The document discusses immunity and the immune system. It describes the different types of white blood cells including phagocytes like neutrophils and macrophages that destroy pathogens through phagocytosis. It also discusses lymphocytes including B cells that produce antibodies and T cells that help activate other immune cells. The immune system provides both active and passive immunity. Vaccines work to stimulate active immunity by exposing the body to antigens in a safe way.

1. Applications of Biology
Immunology

2. Immunity
• This refers to the body’s ability to defend itself
against diseases.
• Immunity is provided by the immune system.
• The immune system recognizes foreign
material and produces chemicals to destroy it.
• The defence provided by the immune system
can be physical, chemical and cellular.

3. Immunity con’t
• Physical defence includes clotting
• Cellular defence includes the barrier created
by epithelia and white blood cells.
• Chemical defence include the secretion of
hydrochloric acid to destroy pathogens.
• White blood cells play a very important role in
the immune system.

4. Immunity con’t
• An antigen is a molecule which the body
recognizes as foreign.
• Antigens have on their surfaces, large
molecules such as proteins, glycoproteins,
lipids and polysaccharides.
• White blood cells are able to recognize
antigens.

5. White blood cells
• White blood cells originate in the bone
marrow.
• The two main groups involved in defence are
phagocytes and lymphocytes.
• Phagocytes can be further classified into
neutrophils and macrophages.

6. Phagocytes
• These are made throughout a person’s
lifetime in the bone marrow.
• They are stored in the bone marrow before
they are distributed around the body.
• Phagocytes act as scavengers by removing
dead cells as well as invasive microorganisms.

7. Neutrophils
• Approximately 60% of white blood cells are
neutrophils.
• They are transported by the blood throughout
the body.
• They are often squeezed through the walls of
the capillaries (by a process known as
diapedesis) to ‘patrol’ the tissues.

8. Neutrophils con’t
• They are short lived cells and are produced in
large amounts during an infection.

9. Macrophages
• These are larger than neutrophils.
• They are usually found in organs such as the
lungs, liver, spleen, kidney and in the lymph
nodes.
• They are made in the bone marrow and travel
in the blood as monocytes.
• Monocytes develop into macrophages once
they settle in the organs.

10. Macrophages con’t
• Macrophages are long-lived.
• They cut up pathogens displaying their
antigens so they can be easily recognized by
lymphocytes.
• They therefore play a major role in initiating
immune response.

11. Phagocytosis
• Cells that are being attacked by pathogens
produce histamine
• Mast cells are body cells that produce
histamine and cause inflammation (see later)
• The pathogens also release chemicals.
• These chemicals from the pathogens along
with the histamine attract passing neutrophils
to the site of infection.

12. Phagocytosis con’t
• Neutrophils have receptor proteins (opsonins)
on their surfaces which allow them to
recognise antibodies and chemicals produced
by the bacteria.
• The pathogens may be clumped together and
covered in antibodies (secreted by
lymphocytes) which would also help to
stimulate action by the neutrophils.

13. Phagocytosis con’t
• The neutrophils move towards the pathogens
and binds with the bacterium.
• The binding stimulates the formation of a
pseudopodia and the formation of a vacuole
called a phagosome.
• Lytic enzymes are released by lysozomes into
the phagosome which break down the
bacterium.

14. Phagocytosis con’t
• Dead neutrophils collect as a site of infection
as pus. (See handout for illustration. Make
sure you can illustrate what is there)
• The histamine released by mast cells cause
dilation of blood vessels making them leak.
• Plasma and white blood cells flow out into the
infected area.

15. Phagocytosis con’t
• Pus is formed from dead bacteria and white
blood cells (mainly phagocytes).
• The inflamed area thus becomes red, hot and
swollen.
• Sometimes a boil is formed which might
eventually burst because of the pressure of
the pus inside.

16. Phagocytosis con’t
• Phagocytosis is enhanced by a group of blood
proteins called complement.
• Complement proteins are made by
macrophages, monocytes and other cells in
the body especially those in the liver.
• They are usually inactive.
• When necessary they stick to invading micro-
organisms (mainly yeasts and bacteria)

17. Phagocytosis con’t
making them conspicuous to phagocytes as
foreign matter.
• Some destroy the membranes of bacteria.

18. Lymphocytes
• These are smaller than phagocytes and have a
large nucleus that fills most of the cell.
• There are two types:
1. B lymphocytes
2. T lymphocytes

19. Origin and maturation of B
lymphocytes
• As you already know, B cells are made in the
bone marrow.
• Here the immature B cells divide by mitosis.
• Each B cell is specific to an antigen.
• It therefore means that many millions of B cell
types exist in our bodies.
• During maturation, each B cell produces
antibodies.

