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AS Biology CIE 

11. Immunity

CONTENTS
11.1 The Immune System
11.1.1 Phagocytes
11.1.2 Antigens
11.1.3 Primary Immune Response
11.1.4 Memory Cells & Immunity
11.2 Antibodies & Vaccination
11.2.1 Antibodies
11.2.2 Making Monoclonal Antibodies
11.2.3 Uses of Monoclonal Antibodies
11.2.4 Types of Immunity
11.2.5 How Vaccines Work
11.2.6 Vaccination to Control Disease

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11.1 The Immune System YOUR NOTES



11.1.1 Phagocytes
Phagocytes: Origin & Mode of Action
Phagocytes are white blood cells that are produced continuously in the bone
marrow
They are stored in the bone marrow before being distributed around the body in
the blood
They are responsible for removing dead cells and invasive microorganisms
They carry out what is known as a non-specific immune response
There are two main types of phagocyte, each with a specific mode of action. The
two types are:
Neutrophils
Macrophages

As both are phagocytes, both carry out phagocytosis (the process of recognising
and engulfing a pathogen) but the process is slightly different for each type of
phagocyte
Neutrophils
Neutrophils travel throughout the body and often leave the blood by squeezing
through capillary walls to ‘patrol’ the body tissues
During an infection, they are released in large numbers from their stores
However, they are short-lived cells
Mode of action:
Chemicals released by pathogens, as well as chemicals released by the body
cells under attack (eg. histamine), attract neutrophils to the site where the
pathogens are located (this response to chemical stimuli is known as
chemotaxis)
Neutrophils move towards pathogens (which may be covered in antibodies)
The antibodies are another trigger to stimulate neutrophils to attack the
pathogens (neutrophils have receptor proteins on their surfaces that recognise
antibody molecules and attach to them)
Once attached to a pathogen, the cell surface membrane of a neutrophil
extends out and around the pathogen, engulfing it and trapping the pathogen
within a phagocytic vacuole
This part of the process is known as endocytosis
The neutrophil then secretes digestive enzymes into the vacuole (the enzymes
are released from lysosomes which fuse with the phagocytic vacuole)
These digestive enzymes destroy the pathogen
After killing and digesting the pathogens, the neutrophils die
Pus is a sign of dead neutrophils

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YOUR NOTES

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The stages of phagocytosis, as carried out by a neutrophil YOUR NOTES


Macrophages 
Macrophages are larger than neutrophils and are long-lived cells
Rather than remaining in the blood, they move into organs including the lungs,
liver, spleen, kidney and lymph nodes
After being produced in the bone marrow, macrophages travel in the blood as
monocytes, which then develop into macrophages once they leave the blood to
settle in the various organs listed above
Mode of action:
Macrophages play a very important role in initiating an immune response
Although they still carry out phagocytosis in a similar way to neutrophils, they
do not destroy pathogens completely
They cut the pathogens up so that they can display the antigens of the
pathogens on their surface (through a structure called the major
histocompatibility complex)
These displayed antigens (the cell is now called an antigen-presenting cell)
can then be recognised by lymphocytes (another type of white blood cell)

 Exam Tip
The vacuole formed around a bacterium once it has been engulfed by a
phagocyte is called a phagosome. A lysosome fuses with the membrane of
the phagosome (to form a phagolysosome) and releases lysozymes
(digestive enzymes) to digest the pathogen.

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11.1.2 Antigens YOUR NOTES



Antigens, Self & Non-Self
Every cell in the human body has markers that identify it
Microorganisms (both pathogenic and non-pathogenic), such as bacteria and
viruses, also have their own unique markers
These markers are called antigens (which are macromolecules) and they allow
cell-to-cell recognition
Antigens are found on cell surface membranes, bacterial cell walls, or the surfaces
of viruses
Some glycolipids and glycoproteins on the outer surface of cell surface
membranes act as antigens
Antigens can be either self antigens or non-self antigens:
Antigens produced by the organism's own body cells (those that the immune
system does not recognise as foreign antigens) are known as self antigens
Self antigens do not stimulate an immune response
Antigens not produced by the organism’s own body cells (those that the
immune system recognises as being foreign eg. the antigens found on
pathogenic bacteria and viruses or if a person receives a different blood type
during a transfusion) are known as non-self antigens
Non-self antigens stimulate an immune response

