Immunity

Natural defence barriers

- Physical
o Skin – Prevents entry of pathogens
- Tough, outer layer of dead cells contains keratin
o Secretes:
- TEARS – Secreted by lachrymal glands – Wash away microbes
- Sebum – Secreted by sebaceous glands containing fatty acids –
Antimicrobial action
- Mucus – Sticky secretion produced by goblet cells – Traps
airborne pathogens
- Mechanical
o Nasal hairs – Filter air drawn into nasal passages
o Cilia – Tiny hairs that beat with wave-like motion
- Chemical
o Lysozyme – Enzyme catalysing hydrolysis of molecules in cell walls of
bacteria
o Sweat – Contains lactate – Slows bacterial growth
o Hydrochloric acid – Kills most microorganisms
o Commensals – Parasitic organisms which don’t harm host – Convert
carbohydrate to lactate – Kills pathogenic bacteria – Found in vagina,
skin and large intestine
- Biological
o Harmless bacteria

Lines of defence

- First line
o External barriers
- Second line
o Internal barriers
o Non-specific  Phagocytosis by macrophages
- Membrane invaginates so that
macrophage can engulf bacteria 
Binds with lysosome
- Third line
o Antigen-antibody complex
o Specific

Immune response

- Antigens
o Substance triggering formation of antibodies
o Self
- Found in cell surface membrane in body cells
- Do not activate immune response - Bodies recognise them as part
of us
o Non-self
- Found on cell walls and membranes of bacteria, viruses, fungi,
animal parasites, pollen, incompatible blood cells
- Produce an immune response- Bodies recognise them as foreign
material
- Antibodies
 o Immunoglobins
o Glycoprotein produced by lymphocytes - Presence of a specific antigen -
Combines with antigen to neutralise, inhibit or destroy it
o Structure:
- Y-shaped molecule
- Heavy chains and light polypeptide chains
• Held by disulphide bridges
- Two identical antigen binding sites
• Variable region
o Function:
- Neutralisation
• Antibodies block sites on bacteria and viruses
• Antitoxins produced to neutralise toxins from bacteria and
viruses
- Agglutination
• Antibodies bind with antigens
• Stick together
• More antibodies attack antigen  Large clumps of antigen-
antibody complexes formed
- Opsinisation
• Antibodies facilitate with phagocytosis of pathogens
o Blood typing
- Antibodies used to find and destroy foreign cells
- Bind tightly  Antigen-antibody complexes – Different types of
blood cells identified
- Determined used antibodies specifically reacting with proteins
- Looking for agglutination
LYMPHOCYTES

B-lymphocytes
- Made by stem cells in bone marrow
- Mature in lymph nodes and spleen
- Divide Plasma B – Secrete
to antibodies into circulation.
produce: Each antibody specific to
antigen. Lives 4 to 5 days
Memory B – Programmed to
remember specific antigen.
Respond very rapidly to any
following infection
Dividing B – Produce more B-
lymphocyte cells
T-lymphocytes
- Made by stem cells in bone marrow
- Mature in thymus gland
- Divide to Cytotoxic T – Destroy
produce: antigen directly. Attaches
to them and releases
chemical perforin to kill
them
Helper T – Attract and
stimulate macrophages.
Promote activity of other
T- and B-lymphocytes.
Increase antibody
production
Memory T – Multiply very
fast in second invasion of
antigen occurs. Produces
bigger clone of T-
lymphocytes
Suppressor T – Slow
down vigorous response
of T-cytotoxic and T-
helper. Slows down
immune response

TYPES OF IMMUNE RESPONSES

Humoral or antibody-mediated response

1. First exposure of antigen engulfed by antigen presenting cell (APC)
 2. Invading bacteria enter body
3. Bacteria detected by B-lymphocytes
a. Surface protein receptors matching shape of bacterial antigens
b. B-lymph binds to antigen
4. B-lymphocyte triggered to differentiate and divide by mitosis
a. Plasma B-cells
b. Memory B-cells
5. Plasma cells secrete large quantities of one type of antibody  Circulate blood
6. Antibodies attach to antigen  Antibody-antigen complexes
7. Destruction of bacterium:
a. Precipitation and agglutination  Easier for phagocytes to destroy
b. Antibodies cause lysis  Rupturing of cell walls of bacteria
8. Plasma cells die – Antibodies remain in blood for small amounts of time –
Memory cells stay in blood for years or even for life