20. Origin and maturation of B
lymphocytes con’t
• The genes that code for antibodies change in a
variety of ways to code for different antibodies
during maturation.
• Each B cell then divides to give a small number
of clones that are able to make the same
antibodies.

21. Origin and maturation of B
lymphocytes con’t
• The antibodies formed during maturation of
the B cells do not leave the cell.
• Rather, they form part of the plasma
membrane.
• A part of each antibody forms a protein
receptor.
• This receptor can combine with one type of
antigen.

22. Origin and maturation of B
lymphocytes con’t
• If that antigen enters the body, there will be
some mature B cells with cell surface
receptors that recognise it. (See hand out for
diagram. Make sure you can illustrate what is
there)

23. Action of B lymphocytes
• When pathogens enters the body for the first
time, some of them are take up by
macrophages (in lymph node etc).
• The macrophages expose the antigens from
the pathogens on their surfaces.
• Any B lymphocyte that has cell surface
receptors that are specific to the antigens
exposed divide repeatedly my mitosis.

24. Action of B lymphocytes con’t
• Within a few weeks, a huge number of
identical B cells are produced.
• Some pathogens have more than one antigen
on their surface.
• This means that several B cells are activated
on entry of the pathogen.
• As each type B cell divides, a polyclone is
formed (each type forms a clone)

25. Action of B lymphocytes con’t
• Some of these B cells become plasma cells.
• Others become memory cells.
• Plasma cells are short lived.
• They produce antibody molecules very quickly
(up to several thousand per second)

26. Action of B lymphocytes con’t
• The antibody molecules are released into the
blood, lymph or onto the linings of the gut or
lungs.
• The antibody molecules last longer than the
plasma cells. However, their concentrations
eventually decrease.

27. Action of B lymphocytes con’t
• The memory cells remain in circulation within
the body for a very long time.
• If the same pathogen enters the body again,
they divide rapidly forming more plasma cells
and memory cells.
• This response occurs every subsequent time
the pathogen enters the body.

28. Action of B lymphocytes con’t
• Thus the pathogen is prevented from causing
a disease. (See diagram on hand out – ensure
you are able to illustrate what is there)
• The immunity offered by B lymphocytes is
called humoral immunity.
• This is because antibodies are produced and
transported in body fluids (blood and lymph)

29. Primary and secondary responses
• When the body encounters an antigen for the
first time, the response is slow because there
are a few B cells that are specific to the
particular antigen.
• This first response is called a primary
response.
• During this response, the body experiences
symptoms of the disease.

30. Primary and secondary responses
con’t
• When the pathogen tries to enter the body
again, the response is much faster.
• This is because there are many memory cells
which divide quickly to give plasma cells. Thus
more antibodies are produced.

31. Primary and secondary responses
con’t
• This is called a secondary response. The body
does not experience symptoms of the disease.
• Memory cells are the basis for immunological
memory. (See graph on handout – be able to
illustrate what is there)

32. Antibodies
• So we’ve been talking about antibodies being
produced by B lymphocytes.
• What really are antibodies?
• They are globular glycoproteins and form the
group of plasma proteins called
immunoglobulins.
• All antibodies has a basic strucure.

33. Structure of an antibody
http://tinyurl.com/77oeght

34. Antibodies con’t
• All are made up of 4 polypeptide chains: two
long or heavy chains and two short or light
chains.
• The chains are held together by disulphide
bridges.
• Each antibody molecule has two identical
binding sites formed by both light and heavy
chains.

35. Antibodies con’t
• The sequence of amino acids form a specific
three-dimensional shape which binds to only
one type of antigen.
• This is called the variable region and varies for
different antibodies.
• There is a hinge region formed between the
two heavy chains.
• This provides flexibility.

36. Antibodies con’t
• Antibodies work in different ways.
• Their actions can be summarized into four
groups;
1. Agglutination – antibodies have two binding
sites. They can therefore bind to antigens on
two different pathogens. This can result in
pathogens being clumped together making
them more vulnerable to attack.

37. Antibodies con’t
2. Precipitation – some antigens are soluble.
Some antibodies bind them together into
large units which are then precipitated out of
solution. This way they are more easily
digested by phagocytes.
3. Neutralization – some antibodies bind to
toxins released by pathogens preventing
harm.

38. Antibodies con’t
4. Lysis – when some antibodies attach to a
pathogen, they act as a binding site for a
number of blood proteins (complement
system). Some of these proteins are
enzymes and cause breakdown of the
pathogen.
• Immunoglobulin E (IgE) binds to the
receptors of mast cells activating them to
release histamine.

39. Origin and maturation of T
lymphocytes
• As you already know, T lymphocytes are made
in the bone marrow.
• Here the immature T cells dived by mitosis.
• They then travel to the thymus gland where
they mature.
• They develop specific receptors which are
displayed in the plasma membrane.