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11.1.3 Primary Immune Response YOUR NOTES



Primary Immune Response (Advanced)
Lymphocytes are another type of white blood cell
They play an important part in the specific immune response
They are smaller than phagocytes
They have a large nucleus that fills most of the cell
They are produced in the bone marrow before birth
There are two types of lymphocytes (with different modes of action). The two
types of lymphocytes are:
B-lymphocytes (B cells)
T-lymphocytes (T cells)

B-lymphocytes
B-lymphocytes (B cells) remain in the bone marrow until they are mature and
then spread through the body, concentrating in lymph nodes and the spleen
Millions of types of B-lymphocyte cells are produced within us because as they
mature the genes coding for antibodies are changed to code for different
antibodies
Once mature, each type of B-lymphocyte cell can make one type of antibody
molecule
At this stage, the antibody molecules do not leave the B-lymphocyte cell but
remain in the cell surface membrane
Part of each antibody molecule forms a glycoprotein receptor that can combine
specifically with one type of antigen

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YOUR NOTES

The maturation of B-lymphocytes – by the time a child is born, it will have millions of
different types of B-lymphocytes, each with a specific antibody receptor

When an antigen enters the body for the first time, the small numbers of B-
lymphocytes with receptors complementary to that antigen are stimulated to
divide by mitosis
This is known as clonal selection
As these clones divide repeatedly by mitosis (the clonal expansion stage) the result
is large numbers of identical B-lymphocytes being produced over a few weeks
During an immune response, these B-lymphocytes then form two types of cell:
Some of these B-lymphocytes become plasma cells that secrete lots of
antibody molecules (specific to the antigen) into the blood, lymph or linings of

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the lungs and the gut YOUR NOTES


These plasma cells are short-lived (their numbers drop off after several 
weeks) but the antibodies they have secreted stay in the blood for a longer
time
The other B-lymphocytes become memory cells that remain circulating in the
blood for a long time
This response to a newly encountered antigen is relatively slow and is known
as a primary immune response

During a primary immune response, B-lymphocytes form two types of cell

T-lymphocytes
Immature T-lymphocytes leave the bone marrow to mature in the thymus
Mature T-lymphocytes have specific cell surface receptors called T cell receptors
These receptors have a similar structure to antibodies and are each specific to
one antigen

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The maturation of T-lymphocytes – some become helper T cells and others become
killer T cells

T-lymphocytes are activated when they encounter (and bind to) their specific
antigen that is being presented by one of the host’s cells (host cells being the
human’s own cells)
This antigen-presenting host cell might be a macrophage or a body cell that has
been invaded by a pathogen and is displaying the antigen on its cell surface
membrane
These activated T-lymphocytes (those that have receptors specific to the antigen)
divide by mitosis to increase in number (similar to the clonal selection and clonal
expansion of B-lymphocytes)
These T-lymphocytes differentiate into two main types of T cell:

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helper T cells YOUR NOTES


killer T cells

Helper T cells release cytokines (hormone-like signals) that stimulate B-
lymphocytes to divide and develop into antibody-secreting plasma cells. Some
helper T cells secrete cytokines that stimulate macrophages to increase their
rates of phagocytosis
Killer T cells attach to the antigens on the cell surface membranes of infected
cells and secrete toxic substances that kill the body cells, along with the
pathogen inside

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Helper T cells and killer T cells carry out different functions during an immune YOUR NOTES
response

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11.1.4 Memory Cells & Immunity YOUR NOTES



Memory Cells & Long-Term Immunity
During an immune response, B-lymphocytes form two types of cell: plasma cells
and memory cells
Memory cells form the basis of immunological memory – the cells can last for
many years and often a lifetime
There are two types of immune response:
Primary immune response (responding to a newly encountered antigen)
Secondary immune response (responding to a previously encountered
antigen)

