Cell recognition and the immune system

Question 1

What is an antigen?

Answer 1

-Cell-surface molecule which stimulate immune response.
-Usually (glyco)protein, sometimes (glyco)lipid or polysaccharide.
- Immune system recognises as ‘self’ or ‘non-self’ = enables identification of cells from other organisms of same species, pathogens, toxins & abnormal body cells.

Question 2

How does phagocytosis destroy pathogens?

Answer 2

1. Phagocyte moves towards pathogen via chemotaxis.
2. Phagocyte engulfs pathogen via endocytosis to form a phagosome.
3. Phagosome fuses with lysosome.
4. Lysozymes digest pathogen.
5. Phagocyte absorbs the products from pathogen hydrolysis.

Question 3

Explain the role of antigen-presenting cells.

Answer 3

Macrophage displays antigen from pathogen on its surface (after hydrolysis in phagocytosis).
Enhances recognition by T helper cells, which cannot directly interface with pathogens / antigens in body fluid.

Question 4

Give 2 differences between specific and nonspecific immune responses.

Answer 4

• Nonspecific (inflammation, phagocytosis) = same for all pathogens.
• Specific: (B & T lymphocytes) = complementary pathogen.
• Nonspecific = immediate.
• Specific = time lag.

Question 5

Name the 2 types of specific immune response.

Answer 5

• Cell-mediated
• Humoral

Question 6

Outline the process of cell-mediated response.

Answer 6

1. Complementary T helper lymphocytes bind to foreign antigen on APC.
2. Release cytokines that stimulate:
   a) clonal expansion of complementary T helper cells (rapid mitosis): become memory cells or trigger humoral response.
   b) clonal expansion of cytotoxic T cells: secrete enzyme perforin to destroy infected cells.

Question 7

Outline the process of the humoral response.

Answer 7

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

Question 8

What is an antibody?

Answer 8

• Protein secreted by plasma cells.
• Quaternary structure: 2 ‘light chains’ held together by disulphide bridges, 2 longer ‘heavy chains’.
• Binding sites on variable region of light chains have specific tertiary structure complementary to an antigen.
• The rest of the molecule is known as the constant region.

Question 9

How to antibodies lead to the destruction of a pathogen?

Answer 9

Formation of antigen-antibody complex results in agglutination, which enhances phagocytosis.

Question 10

What are monoclonal antibodies?

Answer 10

Antibodies produced from a single clone of B cells.

Question 11

What are memory cells?

Answer 11

• Specialised T helper / B cells produced from primary immune response.
• Remain in low levels in the blood.
• Can divide very rapidly by mitosis if organism encounters the same pathogen again.

Question 12

Contrast the primary and secondary immune response.

Answer 12

Secondary response:
- faster rate of antibody production
- shorter time lag between exposure and antibody production
- higher concentration of antibodies
- antibody level remains higher after the secondary response
- pathogen usually destroyed before any symptoms

Question 13

What causes antigen variability?

Answer 13

1. Random genetic mutation changes DNA base sequence.
2. Results in different sequence of codons on mRNA.
3. Different primary structure of antigen = H-bonds, ionic bonds & disulphide bridges form in different places in tertiary structure.
4. Different shape to antigen.

Question 14

Explain how antigen variability affects the incidence of disease.

Answer 14

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

Question 15

Compare passive and active immunity. Give examples of both types.

Answer 15

• Both involve antibodies.
• Can both be natural or artificial.
  Passive natural: antibodies in breast milk / across placenta.
  Passive artificial: anti-venom, needle stick injections.
  Active natural: humoral response to infection.
  Active artificial: vaccination.

Question 16

Contrast passive and active immunity.

Answer 16

Passive:
- No memory cells & 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.
- Lymphocytes produce antibodies.
- Direct contact with antigen necessary.

Question 17

Explain the principles of vaccination.

Answer 17

1. Vaccine contains dead / inactive form of pathogen or antigen.
2. Triggers primary immune response.
   - Memory cells are produced and remain in the blood stream, so secondary response is rapid & produces higher concentrations of antibodies.
3. Pathogen is destroyed before it causes symptoms.

Question 18

What is herd immunity?

Answer 18

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.

Question 19

Suggest some ethical issues surrounding the use of vaccines.

Answer 19

• Production may involve use of animals.
• Potentially dangerous side-effects.
• Clinical tests may be fatal.
• Compulsory vs opt-out.

Question 20

Describe the structure of HIV.

Answer 20

• Genetic material (2 x RNA) & viral enzymes (integrase & reverse transcriptase) surrounded by capsid.
• Surrounded by viral envelope derived from host cell membrane.
• GP120 attachment proteins on surface.

Question 21

How does HIV result in the symptoms of AIDS?

Answer 21

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

Question 22

Why are antibiotics ineffective against viruses?

Answer 22

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.

Question 23

Suggest the clinical applications of monoclonal antibodies.

Answer 23

• 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 specific tertiary structure of binding site.

Question 24

Explain the principle of a direct ELISA test.

Answer 24

Detects presence of a specific antigen.
1. Monoclonal antibodies bind to bottom of test plate.
2. Antigen molecules in sample bind to antibody. Rinse excess.
3. Mobile antibody with ‘reporter enzyme’ attached binds to antigens that are ‘fixed’ on the monoclonal antibodies. Rinse excess.
4. Add substrate for reporter enzyme. Positive result: colour change.

Question 25

Explain the principle of doing an indirect ELISA test

Answer 25

Detects presence of an antibody against a specific antigen.
1. Antigens bind to bottom of test plate.
2. Antibodies in sample bind to antigen. Wash away excess.
3. Secondary antibody with ‘reporter enzyme’ attached binds to primary antibodies from the sample.
4. Add substrate for reporter enzyme. Positive result: colour change.

Question 26

What is the ELISA test and what is it used for?

Answer 26

• Enzyme-linked immunosorbent assay.
• Can be used to see if a patient has any antibodies to a certain antigen. For example, they can be used to test for infections by pathogens or for allergies.

Question 27

Suggest some ethical issues surrounding the use of monoclonal antibodies.

Answer 27

• Production involves animals.
• Drug trials against arthritis & leukaemia resulted in multiple organ failure.