40. Origin and maturation of T
lymphocytes con’t
• The mature T cells circulate in the body. (see
hand out – be able to illustrate)
• Some form T helper cells, some form T
cytotoxic cells, some form T suppressor cells
and some form memory T cells.

41. Action of T lymphocytes
• T cells are activated when they recognize an
antigen in contact with a host cell. Eg. A
macrophage which has cut up a pathogen
displaying its antigen (a help signal).
• The T cell with matching receptors divide by
mitosis to form a clone.
• The cells differentiate to form several types of
cells, the two main types being T helper cells
and killer T cells.

42. Action of T lymphocytes con’t
• Cytokines are secreted by T helper cells when
they are activated.
• Cytokines stimulate appropriate B cells to
divide and develop plasma cells which secrete
antibodies.
• Some secrete cytokines that stimulate
macrophages to carry out phagocytosis more
vigilantly.

43. Action of T lymphocytes con’t
• The cytokines these T cells secrete belong to a
group of proteins called lymphokines.
• Another lymphokine is called interferons.
These inactivate the protein making
machinery of the infected cell. This therefore
inhibits the replication of viruses.

44. Action of T lymphocytes con’t
• T cytotoxic cells search for body cells that are
invaded with pathogens and are displaying the
antigens.
• The killer T cells attach themselves to the
infected cells and secrete toxic substances
such as hydrogen peroxide killing these
infected cells and the pathogens. (see
handout – be able to illustrate)

45. Action of T lymphocytes con’t
• T suppressor cells – these control the immune
system. Once an infection has been
eliminated, these cells suppress the activities
of the lymphocytes.
• T memory cells – these remain in the body
and become very active during a secondary
response to antigens.

46. Active and passive immunity
• Active immunity refers to resistance to disease
derived by the body producing antibodies on
exposure to antigens.
• Active immunity is long term and can be
either natural or artificial.
• When pathogens enter the body by natural
means (air borne, food borne etc.), B
lymphocytes make antibodies to destroy
them.

47. Active and passive immunity con’t
• As you would remember, memory cells are
formed which make the body immune the
next time the pathogen invades the body.
• This is natural active immunity.
• In some cases antigens are injected or taken
orally into the body.
• The body then makes antibodies which
protect the body from those antigens.

48. Active and passive immunity con’t
• Passive immunity refers to resistance to
disease that is short lived and is not derived
by any action of the body.
• Passive immunity can also be natural or
artificial.
• Natural passive immunity is obtained when
antibodies pass by natural means into the
body.

49. Active and passive immunity con’t
• Babies have natural passive immunity.
• This is a result of antibodies passing across the
placenta from the mother to the foetus.
• After birth, the colostrum which the baby
receives is rich in IgA which prevents the
growth of bacteria.
• Because immunity is passive it is short lived.

50. Active and passive immunity con’t
• Depending on the nature of a disease or
infection, antibodies may need to be injected
into the body.
• If the body were allowed to make its own
antibodies, the person would die. Eg. Tetanus.
• This is artificial passive immunity.

51. Vaccinations
• A vaccine is a preparation of antigenic
material designed to stimulate the production
of antibodies and develop immunity within
the body.
• Immunity derived from exposure to live
pathogens is the best but not always realistic.
• Some vaccines are very effective and one
injection is sufficient. Some need
vaccinations.

52. Vaccinations con’t
• The materials used in vaccinations can be
grouped:
1. Living attenuated organisms – these are
pathogens that are treated (for example,
using heat) so that they can multiply but are
unable to cause the symptoms of the
disease. Even though they are harmless,
they stimulate the production of antibodies.
Eg. Measles, tuberculosis, poliomyelitis

53. Vaccinations con’t
2. Toxoids – the toxins which result from certain
diseases can stimulate the body to produce
antibodies. These toxins are modified to
prevent them causing symptoms of the
disease (eg. Treating it with formaldehyde)
and then administered by injection. Eg.
Diphtheria, tetanus

54. Vaccinations con’t
3. Dead microorganisms – the pathogens are
killed and then injected. Even though they are
dead, they are able to stimulate the
production of antibodies in the same way they
would if they were living. Eg. Typhoid,
cholera, whooping cough.

55. Vaccinations con’t
4. Extracted antigens – chemicals with antigenic
properties are extracted from the pathogens
and injected. Eg. Influenza vaccine
5. Artificial antigens – Genetic engineering is
used to transfer genes for the production of
antigens from the pathogen to a harmless
organism. These are grown in a laboratory
for the production of antigens which are later
used. Eg. Hepatitis B

56. Problems with vaccines
• Despite the benefits derived from vaccines,
there are several problems associated with
them.
1. Poor response – due to weakened immune
systems or malnourishment some persons do
not develop the necessary B and T cell clones.
Persons that are vaccinated with live viruses
can pass it to others in faeces. Herd immunity
is therefore ideal.