Primary immune response


When an antigen enters the body for the first time, the small numbers of B-
lymphocytes with receptors complementary to that antigen are stimulated to divide
by mitosis
This is known as clonal selection
As these clones divide repeatedly by mitosis (the clonal expansion stage) the result
is large numbers of identical B-lymphocytes being produced over a few weeks
Some of these B-lymphocytes become plasma cells that secrete lots of antibody
molecules (specific to the antigen) into the blood, lymph or linings of the lungs
and the gut
These plasma cells are short-lived (their numbers drop off after several weeks) but
the antibodies they have secreted stay in the blood for a longer time
The other B-lymphocytes become memory cells that remain circulating in the
blood for a long time
This response to a newly encountered pathogen is relatively slow
Secondary immune response
If the same antigen is found in the body a second time, the memory cells
recognise the antigen, divide very quickly and differentiate into plasma cells (to
produce antibodies) and more memory cells
This response is very quick, meaning that the infection can be destroyed and
removed before the pathogen population increases too much and symptoms of the
disease develop
This response to a previously encountered pathogen is, relative to the primary
immune response, extremely fast

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YOUR NOTES

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YOUR NOTES

During a secondary immune response, memory cells that remained in the blood divide
very quickly into plasma cells (to produce antibodies) and more memory cells

T-lymphocytes also play a part in the secondary immune response


They differentiate into memory cells, producing two main types:
Memory helper T cells
Memory killer T cells

Just like the memory cells formed from B-lymphocytes, these memory T cells
remain in the body for a long time
If the same antigen is found in the body a second time, these memory T cells
become active very quickly

 Exam Tip
Immunological memory (made possible by memory cells) is the reason why
catching certain diseases twice is so unlikely. For example, there is only one
strain of the virus that causes measles, and each time someone is re-
infected with this virus, there is a very fast secondary immune response so
they do not get ill.However, some infections such as the common cold and
influenza are caused by viruses that are constantly developing into new
strains. As each strain has different antigens, the primary immune response
(during which we often become ill) must be carried out each time before
immunity can be achieved.

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11.2 Antibodies & Vaccination YOUR NOTES



11.2.1 Antibodies
Antibodies: Structure & Functions
Structure
Antibodies are globular glycoproteins called immunoglobulins
Antibodies have a quaternary structure (which is represented as Y-shaped), with
two ‘heavy’ (long) polypeptide chains bonded by disulfide bonds to two ‘light’
(short) polypeptide chains
Each polypeptide chain has a constant region and variable region
The constant regions do not vary within a class (isotype) of antibodies but do vary
between the classes. The constant region determines the mechanism used to
destroy the antigens
There are 5 classes of mammalian antibodies each with different roles
The amino acid sequence in the variable regions of the antibodies (the tips of the
"Y") are different for each antibody. The variable region is where the antibody
attaches to the antigen to form an antigen-antibody complex
At the end of the variable region is a site called the antigen-binding site. Each
antigen-binding site is generally composed of 110 to 130 amino acids and
includes both the ends of the light and heavy chains
The antigen-binding sites vary greatly giving the antibody its specificity for
binding to antigens. The sites are specific to the epitope (the part of the antigen
that binds to the antibody)
A pathogen or virus may therefore present multiple antigens different antibodies
need to be produced
The ‘hinge’ region (where the disulfide bonds join the heavy chains) gives
flexibility to the antibody molecule which allows the antigen-binding site to be
placed at different angles when binding to antigens
This region is not present in all classes of antibodies

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YOUR NOTES

A model of the generalised structure of an antibody molecule

Function
Antibodies are produced by B-lymphocytes
Antibodies bind to specific antigens that trigger the specific immune response.
Every antigen has one antibody
Antigens include pathogens and their toxins, pollen, blood cell surface molecules
and the surface proteins found on transplanted tissues
Antibodies are divided into five major classes (isotypes), each with a different role
The function of antibodies differ:
Antibodies can combine with viruses and toxins of pathogens (e.g. bacteria) to
block them from entering or damaging cells
Antibodies can act as anti-toxins by binding to toxins produced by pathogens
(e.g. the bacteria that cause diphtheria and tetanus) which neutralises them
making them harmless
Antibodies can attach to bacteria making them readily identifiable to
phagocytes, this is called opsonisation. Once identified, the phagocyte has
receptor proteins for the heavy polypeptide chains of the antibodies, which
enables phagocytosis to occur
Antibodies can attach to the flagella of bacteria making them less active,
which makes it easier for phagocytes to do phagocytosis

