Cell Recognition And The Immune System Flashcards

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
    e
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4
Q

Describe phagocytosis of pathogens (non-specific immune response)

A
  1. Phagocyte attracted by chemicals / recognises (foreign) antigens on pathogen
  2. Phagocyte engulfs pathogen by surrounding it with its cell membrane
  3. Pathogen contained in vesicle / phagosome in cytoplasm of phagocyte
  4. Lysosome fuses with phagosome and releases lysozymes (hydrolytic enzymes)
  5. Lysozymes hydrolyse / digest pathoge
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5
Q

Phagcytosis leads to …

A

Phagocytosis leads to presentation of antigens where antigens are displayed on the phagocyte cell-surface
membrane, stimulating the specific immune response (cellular and humoral response)

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6
Q

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

A
  • T lymphocytes recognise (antigens on surface of) antigen presenting cells eg. infected cells, phagocytes
    presenting antigens, transplanted cells, tumour cells etc.
    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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7
Q

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

A

B lymphocytes can recognise free antigens eg. in blood or tissues, not just antigen presenting cells.
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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8
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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9
Q

Struc of antibody

A

2x antigen binding sites
2x variable regions
2x constant region
2x light chain
2x heavy chain
1x disulphide bridge between heavy and light chain
2x disulphide bridge between 2 heavy chains

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10
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 onc

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11
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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12
Q

What is a vaccine?

A

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

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13
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
  6. These release antibodies faster and at a higher concentration
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14
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 diseas

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15
Q

Describe the differences between active and passive immunity

A

Initial exposure to antigen eg.
vaccine or primary infection
Vs No exposure to antigen
Memory cells involved vs No memory cells involved
Antibody produced and secreted
by B plasma cells
Vs Antibody introduced from another organism eg.
breast milk / across placenta from mother
Slow; takes longer to develops Faster acting
Long term immunity as antibody can be produced
in response to a specific antigen again vs
Short term immunity as
antibody hydrolysed (endo/exo/dipeptidases)

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16
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

17
Q

Describe the struc of a HIV particle

A

Attachment protein on lipid envelope
Capsid surrounds RNA and reverse transcriptase

18
Q

Describe the replication of HIV in helper T cells

A

1.HIV attachment proteins attach to receptors on helper T cell
2. Lipid envelope fuses with cell-surface membrane, releasing capsid into cell
3. Capsid uncoats, releasing RNA and reverse transcriptase
4. Reverse transcriptase converts viral RNA to DNA
5. Viral DNA inserted / incorporated into helper T cell DNA (may remain latent)
6. Viral protein / capsid / enzymes are produced
a. DNA transcribed into HIV mRNA
b. HIV mRNA translated into new HIV proteins
7. Virus particles assembled and released from cell (via budding)

19
Q

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

A

● HIV infects and kills helper T cells (host cell) as it multiplies rapidly
○ So T helper cells can’t stimulate cytotoxic T cells, B cells and phagocytes
○ So B plasma cells can’t release as many antibodies for agglutination & destruction of pathogens
● Immune system deteriorates → more susceptible to (opportunistic) infections
● Pathogens reproduce, release toxins and damage cells

20
Q

Explain why antibiotics are ineffective against viruses

A

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

21
Q

What is a monoclonal antibody?

A

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

22
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

23
Q

Explain why antibiotics are ineffective against viruses

A

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

24
Q

What is a monoclonal antibody?

A

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

25
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

Some monoclonal antibodies are also designed to block antigens / receptors on cells

26
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

27
Q

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

A

Example method 1 (direct ELISA):
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)

Example method 2 (sandwich ELISA):
1. Attach specific monoclonal antibodies to well
2. Add sample with potential antigens, then wash well
3. Add complementary monoclonal antibodies with enzymes attached → bind to antigens if present
4. Wash well → remove unbound antibodies (to prevent false positive)
5. Add substrate → enzymes create products that cause a colour change (positive result)

28
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)
29
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

30
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

31
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

32
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?
● Were placebo / control groups used for comparison?
● Was the duration of the study long enough to show long-term effects?
● Was the trial double-blind (neither doctor / patient knew who was given drug or placebo) to reduce bias?

33
Q

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

A

Suggest some points to consider when evaluating evidence and data
relating to the use of vaccines and monoclonal antibodies
● 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?
● Was the standard deviation of final results large, showing some people did not benefit?
● Did standard deviations of start & final results overlap, showing there may not be a significant difference?
● What dosage was optimum? Does increasing dose increase effectiveness enough to justify extra cost?
● Was the cost of production & distribution low enough?