2.4 Cell recognition and the immune system

What is an antigen?

● 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.

How does phagocytosis destroy
pathogens?

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

Explain the role of antigen-presenting
cells (APCs).

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

Give 2 differences between specific and
nonspecific immune responses.

nonspecific (inflammation, phagocytosis) = same for all
pathogens
specific (B & T lymphocytes) = complementary pathogen
nonspecific = immediate
specific = time lag

Name the 2 types of specific immune
response.

● cell-mediated
● humoral

Outline the process of the cell-mediated
response.

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

Outline the process of the humoral
response.

1. Complementary T H 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.

What is an antibody?

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.

How do antibodies lead to the
destruction of a pathogen?

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

What are monoclonal antibodies?

Antibodies produced from a single clone
of B cells

What are memory cells?

● Specialised T H
/ 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.

Contrast the primary and secondary
immune response.

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.

What causes antigen variability?

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

Explain how antigen variability affects
the incidence of disease.

● 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.

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

● 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

Contrast passive and active immunity.

Explain the principles of vaccination.

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

What is herd immunity?

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.

Suggest some ethical issues surrounding
the use of vaccines.

● production may involve use of animals
● potentially dangerous side-effects
● clinical tests may be fatal
● compulsory vs opt-out

Describe the structure of HIV.

● 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.

How does HIV result in the symptoms of
AIDS?

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

Why are antibiotics ineffective against
viruses?

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.

Suggest the clinical applications of
monoclonal antibodies.

● 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

Explain the principle of a direct ELISA
test.

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.

Explain the principle of an indirect ELISA
test.

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.

Suggest some ethical issues surrounding
the use of monoclonal antibodies.

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