Immunology

2. Immunology
Objectives
Students should be able to:

– describe the mode of action of phagocytes; Review phagocytosis; include the role of mast cells and
histamine production; complement; phagocytes as antigen-preventing cells.

– define the term “immune response”

– compare the origin and maturation of B- and T- lymphocytes;Include the types of T-cells and their
function (refer to HIV); B- cells and their functions

-distinguish between the humoral and cell-mediated immune responses; Details required.

- explain the role of memory cells in long-term immunity; T- and B- memory cells.

– relate the molecular structure of a typical antibodies to its function;

Labelled diagram of a typical antibody showing its “Y-shaped structure; include

the function of the various parts; specificity of antibody to antigen.
 Objectives
– distinguish between active and passive, natural and artificial immunity; Include examples.

– explain the role of vaccination in providing immunity;

– state what is meant by a monoclonal antibody;

– describe the use of monoclonal antibodies in diagnosis and treatment.

The anticancer drug, MabThera; details required of the use of monoclonal
antibodies in pregnancy testing.
 Immunology
Immunology : the ability to tell self from non self and
respond

Pathogen : any organism that causes illness. Tend to be

microorganisms e.g viruses, bacteria, fungi
Parasites : organisms living on or inside another
organism called a host. Tend to refer to tapeworm ,
round worms, fleas
 The Immune System
The Skin and mucus membranes are the body’s Primary
Defense Mechanism
– Skin
• Physical barrier: blocks pathogens
• Chemical barrier: produce antimicrobial substances which lower
pH and inhibit growth of pathogens
– Mucus membranes protect openings to the environment
such as mouth, eyes , ears, nostril anus genitals
• Physical barrier: Secrete sticky mucus to trap pathogens
• Chemical barrier: Contain antimicrobials to inhibit growth of
pathogens e.g lysozymes in tears & HCL in stomach acid
 The Immune System
The Secondary Defense Mechanism is the Immune
System.
An Immune response is the way the body deals with a
foreign body or anything that is non self.
It involves:
Action of White blood cells (WBC’s)or Leukocytes
Antigens: protein and ploysaccharide molecules that
help the body distinguish self from non self. Any
molecule that the body recognizes as foreign is called
an antigen.
Type Of White Blood Cells % By Volume Of WBC Description Function

Neutrophils 60 – 70 % Nucleus has many Phagocytize and destory

interconnected lobes; blue bacteria; most numerous WBC
granules

Eosinophils 2–4% Nucleus has bilobed nuclei; red or Play a role in ending allergic
yellow granules containing reactions
digestive enzymes

Basophils <1% Bilobed nuclei hidden by large Function in inflammation

purple granules full of chemical medication; similar in function to
mediators of inflammation mast cells

Lymphocytes (B Cells and T 20 – 25 % Dense, purple staining, round the most important cells of the
Cells) nucleus; little cytoplasm immune system; effective in
fighting infectious organisms;
act against a specific foreign
molecule (antigen)

Monocytes 4–8% Largest leukocyte; kidney Transform into macrophages;

shaped nucleus phagocytic cells
 Three Types of Leukocytes
Neutrophils:
– Multi-lobed nucleus
– Destroy bacteria by phagocytosis
– Short life span hours – few days

Monocytes:
– Kidney shaped nucleus
– Life span : months
– Involved in Phagocytosis
– Migrates out of the blood
– Differentiate (develop into macrophages when in tissue)e.g alvelolar
macrophage in alveolar of lungs, Kuffer cells in Liver
 Three types of Leukocytes
Lymphocytes:
– Dark oval nucleus with thin blue/purple cytoplasmic rim
– Lifespan : variable ( hours – years)
– Mount the cell immune response
• B cells :
– Remain in bone marrow
– Become Plasma cells(produce antibodies)
– Destroy bacteria and toxins
• T Cells:
– Migrate to Thymus where they differentiate ( mature)
– Cell mediated immunity
– Attack viruses fungi some bacteria , transplant organs , Cancer cells
• Natural Killer cells NK
– Attack many microbes
– Direct Attack on cells
– Part of the innate immunesystem
 Processes involved in the Immune Response
Words to know
“Immunity Is the ability to recognize self from non self “ sec14.
The immune response – the body’s reaction to foreign antigen