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Antibodies act as agglutinins causing pathogens carrying antigen-antibody YOUR NOTES


complexes to clump together (agglutination). This reduces the chance that the 
pathogens will spread through the body and makes it possible for phagocytes
to engulf a number of pathogens at one time
Antibodies (together with other molecules) can create holes in the cell walls of
pathogens causing them to burst (lysis) when water is absorbed by osmosis

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The functions of antibodies vary according to which type of antigen they act on

 Exam Tip
You must know that each antibody will have a different variable region with
an antigen-binding site that matches one antigen or toxin produced by a
pathogen. The antigen-binding site (and therefore the antibody) is specific
to one antigen.

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11.2.2 Making Monoclonal Antibodies YOUR NOTES



The Hybridoma Method
Monoclonal antibodies are artificially produced antibodies produced from a single
B cell clone
The hybridoma method is a method used to make monoclonal antibodies (Mabs)
The method enables large quantities of identical antibodies to be produced
The hybridoma method solved the problem of having B cells that could divide by
mitosis but not produce antibodies and plasma cells that could produce antibodies
but not divide
This method was established in the 1970s
Monoclonal antibodies bind antigens, in the same way naturally produced
antibodies do
They are produced by injecting mice with an antigen that stimulates the production
of antibody-producing plasma cells
Isolated plasma cells from the mice are fused with immortal tumour cells, which
result in hybridoma cells
These hybrid cells are grown in a selective growth medium and screened for the
production of the desired antibody
They are then cultured to produce large numbers of monoclonal antibodies
Monoclonal antibodies have multiple applications to include diagnostics, treating
disease, food safety testing and pregnancy testing

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The hybridoma method is used to produce monoclonal antibodies

 Exam Tip
Remember monoclonal antibodies are produced from a hybridoma cell - a
cell formed by the fusion of plasma cells and tumour (cancer) cells, which
divide continuously therefore producing large quantities of a wanted
antibody.

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11.2.3 Uses of Monoclonal Antibodies YOUR NOTES



Use of Monoclonal Antibodies
Diagnostic uses of monoclonal antibodies
Monoclonal antibodies can be used diagnostically for:
Pregnancy tests
Diagnosing HIV
Detecting the presence of pathogens such as Streptococcus bacteria
Distinguishing between Herpes I and Herpes II
Blood typing before transfusions and tissue typing before transplants
Detecting the presence of antibiotics in milk
Detecting cancer cells
Monoclonal antibodies can also be used to locate the position of blood clots for
patients thought to have deep vein thrombosis. This occurs by:
Injecting a mouse with human fibrin (the main protein found in blood clots)
This activates the plasma cells to produce antibodies against fibrin
These cells are collected from the mouse spleen
The plasma cells are then fused with tumour cells forming hybridomas that
produce antifibrin antibodies
To detect where the antibodies are binding to fibrin molecules, a radioactive
chemical (producing gamma radiation) is attached to the antibodies making
them radioactively labelled
A gamma-ray camera is used to detect where these radioactively labelled
antibodies have attached to a fibrin molecule, hence indicating where blood
clots can be found
Generally monoclonal antibodies are used only once

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YOUR NOTES

Another example of the diagnostic use of monoclonal antibodies - test for HIV

Therapeutic uses of monoclonal antibodies


Therapeutically monoclonal antibodies have multiple applications to include:
Treatment for the rabies virus, (which can be potentially fatal), by injecting
purified antibodies
The prevention of transplanted organ rejection, achieved by intervening with
the T cells involved in the rejection process
Autoimmune therapies for allergic asthma and rheumatoid arthritis; here
monoclonal antibodies are able to bind and deactivate factors involved in the
inflammatory response

