3.2.4

Question 1

What is an antigen

Answer 1

-cell surface molecule which stimulate immune response
-usually glycoprotein sometimes glycolipid or polysaccharide
-immune system recognises as “self” or “non-self” = enables identification of cells from other organisms of the same species, pathogens, toxins & abnormal body cells

Question 2

How does phagocytosis destroy pathogens?

Answer 2

1. phagocyte moves towards pathogen by chemotaxis
   2.phagocyte engulfs pathogen via endocytosis to form a phagosome
2. Phagosome fuses with lysosome (phagolysosome)
3. lysozymes digest pathogen
4. phagocyte absorbs the products from pathogen hydrolysis

Question 3

Explain the role of antigen presenting cells (APCs)

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 + immediate
specific (B&T lymphocytes) = complementary pathogen + not immediate

Question 5

Name the 2 types of specific immune response

Answer 5

-cell mediated
-humoral

Question 6

Outline the process of the cell mediated response

Answer 6

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

Question 7

Outline the process of the humoral response.

Answer 7

1. Complementary T lymphocytes bind to foreign
   antigen on antigen-presenting T cells.
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

-proteins secreted by plasma cells

-Quaternary structure: 2 ‘light chains’ held together by disulfide 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 do 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/ 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 & 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 & disulfide bridges form in different places in tertiary structure.
4. Different shape of 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
the 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 an 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 a pathogen or antigen.
2. Triggers primary immune response.
3. Memory cells are produced and remain in the bloodstream, so secondary response is rapid & produces higher concentration of antibodies.
4. 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-cells.
2. HIV particles replicate inside T-cells, killing or damaging
   them.
3. AIDS develops when there are too few T-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 specificity of 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 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 enzvme’ attached binds to primary antibodies from the sample.
4. Add substrate for reporter enzyme. Positive result: colour change.

Question 26

Suggest some ethical issues surrounding the use of monoclonal antibodies.

Answer 26

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

Question 27

Describe how HIV is replicated.

Answer 27

1. Attachment proteins attach to receptors on helper T cell/lymphocyte;
2. Nucleic acid/RNA enters cell;
3. Reverse transcriptase converts RNA to DNA;
4. Viral protein/capsid/enzymes produced;
5. Virus (particles) assembled and released (from cell);