• Phagocytosis: a non specific response

– Amoeboid movement : crawling by flowing of their cytoplasm
– Phagocytes engulf invading bacteria and clean up debris
– Phagocytic vesicles are formed. Lysosomes with hydrolytic
enzymes and acids fuse with them to digest the pathogen.
– Phagocytes are the first line of defense against microbes E.g
Neutrophils and monocytes
• Involve use of Complements: group of about 20 proteins
which are always present in the blood. They help phagocytes
fight bacterial infections.
• attract phagocytes to the site of infection by chemotasis : Cell
movement towards a chemical stimulus
• Destroy foreign cells: punch holes in cell surface membrance of
bacteria
• Opsonisation : coating/tagging bacteria with opsonins(protein) which
make them easily recognised by phagocytes
 Processes involved in the Immune Response
Words to know
• Antigen presentation: a specific response
– Involve the action of lymphocytes
– Antigens (molecules that cause the production of antibodies) are
markers on the cell membrane of all cells that help them to recognize
each other
– Antigens are usually protein or polysaccharide e.g glycoprotein(protein
with a carbohydrate tail)
– The body identifies antigens on a microorganism as a foreign antigen
and makers antibodies against it .
– Macrophages called Antigen Presenting Cells(APC), engulf and digest the
antigen.
– The APC display some of the bacteria (antigen) on their cell membrane .
– Lymphocytes ( B cells) with a complementary antibody for that specific
bacterial antigen bind to the antigen.
– This antigen -antibody complex leads to stimulation of more B cells producing
more antibody; t cells (T8-Natural killer and T4-helper cells )to destroy the
pathogen

• Antibody production
– Antibodies are glycoprotein ( consist of amino acid and sugar units)
– Made by the plasma cell ( B -lymphocytes)
 The Characters
– The Bacteria or pathogen with its foreign antigen
– Phagocytes: Neutrophils and Macrophages(non
specific/ innate)
– Lymphoctyes (specific/adaptive)
• B cells: differentiate to plasma cells which release
antibodies and memory cells
• T Cells
– T4 Helper cells(effector cells & memory cells)
– T8 cells (effector killer cells, memory cells, suppressor cells)
• Natural Killer cell( innate immunity)
Two systems of Immune Responses
• Humoral Immune Response (fluid)
• B-Lymphocytes
– Become plasma cells which produce antibodies against pathogens while
they are in the blood, lymph, or between cell.

• Cell mediated Immune Response

• T-Lymphocytes:
– T cell made in the bone marrow but differentiated in the Thymus (in the
thorax above he heart ). Importance:
» Early removal – death due to deficiency of lymphocytes
» Graft from older thymus to baby mouse – no antigen recognition
» Removal from an older mouse – no adverse effects
 Humoral Response
• Each B lymphocyte recognizes and responds to a particular antigen
• B cell produce a specific antibody (a glycoprotein) against each specific antigen
• The antibodies are placed on the cell membrane of the B cell and act as receptors for foreign
antigens
• If a B lymphocyte meets a bacterial antigen specifically matching the antibodies on its cell
membrane, (either in the blood or displayed on a APC)it binds to it. (Clonal selection)
• This antibody- antigen complex trigger an immune response:
– B lymphocyte divides by mitosis making clones of itself and memory cells (Clonal
proliferation/clonal expansion)
– Some of the new B lymphocytes differentiate into
• Plasma cells/ effector cells: rapidly produce and release antibodies at a rate (2000
per sec.)
• Memory cells: don’t secrete antibodies but remain in blood to quickly mount a
second response if the pathogen re: enters the body.
 Cell Mediated Response
• T Lymphocytes are stimulated when they come in
contact with an antigen ( free floating in the blood
from invading virus / bacteria, or on APC
Macrophage, or on membrane of an infected viral
cell)
• Antigen binds to receptors on the cell membrane of
the T lymphocyte and begins to divide by mitosis(
clonal proliferation)
• Each T lymphocyte recognizes a specific antigen (
specific response) and reacts to the foreign antigen
differently
 Cell Mediated Response
T 4cell or helper cells help APC macrophages.
(NB HIV infects and destroying T4 Helper cells)
• The cloned T4 helper cell produces substances called
cytokines/lymphokines / interleukins which: are protein
mediators to direct/stimulate the immune system
response by causing signaling between its cells
– Stimulate T killer cells to destroy the infected cell. E.g
infected cells marked with viral particles & cancer cells
– Promote inflamation
– Stimulate and activates B cells specific to the antigen to
differentiate into plasma cells producing antibodies
– Stimulate Macrophages to carry out phagocytosis
 Cell Mediated Response
T killer cells destroy the cells with the specific antigen
to its receptors.
• Attack virus infected cells and cancer causing cells
• They are involved in rejection of transplanted organs
• They are the bodies main defense against viruses
– After binding to the infected cell, T killer cells secrete
chemicals e.g hydrogen peroxide to destroy it