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Treatment for diseases caused by the overproduction or inappropriate YOUR NOTES


production of B-cells (eg. leukaemia, multiple sclerosis and myasthenia 
gravis); the antibody (rituximab) binds to cell surface receptor proteins on B-
cells (not plasma cells) and causes the death of the cells
Prevention of blood clotting following angioplasty procedures; here
monoclonal antibodies bind to receptors on the platelet surface thereby
inhibiting fibrinogen from binding and subsequent clotting from ensuing
Targeted treatment of breast cancer; Herceptin (trastuzumab) is a monoclonal
antibody used to treat breast cancer, it recognises receptor proteins on the
surface of cancer cells and binds to them allowing the immune system to
identify and destroy them
Treatment of melanoma (a type of skin cancer); the antibody (ipilimumab)
binds to a protein produced by T-cells (whose role is to reduce the immune
response) which results in the immune system remain active against the
cancer cells
Using monoclonal antibodies as a treatment requires multiple administrations and
this can cause problems
Initially the monoclonal antibodies were produced by mice, rabbits or other
laboratory animals (as these were easier to produce), however this triggered an
immune response when they were introduced to humans
Scientists have largely overcome this by:
Genetically modifying the antibody polypeptide chains so that the amino acid
sequences are now human not mouse or rabbit sequences
Altering the type and position of the sugar groups (antibodies are
glycoproteins) attached to the heavy polypeptide chains to reflect those found
on human antibodies

 Exam Tip
Know specific examples of how monoclonal antibodies can be used as a
diagnostic tool and for treatment. You can use a well-annotated diagram to
explain how monoclonal antibodies can be used as a diagnostic tool.

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11.2.4 Types of Immunity YOUR NOTES



Types of Immunity
Active immunity
Active immunity is acquired when an antigen enters the body triggering a specific
immune response (antibodies are produced)
Active immunity is naturally acquired through exposure to microbes or artificially
acquired through vaccinations
The body produces memory cells, along with plasma cells, in both types of active
immunity giving the person long-term immunity
In active immunity, during the primary response to a pathogen (natural) or to a
vaccination (passive), the antibody concentration in the blood takes one to two
weeks to increase. If the body is invaded by the same pathogen again or by the
pathogen that the person was vaccinated against then, during the secondary
response, the antibody concentration in the blood takes a much shorter period of
time to increase and is higher than after the vaccination or first infection

The primary and secondary response to the same antigen

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Passive immunity YOUR NOTES


Passive immunity is acquired without an immune response. Antibodies are not 
produced by the infected person
As the person’s immune system has not been activated then there are no memory
cells that can produce antibodies in a secondary response. If a person is reinfected
they would need another infusion of antibodies
Depending on the disease a person is infected with (eg. tetanus) they may not have
time to actively acquire the immunity, that is, there is no time for active immunity.
So passive immunity occurs either artificially or naturally
Artificial passive immunity occurs when people are given an injection /
transfusion of the antibodies. In the case of tetanus this is an antitoxin. The
antibodies were collected from people whose immune system had been triggered
by a vaccination to produce tetanus antibodies
Natural passive immunity occurs when:
Foetuses receive antibodies across the placenta from their mothers
Babies receive the initial breast milk from mothers (the colostrum) which
delivers a certain isotype of antibody (IgA)
Comparing Active & Passive Immunity Table

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YOUR NOTES
 Exam Tip
Active immunity is when the body produces the antibodies whereas in 
passive immunity the body is given the antibodies.

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11.2.5 How Vaccines Work YOUR NOTES



How Vaccines Work
A vaccine is a suspension of antigens that are intentionally put into the body to
induce artificial active immunity. A specific immune response where antibodies
are released by plasma cells
There are two main types of vaccines:
Live attenuated
Inactivated