Cell-mediated response
1. APC engulfs antigen
2. Infection of body cells with virus causes surface antigens to be present
3. Correct T-lymphocyte recognises antigen
a. Due to match in shape
b. T-lymphocytes binds to antigen
4. T-lymphocyte triggered to divide by mitosis
a. Memory T-cell
b. Helper T-cell
c. Cytotoxic (killer) T-cell
5. Cytotoxic-T are specific to infected cell’s antigen
a. Circulate in body
b. Attach to antigens of infected cells
c. Kill the cells
6. Memory-T cells remain in blood for long time
a. Multiply rapidly in second invasion of antigen

TYPE OF IMMUNITY MAIN FEATURES

Natural active - Lymphocytes activated by antigens - Present on the
immunity surface of the pathogen
- Takes place during the natural course of an infection.
Examples : Chickenpox
Artificial active - Antigens injected into the body
immunity - Lymphocytes activate
- Doesn’t take place through natural course
- Attenuated, inactivated or dead pathogens are vaccinated
E.g. MMR, Tetanus, Diphtheria.
Natural passive - Pre-formed antibodies from mother to baby across the
immunity placenta and colostrum (first secretion of mammary gland)
- Passive - Baby not forming own antibodies - Still provides
the baby with protection
E.g. Maternal antibodies through placenta, Immunoglobulin A in
breast milk protects from bacterial infections.
Artificial passive - Pre-formed antibodies extracted from individual and
immunity injected into another as serum
- Short-term immunity - Injected antibody possess non-self
antigens – Causes body to produce antibodies against it
 E.g. Normally used in immunodeficiency diseases, acute infection
and to treat poisoning.

VACCINATION

- Vaccine – Antigen injected or swallowed – Causing development of active

immunity
- Long term – Able to produce memory cells

Most vaccines contain one of the following:

- Killed virulent organisms

o Microbe killed by heat or chemicals
o Dead pathogens possess antigenic sites
 Recognised by T- and B-lymphocytes  Produces antibodies
o E.g. Whooping cough bacteria
- Live non-virulent strains
o Pathogen weakened – Ensure it doesn’t cause severe infection
o E.g. Rubella vaccines, BCG and Sabin vaccine
- Modified toxins
o Toxoids produced by bacteria made harmless
o Stimulate antibody production
o NO risk of infection by pathogen
o E.g. Vaccine against diphtheria and tetanus
- Isolated antigens
o Antigens separated from microbes
o E.g. flu vaccines – Contains mixture of antigens from various strains of
influenza
o Antigenic variation – Occur in microorganisms with high mutation rate
- Genetically engineered antigens
o Restriction endonucleases - Extract genes coding for particular antigen
from pathogen
o Inserted into harmless plasmid vector
o Cells replicate to produce large amounts of antigen

PRIMARY AND SECONDARY IMMUNE RESPONSES

Primary response
- Triggered by body’s
first contact with
antigen
- B-lymphocytes divide
to form plasma cells
 Produce antibodies

Secondary response:
- Triggered by
subsequent contact
with same antigen
previously caused
 - B memory specific to antigen present  Activated by antigen
o Stimulate plasma B to produce antibodies

Primary response Secondary response

- Slower to start – Greater delay
- Maximum antibody production
is less
- Lasts in blood for shorter time
- Quicker to start – Immediate
response
- Maximum antibody production
is greater
- Lasts in blood for longer time

AIDS

AIDS – Acquired immunodeficiency syndrome

HIV – Human Immunodeficiency Virus
- Destroys helper T-cells
- Retrovirus – Uses RNA to produce single strand of “copy DNA”
- Enzyme reverse transcriptase catalyses reverse transcription of DNA from RNA
- Virus can remain latent for many years before activated
- 3 STAGES:
1. HIV positive – Little or no symptoms
2. Low helper T-cell count
3. Clinical AIDS with symptoms – E.g. cancer, weight loss, fever,
deteriorating brain function

Replication of HIV
 2. Binding and fusion:
a. Glycoprotein on outer surface of virus attaches to receptors on host
cell
b. Lipid bilayer of virus fuses with host cell’s membrane - Virus enters
the host cell
4. Reverse transcription:
a. Stimulates cell to make copy DNA from viral RNA template
5. Integration:
a. Viral DNA insert into host cell’s chromosomes
6. Transcription:
a. Viral DNA codes for production of thousands of
new viruses

OPPORTUNISTIC INFECTIONS:
- An infection caused by pathogens
o Usually doesn’t cause disease in healthy host (with healthy immune
system)
o Weakened immune system presents “opportunity” for pathogen to
infect