T memory cells remain in the body to help mound a

faster second response if the pathogen re:enters the
cell again
 Cell Mediated Response
Involve use of Complements: group of about 20 proteins which are always
present in the blood.
• They help phagocytes fight bacterial infections.
• Precursers of enzymes ( Zymogen or un reactive form of an enzyme.
• Upon activation , it causes a cascade effect involving large number of
protein molecules. This activation and cascade rxn occurs due to :
• Complement bind to an Antigen antibody binding complex
• Complements bind directly to a pathogen
• Complements help destroy pathogens by
• attract phagocytes e.g macrophage to the site of infection by chemotasis :
Cell movement towards a chemical stimulus e.g in the inflammatory
response
• Destroy foreign cells: punch holes in cell surface membrane of bacteria
• Opsonisation : proteins produced in the cascade (opsonin) , coats/tagging
bacteria making them easily recognised by phagocytes
B Lymphocyte Response to
antigen

(Ramesar,2011)
Lymphocytes Response to antigen

(Ramesar,2011)
B & T cells Response to Antigen

(Ramesar, 2011)
Cell Mediated & Humoral Responses

(Taylor ,2012)
 Summary

• Although the Immune system response is

presented as two separate mechanisms,
In reality, there are constant interactions
between cells- in the Cell mediated response
and chemicals in the Humoral response.
• The Skin and mucus membrnes re the bodies
Primary Defences
 The Inflammatory Response
• The process by which damaged cells release chemicals to bring lymphocytes and
macrophages to the site of infection
• These chemicals include Bradykinins and prostaglandins
• The result is:
– Vasodilation : There is a larger blood flow to the area bringing cells to fight the infection . This
causes redness and increased temperature
– Capillaries become more permeable to allow leakage of fluids into the tissue where the damage is .
This causes localized swelling (oedema)
• Pus may accumulate :this consist of dead bacteria ,lymphocytes and phagocytes
• Mast cells (similar to basophils) found in tissue near blood vessels and nerves ,
also release chemicals
– Heparin; prevent clotting
– Histamine : which is responsible for the reactions associated with an allergic response .
Where potentially harmless antigens e.g pollen grains cause strong immune reactions
• Mast cells may become activated by binding to IgE antibodies, or to
complements.
• They result in dilation of blood vessels, contraction of smooth muscles eg
in air ways, appearance of skin rashes ,tissue fluid accumulation.
• Mast cell are also involved in auto immune diseases e.g rheumatoid
arthritis, Multiple sclerosis
 Words to note
• Innate
• Acquired
• Active
• Passive
• Artificial
• Natural
• Primary response
• Secondary response
 Innate vs Adptive /Acquired
Innate immune system consists of cells and proteins that are
always present and ready to mobilize and fight microbes at
the site of infection. T 1) physical epithelial barriers, 2)
phagocytic leukocytes, 3) dendritic cells, 4) a special type of
lymphocyte called a natural killer (NK) cell, and 5) circulating
plasma proteins.
Adaptive immune system, /learnt becomes activated by intrusion of a pathogen the
resultant effect is to cause proliferation and potent mechanisms for
neutralizing or eliminating the microbes involving the:
– humoral immunity, mediated by antibodies produced by B lymphocytes,
– cell-mediated immunity, mediated by T lymphocytes.
 Antibodies
– Glycoproteins: Their polypeptide chains are held by disulphide bridges
– There are may different kind of antibodies. Collectively they are known as
Immunoglobulins and are represented as IgG, IgA etc.