Vaccines are administered either by injection or orally (by mouth). When a person
is given a vaccine they have been given a vaccination
The vaccinations given by injection can be into a vein or muscle
Vaccinations produce long-term immunity as they cause memory cells to be
created. The immune system remembers the antigen when reencountered and
produces antibodies to it, in what is a faster, stronger secondary response
Vaccines can be:
Highly effective with one vaccination giving a lifetime’s protection (although
less effective ones will require booster / subsequent injections)
Generally harmless as they do not cause the disease they protect against
because the pathogen is killed by the primary immune response
Unfortunately there can be problems with vaccines:
People can have a poor response (eg. they are malnourished and cannot
produce the antibodies – proteins or their immune system may be defective)
A live pathogen may be transmitted (e.g. through faeces) to others in the
population (ideally enough number of people are vaccinated at the same time
to give herd immunity)
Antigenic variation – the variation (due to major changes) in the antigens of
pathogens causes the vaccines to not trigger an immune response or diseases
caused by eukaryotes (eg. malaria) have too many antigens on their cell
surface membranes making it difficult to produce vaccines that would prompt
the immune system quickly enough
Antigenic concealment – this occurs when the pathogen ‘hides’ from the
immune system by living inside cells or when the pathogen coats their bodies
in host proteins or by parasitising immune cells such as macrophages and T
cells (eg. HIV) or by remaining in parts of the body that are difficult for
vaccines to reach (eg. Vibrio cholerae – cholera, remains in the small intestine)
The principles underpinning vaccinations were discovered by Edward Jenner in the
1700s when he developed the first smallpox vaccine
Live attenuated vaccines
Live attenuated vaccines contain whole pathogens (e.g. bacteria and viruses) that
have been ‘weakened’
These weakened pathogens multiply slowly allowing for the body to recognise the
antigens and trigger the primary immune response (plasma cells to produce

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antibodies) YOUR NOTES


These vaccines tend to produce a stronger and longer-lasting immune response 
They can be unsuitable for people with weak immune systems as the pathogen
may divide before sufficient antibodies can be produced
An example of this type of vaccine is the MMR (Measles, Mumps and Rubella)
Inactivated vaccines
Inactivated vaccines contain whole pathogens that have been killed (‘whole killed’)
or small parts (‘subunit’) of the pathogens (eg. proteins or sugars or harmless
forms of the toxins – toxoids)
As inactivated vaccines do not contain living pathogens they cannot cause disease,
even for those with weak immune systems
However these vaccines do not trigger a strong or long-lasting immune response
like the live attenuated vaccines. Repeated doses and / or booster doses are often
required
Some people may have allergic reactions or local reactions (eg. sore arm) to
inactivated vaccines as adjuvants (eg. aluminium salts) may be conjugated (joined)
to the subunit of the pathogen to strengthen and lengthen the immune response
An example of a whole killed vaccine is polio vaccine
An example of a toxoid subunit vaccine (where inactivated versions of the toxins
produced by pathogens are used) is Diphtheria

 Exam Tip
Remember vaccines trigger the primary immune response (T helper cells
trigger B plasma cells to secrete specific antibodies) which leads to the
production of memory cells which will give a faster and greater (higher
concentration of antibodies) during the secondary response.

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11.2.6 Vaccination to Control Disease YOUR NOTES



Vaccination to Control Disease
With the exception of the great success story surrounding the eradication of
Smallpox following a ten year global initiative in 1980 no other pathogen has been
eradicated globally since
Smallpox was able to be eradicated because a ‘live attenuated’ vaccine was used
against the only strain of the virus. There was also a programme of surveillance,
contact tracing and ‘ring’ vaccinations
There are many safe and effective vaccines that do exist against many pathogens
and these have managed to push a number of childhood diseases to the verge of
extinction
Vaccines against such diseases as mumps, chicken pox and whooping cough are
administered to children as part of an immunisation schedule and they
successfully confer immunity
As a result many childhood diseases are kept at low levels within populations due
to herd immunity
Herd immunity arises when a sufficiently large proportion of the population has
been vaccinated (and are therefore immune) which makes it difficult for a pathogen
to spread within that population, as those not immunised are protected and
unlikely to contract it as the levels of the disease are so low
Although most vaccinations are given to children there are some vaccines that are
provided at later stages in life, for example vaccinations for tuberculosis (TB) and
Hepatitis B are offered to frontline medical workers who have a higher risk of
coming into contact with such diseases in the hospital setting;
Travellers may be advised to take particular vaccines if travelling to areas where
certain diseases are endemic such as Yellow Fever in parts of Africa

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