57. Problems with vaccines con’t
• Antigenic variation – when pathogens mutate
causing minor changes in the antigens they
produce, this is called antigenic drift.
Sometimes the memory cells will still
recognise them and cause a secondary
response. Sometimes there is an antigenic
shift where the mutation is so great that there
is a drastic change in antigen structure (eg.
Influenza). This results in the vaccine being

58. Problems with vaccines con’t
changed every year. Also, some pathogens are
eukaryotes eg. Plasmodium which causes
malaria and Trypanosoma which causes
sleeping sickness. Being eukaryotes, they
have many more genes than viruses and
bacteria and can have many hundreds or
thousands of antigens (each stage in the life
cycle has different antigens). There are
therefore no effective vaccines against these
diseases.

59. Problems with vaccines con’t
• Large invaders like nematodes and
platyhelminthes of the body are too large to
be dealt with by the phagocytes.
Eosinophils produce materials including
enzymes that breakdown the body walls of
these parasites and protect the body.
Basophils and mast cells produce chemicals like
histamine that stimulate action of the immune
system.

60. Problems with vaccines con’t
• Antigenic concealment – some pathogens are
able to hide inside body cells before an
immune response can be waged. They are
‘protected’ by being in the body cell eg.
Plasmodium in red blood cells. Some remain
in the intestines eg. Vibrio cholerae where
they cannot be reached by antibodies. To
combat this oral vaccines have been
developed against cholera

61. Problems with vaccines con’t
Some pathogens parasitize macrophages eg.
Myobacterium tuberculosis. Others parasitize
T helper cells eg. HIV. These suppress the
immune system.
• Recently, there have been concerns about
vaccines influencing the development of
autism. There have also been concerns about
chemicals used to treat pathogens. Eg.
Mercury and chloroform

62. Monoclonal antibodies
• Since B lymphocytes produce specific
antibodies, it would be ideal to be able to
produce antibodies outside the body.
• Until recently it was difficult to produce pure
cultures.
• In 1975 two persons (Cesar Milsten and
Georges Kohler) succeeded in producing pure
cultures.

63. Monoclonal antibodies con’t
• They did this by fusing antibody secreting cells
with tumour cells.
• The resulting cells are called HYBRIDOMAS.
• These hybridomas secrete antibodies and are
considered ‘immortal’.
• These hybridoma cells can be cultured as pure
clones and each type of antibody collected.

64. Monoclonal antibodies con’t
• The antibodies collected this way are called
monoclonal antibodies.

65. Using monoclonal antibodies
1. They can be used to treat a range of
infections.
2. They can be used to separate a particular
antigen from a complex mixture – to do this
the monoclonal antibodies for the required
antigen are immobilized on resin beads
which are then packed in a column. When
the mixture is passed over the beads, only
the required antigen is removed.

66. Using monoclonal antibodies con’t
• The antigen can then be washed from the
beads using a chemical which causes the
antibodies to release it.
3. They can be used in immunoassays – this is
the use of monoclonal antibodies to
determine the amount of a particular antigen
in a mixture. The antibodies are labelled eg.
With radioactive or fluorescent material for
easy detection.

67. Using monoclonal antibodies con’t
• If they are added to a test sample they will
attach to their specific antigen. If the sample
is washed in a special solution, the unattached
antibodies are removed. The amount of
antigens in the sample is revealed by the
degree of radioactivity or fluorescence.
4. ELISA (Enzyme Linked Immunosorbant Assay)
– this is used in athletes drugs tests,
pregnancy test kits and HIV tests.

68. Using monoclonal antibodies con’t
• The antibodies are immobilized and the test
solution passed over them. If the antibody is
specific for antigen X and X is present in the
test solution, it will bind to the antibody. A
second set of antibodies with an enzyme
attached is added to the solution. It combines
with antibody/antigen X complex. If a
substrate is added whose colour the enzyme
will change , the amount of chemical X can be

69. Using monoclonal antibodies con’t
determined.
5. Anticancer drugs are linked to monoclonal
antibodies which are attracted to the cancer
cells.
6. ADEPT (Antibody Direct Enzyme Prodrug
Therapy) – Monoclonal antibodies are tagged
with an enzyme which converts an inactive
form of the cytotoxic drug (prodrug) into an
active form.

70. Using monoclonal antibodies con’t
• Once injected these antibodies link with the
cancer cells. The inactive form of the drug is
administered in large doses. It is only effective
on the cancer cells.
• Monoclonal antibodies are used in the cancer
treatment Mabthera. The active ingredient is
rituximab and is used to treat non-Hodgkins
lymphoma which is a cancer affecting B cells.

71. Using monoclonal antibodies con’t
• Rituximab binds to a specific protein on the
surface of the affected B lymphocytes
stimulating the immune system to get rid of
the cancer cells.