Structure :
– Variable region:
• Antigen binding site (epitope)
• The shape is complementary to a particular antigen
– Hinge region: allows flexibility for binding to antigen
– Constant region: is the same for all antibiotics
 Antibodies
Types of Antibodies
– IgA: bacterial infection
– IgE: activate mast cells to release histamine
(allergic reactions)
– IgG: helps macrophage engulf pathogens,
neutralize toxins
– IgM: agglutination of bacteria activate
complements
 Antibodies
Antibodies function by causing:
• Agglutination: pathogen clump together at the
variable end ( hold them together to make bigger
targets for phagocytes)
• Neutralize toxins: bind to and neutralize toxins
• Prevent pathogen binding to host
• Immobilize some bacteria by bind to their flagella
• Opsonisation: coates the pathogen to facilitate
phagocytosis.
• Activate complements
Antibodies
 The Immune System
Primary response Slow…
This occurs when a pathogen enters the body for first time. There are not
many B cell differentiated into plasma cells with antibodies for the
antigen.
The body takes time to produce the right antibodies against the pathogen .
Until then, the pathogen multiplies and the person shows symptoms of the
disease.

The Secondary response is faster…

Memory cells are produced which remember the specific antigen so a
stronger quicker immune response is made upon re: infection. The person
is now immune.
Primary and Secondary Response
Primary and secondary Response
 Immunity
Active Immunity
– Immunity developed when the body makes its
own antibodies after being stimulated by an
antigen.
• Natural: Becoming immune after catching the disease
• Artificial: after being given a vaccine contains a
weakened attenuated form of the antigen

– Herd immunity: immunity to a disease in a population over

time by vaccinating most persons thus reducing the likelihood
of contracting the disease. At least 80% of the population
must be vaccinated for it to work.
Vaccination
Vaccination
 Vaccination
Types of vaccines:
Toxoids: toxins produced by tetanus and diphtheria are detoxified bit their
antigenic properties remain can stimulate antibody production.
Killed organisms: invove use of dead bacteria and viruses for immunisation e.
g flu vaccine.
Live vaccines: is attenuated or weakened organism but still containing the
antigens to stimulate immunizations e.g for Tuberculosis, Measels, Mumps
,Rubella, Polio. For small Pox , an un attenuated virus was used. This was
a different strain which was harmless.
New vaccines are developed using only the proteins coded for the antigen for
the pathogen in question. Large amounts of antigens can be prepared in
this way. E.g cholera, thyphoid, hepatitist B vaccines
 Immunity
Passive Immunity
– Immunity developed from being given antibodies
made by a different organism. Not long lasting as
no lymphocytes have been activated.
• Natural: Baby becomes immune due to antibodies
received from its mother through the placenta and
breast milk
• Artificial: immunity after being injected with
antibodies from someone else e.g Urgent passive
immunity using antitoxins against Tetanus toxin from
the bacterium Clostridium tetani if too late for
vaccination.
 Crash course Videos
Part 1
https://www.youtube.com/watch?
v=GIJK3dwCWCw
Part 2
https://www.youtube.com/watch?
v=2DFN4IBZ3rI
Part 3
https://www.youtube.com/watch?
v=rd2cf5hValM
 Questions

• Name two Primary defense against pathogens and parasites

• Define the term immune response
• What are antigens?
• What are structures found on the surface of T lymphocytes?
• Draw and label the structure of a B Lymphocyte
• Draw and label the structure of an antibody
• Give two differences between the primary and secondary
response
 Questions
• Describe how a phagocyte responds to an
invading pathogen.
• Describe the function of Antibodies
• Emily had chickenpox as a child. She was
exposed to the virus that causes it as a
teenager but did not experience any
symptoms. Explain why.
 Questions
• What is the difference between active and
passive immunity?
• Explain the difference natural passive and
artificial passive immunity.
• Give two advantages of vaccinations
• Why is protecting biodiversity important for
the development of new medicine?
 Question
How does the plasma cell in passive immunity
not get destroyed as foreign .

