immune response Flashcards

1
Q

Describe how T lymphocytes recognise and respond to the influenza virus.

A

T lymphocyte receptors recognise shape of viral antigen;
clone (once only);
destroy virus;

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2
Q

Describe how B lymphocytes respond to the influenza virus

A

clone (once only);
produce antibodies;
effect of antibody e.g. stimulation of phagocytosis /
precipitation of toxins;

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3
Q

The MMR vaccine contains attenuated microorganisms.

What is an attenuated microorganism?

A

Microorganism alive/active;

But does not cause symptoms of disease/Avirulent

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4
Q

graph of influenza deaths: slowly decreases sudden rise explain why

A

fall in deaths due to rise in number of people with immunity / better care / targeting vaccination at vulnerable;

mutation of virus / new strain;
mutant form not recognised by memory cells (allow antibodies);

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5
Q

Neuraminidase is an enzyme which breaks down molecules in the surface membrane of epithelial cells and allows the viruses to be released from the cells.
New drugs have recently become available for treating influenza. One type is a neuraminidase inhibitor. Explain how this type of drug would act as a treatment for influenza.

A

alter shape of active site of neuraminidase / block active site;
virus unable to leave host cells;

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6
Q

Describe how HIV is replicated after it has entered a human cell.

A

Reverse transcriptase;
Enzyme uses (HIV) RNA to make DNA (copy);
DNA joined to (host) cell’s DNA/chromosome;
DNA used to make HIV RNA (copies);
And HIV capsid proteins/enzymes;
Made at (host) ribosomes;
Assembly of new virus particles;
Budding off from membrane (of host cell);

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7
Q

The destruction of T-cells by HIV leads to the death of an infected person.
Explain how.

A

Not enough/no T-cells to activate B-cells/lead to antibody production/activate immune system;
Person unable to fight /more prone to (opportunistic) infections/cancer;
Accept diseases
Example of infection/cancer;

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8
Q

A child was given the MMR vaccine and was given a second dose of the vaccine as a booster later.
(i) It took more than a week for antibodies to appear in the child’s blood after the first vaccination. Explain why.

A

primary response
(Takes time for) antigen to be recognised;
(Takes time for) T cells to be activated;
B-cell activation/clonal selection/expansion;
Plasma cells to make (specific) antibodies;
Time for enough antibodies to measure;

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9
Q

A child was given the MMR vaccine and was given a second dose of the vaccine as a booster later.

The concentration of antibodies increased immediately after the second vaccination.
Explain why.

A

secondary response:
Memory cells (present);
Respond immediately / can produce antibodies immediately;

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10
Q

Give two factors, other than cost, that should be considered when selecting an antibiotic to treat a bacterial disease.

A

side effects / allergic reactions / low toxicity to cells;
interaction with other drugs / effective in conditions of use / reasonably stable;
should only act on the problem bacteria / narrow spectrum;
how much resistance the bacteria have built up;

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11
Q

Tetracycline prevents tRNA binding
Explain how this antibiotic slows down the rate of growth of bacteria.

Suggest why tetracycline has no effect on human cells.

A

prevents tRNA binding to ribosomes / amino acid / mRNA;
amino acids not available / brought / picked up;

only prevents tRNA binding to 70S / prokaryotic / bacterial
ribosomes / human ribosomes are different sizes / shapes / structure;

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12
Q

Chloramphenicol prevents peptide bonds forming

Explain how this antibiotic slows down the rate of growth of bacteria.

A

chloramphenicol
prevents amino acids being joined / prevents primary structure forming;
no enzymes / no structural proteins formed;

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13
Q

Changes to the protein coat of the influenza virus cause antigenic variability. Explain how antigenic variability has caused some people to become infected more than once with influenza viruses.

A

memory B / T cells do not recognise (new antigens);
antibodies previously produced are not effective
as shape not complementary to new antigen;

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14
Q

Describe the role of macrophages in stimulating B lymphocytes

A

antigen in membrane presented to lymphocytes /

produce cytokinins;

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15
Q

Explain how the changes shown in the drawings (larger cell and more organelles) are related to the function of B lymphocytes.

A

mitochondria provide (more) ATP / energy;
(more) RER / ribosomes synthesise proteins;
(more) Golgi body secretes / modifies or packages proteins /
produces glycoproteins;
(B lymphocytes) produces antibodies;

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16
Q

What is an antigen?

A

protein / glycoprotein / glycolipid / polysaccharide / molecule;
on surface / membrane (of cell);
causes immune response / description / triggers antibody
production;

17
Q

What is a monoclonal antibody?

A

hybrid cell from tumour / cancer and
B-lymphocyte / hybridoma;
antibodies all the same / from one type of plasma cell;
specific to / complementary to / fits only one antigen;

18
Q

Explain why this test detects prostate cancer, but not any other disease.

A

antibodies specific / only binds to PSA;
PSA only associated with prostate cancer / not with other
diseases;

19
Q

Explain why there will not be a colour change if the blood sample does not contain PSA.

