → bind to antigens if present
  3. Wash well → remove unbound antibodies (to prevent false positive)
  4. Add substrate → enzymes create products that cause a colour change (positive result)
24
Q

Explain the use of antibodies in the ELISA test to detect antibodies

A
  1. Attach specific antigens to well
  2. Add sample with potential antibodies, wash well
  3. Add complementary monoclonal antibodies
    with enzymes attached → bind to antibodies if
    present
  4. Wash well → remove unbound antibodies
  5. Add substrate → enzymes create products that
    cause a colour change (positive result)
25
Q

Suggest the purpose of a control well in the ELISA test

A

● Compare to test to show only enzyme causes colour change
● Compare to test to show all unbound antibodies have been washed away

26
Q

Suggest why failure to thoroughly wash the well can result in a false positive
in the ELISA test

A

● Antibody with enzyme remains / not washed out
● So substrate converted into colour product

27
Q

Discuss some general ethical issues associated with the use of vaccines and
monoclonal antibodies

A

● Pre-clinical testing on / use of animals - potential stress / harm / mistreatment
○ But animals not killed & helps produce new drugs to reduce human suffering
● Clinical trials on humans - potential harm / side-effects
● Vaccines - may continue high risk activities and still develop / pass on pathogen
● Use of drug - potentially dangerous side effects

28
Q

Suggest some points to consider when evaluating methodology relating to
the use of vaccines and monoclonal antibodies

A

● Was the sample size large enough to be representative?
● Were participants diverse in terms of age, sex, ethnicity and health status?

29
Q

Suggest some points to consider when evaluating evidence and data
relating to the use of vaccines and monoclonal antibodies

A

● What side effects were observed, and how frequently did they occur?
● Was a statistical test used to see if there was a significant difference between start & final results?