http://www.bbc.co.
uk/schools/gcsebitesize/science/ocr_gateway
_pre_2011/ourselves/2_keeping_healthy3.
shtml
 Monoclonal Antibodies
In 1970 Scientists developed a way to select a type of B lymphocytes to
produce large amounts of its antibodies . Monoclonal Antibodies.
Problem:
B lymphocytes that made clones of plasma cells did not produce antibodies
Plasma cells that made antibodies did not clone

The concept is based on the principle that B lymphocytes are fused with
cancer cells to form hybridoma cell. These Hybridoma cells in turn form
clones of cells secreting monoclonal antibodies.
 Monoclonal Antibodies
How to make monoclonal antibodies
https://www.youtube.com/watch?v=Gykx5FrQbvU
Steps
Mouse is immunized against an antigen
Mouse antibodies are produced and tested
Mouse cell are mixed with rapidly cloning cells to form a hybrid.
Hybrid cells are allowed to grow and are tested to ensure production of the
right antibodies
Hybrid cells are modified to be used( humanized)
 Monoclonal Antibodies in
Diagnosis
Used to locate where blood clots occur in a body suspected of a blood thrombosis( dislodged clot)
– Mouse injected with human fibrin ( a protein found in blood clot)
– Fibrin acts as the antigen in the mouse
– Mouse B lymphocytes proliferate producing antibodies for human fibrin especially in spleen
(an abdominal organ involved in the production and removal of blood cells in most
vertebrates and forming part of the immune system)
Spleen cells with B plasma cells releasing fibrin antibodies are mixed with
cancer cells.
This hybridoma cells are cultured producing large amounts of antibodies
Antibodies are labeled using a radioactive chemical that produces gamma
radiation
Labeled antibodies are used in a patients blood bind to fibrin molecules
These show up on a gamma film to indicate the areas where the blood clot
releasing fibrin is located
Monoclonal Antibodies in
Diagnosis
 Monoclonal Antibodies in
Diagnosis
Used to test pregnancy to detect the presence of a hormone HCG- Human
Chorionic Gonadotrophin in the urine. (Only secreted in Pregnancy)
– In the pregnancy kit, Monoclonal antibodies are made using mouse
lymphocytes specific to HCG in the urine.
– Urine added to the sample window saturates the absorbent pad and begins to
moves up the test strip.
– HCG antibodies bound to coloured latex particles form an antibody-particle
complex . If HCG is present in the urine it bind to the mobile antibody-particle
complex.
– A fixed monoclonal antibody for HCG is found in the Results window. As the
HCG- antibody-latex complex passes this region ,a coloured line is seen. This is
region called the Test Results Region.
– There is yet another region containing another monoclonal antibody ( an anti-
mouse antibody) .This react against the antibody – latex complex whether or
not it has HCG bound to it. This is called the Control Region and confirms that
the test has worked properly.
 Monoclonal Antibodies in
Diagnosis of Disease
Differentiate between diseases with similar symptoms.E.g:
-STDs Chlamydia &Gonorrhoea: both caused by a bacterium that causes
pelvic inflammation and possibly infertillity. Monoconal antibodies
make diagnosis faster and more reliable
-Herpes 1 ( Cold sores) and Herpes 2 ( genital infection)
-Leukemia and Lymphomas ( Cancers of WBC’S)
Early Diagnosis of other cancers Lung, breast ,colon rectal
-Testing body fluid samples
-By directly locating tumors : using monoclonal antibodies attached
to radioactive tracer e.g Iodine -131 specific to a cancer antigen. The
antibody would find the location of the antigen which would be
identified due to the radioactive tracer used.
Diagnosis of streptococcal infections
 Monoclonal Antibodies in
Treatment of diseases
Treatment of Disease (Magic bullet) Paul Ehrlich
Ehrlich reasoned that since a compound could selectively target a disease-causing
organism, then a toxin for that organism could be delivered along with the agent
of selectivity. "magic bullet" – referred to an ideal therapeutic agent created to kill
only the organism targeted. This lead to the development of antibody-drug
conjugates(a monoclonal antibody linked to a cytotoxic biologically active drug),
selectively delivered to their designated targets (e.g. cancer cells).
This mechanism of action of Monoclonal antibodies can be an effective in
treating disease.e.g If attached to a isotope or a toxic drug the antibody
would be able to destroy the target cell
limitations
-Normal cells may also be destroyed since similar markers on cancer cells
are present on normal cells
-Antibody attach to the surface of the cell but does not enter it to deliver
the toxin
 Monoclonal Antibodies for
Treatment (MabThera drug)
MabThera : (rituximab)an anticancer drug is a
monoclonal antibody for a protein(CD20)
found on the membrane of B lymphocytes
• In the cancer no-Hodgkin Lymphoma , B Lymphocytes
are the cancerous cells
• Binding of rituximab kills the B lymphocyte as well as
normal ones since they have the same CD20 receptor
• Rituximab is also use din treating other autoimmune
diseases involving over active Blymphocytes e.g
rheumatoid arthritis.
 Monoclonal Antibodies in organ
transplants
Prevent rejection of transplants:
– Monoclonal antibodies are used to suppress T cells which normally
destroy transplanted organs
– This is more effective than drugs used to suppress the entire immune
system since only the Tcells are suppressed .