A

antibody with enzyme only attaches if PSA present / washed
away if no PSA;
no colour change without enzyme;

20
Q

Give two ways in which pathogens can cause disease when they enter the body of their host.

A

Damage / destruction of cells / tissues;

Production of toxins;

21
Q

Vaccines provide protection against disease. What is a vaccine?

A

Contains antigen / proteins / dead / weakened microorganism / pathogen / virus / bacteria;
Stimulates production of antibodies / plasma cells / memory cells;

22
Q

What is an antibody?

A

protein / immunoglobulin;
specific to antigen;
idea of ‘fit’ / complementary shape;

23
Q

Describe how antibodies are produced in the body following a viral infection.

A
  1. virus contains antigen;
  2. virus engulfed by phagocyte / macrophage;
  3. presents antigen to B-cell;
  4. memory cells / B-cell becomes activated;
  5. (divides to) form clones;
  6. by mitosis;
  7. plasma cells produce antibodies;
  8. antibodies specific to antigen;
  9. correct reference to T-cells / cytokines;
24
Q

Taking a course of these antibodies from plants to treat a herpes infection would not produce long-term protection against disease. Explain why.

A

passive / person is not making own antibodies / antibodies not replaced;
memory cells not produced;

25
Q

Describe how the antibody gene could be isolated from an animal cell and introduced into a crop plant such as maize

A
  1. antibody gene located using gene probe;
  2. cut using restriction enzyme;
  3. at specific base pairs;
  4. leaving sticky ends / unpaired bases;
  5. cut maize / DNA / vector using same restriction enzyme;
  6. join using DNA ligase;
  7. introduce vector into maize / crop / recombinant DNA into maize;
26
Q

Explain one advantage of using antibodies from plants to treat a disease, rather than antibodies produced in an experimental animal

A

fewer ethical difficulties / less risk of infection;

27
Q

Some white blood cells are phagocytic. Describe how these phagocytic white blood cells destroy bacteria.

A
  1. Phagocyte attracted to bacteria by chemicals / recognise antigens on bacteria as foreign;
  2. Engulf / ingest bacteria;
  3. Bacteria in vacuole / vesicle;
  4. Lysosome fuses with / empties enzymes into vacuole;
  5. Bacteria digested / hydrolysed;
28
Q

When a pathogen causes an infection, plasma cells secrete antibodies which destroy this pathogen.
Explain why these antibodies are only effective against a specific pathogen.

A

Antigens (on pathogen) are a specific shape / have specific tertiary / 3D structure;
Antibody fits / binds / is complementary to antigen / antibody-antigen complex forms;

29
Q

People with AIDS die because they are unable to produce an immune response to pathogens (lines 2-4).
Explain why this leads to death.

A

Infected by / susceptible to (other) pathogen(s) / named disease caused by a pathogen (from environment);

  1. Pathogen(s) reproduce / cause diease (in host);
  2. Damage cells / tissues / organs;
  3. Release toxins;
30
Q

Explain why each of the following means that a vaccine might not be effective against HIV.
(i) HIV rapidly enters host cells

A

(HIV enters cells) before antibodies can bind to / destroy it;
Antibodies cannot enter cells (to destroy HIV) / stay in blood;

31
Q

HIV shows a lot of antigenic variability

Explain why ethis means that a vaccine might not be effective against HIV.

A

Antigen (on HIV) changes;

(Specific) antibody / receptor no longer binds to (new) antigen;

32
Q

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

A
  1. Vaccine contains antigen from pathogen;
  2. Macrophage presents antigen on its surface;
  3. T cell with complementary receptor protein binds to antigen;
  4. T cell stimulates B cell;
  5. (With) complementary antibody on its surface;
  6. B cell secretes large amounts of antibody;
  7. B cell divides to form clone all secreting / producing same antibody.
33
Q

Describe the difference between active and passive immunity.

A
  1. Active involves memory cells, passive does not;
  2. Active involves production of antibody by plasma cells / memory cells;
  3. Passive involves antibody introduced into body from outside / named source;
  4. Active long term, because antibody produced in response to antigen;
  5. Passive short term, because antibody (given) is broken down;
  6. Active (can) take time to develop / work, passive fast acting.
34
Q

The percentage of the population vaccinated does not need to be 100% to be effective in preventing the spread of whooping cough.
Suggest why.

A

More people are immune / fewer people carry the pathogen;

So susceptible / unvaccinated people less likely to contact infected people.

35
Q

Vaccines protect people against disease. Explain how.

A
  1. Vaccines contain antigens / dead / weakened pathogens / antigens dead / weakened
    pathogens are injected;
  2. Memory cells made;
  3. On second exposure memory cells produce antibodies / become active / recognise pathogens;
  4. Idea of memory cells responding.
  5. Rapidly produce antibodies / produces more antibodies;
  6. Production of antibodies must be qualified for mark.
  7. Antibodies destroy pathogens;
  8. Accept bacteria / viruses etc but not disease
36
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;