Tissue Typing to reduce the risk of rejection before carrying out

a transplant
– Find a compatible donor whose antigens is a close match to the
recipient
– Monoclonal antibodies are cultivated to find out the types of antigens
present in the donor to increase the accuracy of the match
 Monoclonal Antibodies in
Diagnosis
https://www.youtube.com/watch?
v=B0y811xI2mk
 Blood Groups
• In order to give or receive blood, both donor and recipient must be
compatible with each other.
• If this does not occur then agglutination occurs.
• Agglutination (or clumping of cells) is one process by which antibodies
function to destroy pathogens. In this case, the immune response occurs
due to reaction between glycoproteins on the cell membrane of the
donors red blood cells called agglutinogens (these act as antigens) and
antibodies (agglutinins) in the recipients plasma

• AB,O are alleles of one gene. A and B alleles make A and B antigens
respectively . The protein produced by the O is non functional
 Blood Group
Fact1: The two antigens that exist are A and B. The two complementary
plasma antibodies in the plasma are a and b
Fact 2:A person with a specific antigen does not have the corresponding
antibody in their plasma. E.g A person with antigen A on their RBC cell
membrane does not have a antibodies in their plasma . That individuals is
said to have blood group A. Similarly, a person with B antigens on their
cell membrane is said to have blood group B and so does not have b
antibodies in their plasma.
Fact 3: If there are no Specific antigens on the Rbcs cell membrane, then the
individual has blood group O and has antibody a and b
Fact 4: If both specific antigens are on the RBC the individual has blood group
AB. There are no antibodies in the plasma
 Blood Groups
Mixing two blood groups together may result in
different consequences.
Figure 14.6 Blood groups
Blood Group O A B AB
% Population 46 42 9 3
Antigen - A B A+B
Antibody a+b b a -

Blood group O is called the Universal donor no antigens to cause

agglutination by the recipients antibodies. Little agglutination – donor
blood diluted by recipients.

Blood group AB is called the Universal Recipient no antibodies to cause

agglutination. They can only donate to AB.Why?
 Blood groups
Figure 14.43 Interactions between human blood groups. In
major transfusion blood groups are matched more accurately.
Recipient O A B AB
----------- a+b b a ---
Donor
O ---- ---- ---- -----
a +b

A Clump ---- Clump -----

b

B Clump Clump ------ ------

a

AB Clump Clump Clump ------

---
 Blood Groups
Recipient O A B AB
----------- a+b b a ---
Donor
O
a +b
A
b
B
a
AB
---
 Blood Groups Summary
Donate Receive

Blood group O: O,A,B,&AB O

Blood group A: A, AB O,A
Blood Group B: B,AB O,B
Blood group AB AB O,A,B,AB
 Major Histocompatibility Complex
Marker (MHC)
Major Histocompatibility Complex (MHC)are :
– special markers found on all cells ( except red blood cells) and are used
by the immune system to recognize self.
– coded for by genes on chromosome 6
– glycoproteins and are attached to the cell membrane with the
carbohydrate tail extended as a flag.
– act as antigens and are attacked by T –cells if they are foreign(e.g
rejection of transplanted organs)
There are three classes:
MHCI- are recognized by CD 8 receptors on T 8cells,
MHC II- are recognized by CD 4 receptors on T4cells
MHCIII
 The rhesus Factor
A special antigen found on red blood cells of 85% of the population. These
persons are rhesus positive: RhD positive (Dominant)
The 15% lacking this rhesus antigen are called rhesus negative RhD negative (
Recessive)
– rhesus negative blood does not usually have antibodies angainst rhesus positive blood
– If rhesus negative individual is given rhesus positive blood antibodies for the antigen
are produce. This can be problematic.
Eight blood groups:
– A RhD positive (A+)
– A RhD negative (A-)
– B RhD positive (B+)
– B RhD negative (B-)
– O RhD positive (O+)
– O RhD negative (O-)
– AB RhD positive (AB+)
– AB RhD negative (AB-)

NHS,2015
 The rhesus Factor
E.g in pregnancy if a rhesus negative mother has a rhesus
positive baby .
– rhesus positive blood gets into the mother during ate pregnancy .
– Antibodies are produced against the red blood cells of the fetus which
may not be in sufficient quantities to affect the first child but may
cause haemolytic disease of other rhesus positive babies.

In UK 85% of the population is RhD positive , (36% of the

population has O+, the most common type).
– As aresult in cases of uncertainty or emergency, O RhD negative blood
(O-) can safely be given to anyone because it doesn't have any A, B or
RhD antigens on the surface of the cells, and is compatible with every
other ABO and RhD blood group.
Questions
 Questions
ai • First line of defence against invading organisms to
eliminate them and prevent infection
• Antigen-nonspecific defence mechanisms that a host
uses immediately on exposure to antigen/response is
same for all pathogens
• There is no memory or lasting protective
immunity/resistance to disease is unchanged after
infection 2–3 points [1)

ii • Physical barriers – epidermis of skin, mucous

membranes
• Chemical factors – lysozyme, complement proteins,
histamines
• Phagocytic cells – neutrophils, monocytes and
macrophages
• Cells that release inflammatory compounds – basophils,
mast cells and eosinophils
• Any valid point
b.i Histamine [1]
ii • Causes cells of capillary wall to pull away from each
other/capillaries become ‘leaky’/diapedesis [1]
• Relaxes the smooth muscles of arterioles causing
increased blood flow to area [1]

iii Cell 1 – neutrophil

Cell 2 – monocyte
Cell 3 – macrophage

iv • Attract the phagocytes (neutrophil, monocyte,

macrophage) to the site of infection by a process called
chemotaxis
• Destroys bacteria by making holes in them/lysis
• Coat/tags the bacteria so phagocytosis can take
place/opsonisation
• Causes local vasodilation
v • Second line of defence against invading organisms to
eliminate them and prevent infection
• Antigen-specific defence mechanism which involves
humoral and cell mediated immunity
• Involves the formation of antibodies and cytokines
secreted by B- and T-lymphocytes
• There is lasting protective immunity/resistance to
disease improves after infection

vi • Ingests pathogen and digests it

• Pieces of antigen are displayed on the cell surface of
macrophage in grooves within MHC proteins
• Acts as antigen presenting cells (APC)
• The displayed antigens on the APCs are shown to Thelper
cells
• Appropriate T-helper cells selected
• T-helper activates appropriate B-cells – clone selected
which produce antibodies
1ai)What is non –specific immunity? 1mk
ii)Give two examples of non specific immunity?2mks
b)The diagram shows the events of a non specific response.
i)Name the substance produces by the mast cell. 1mks
ii) What are the functions of the substances identified in bi)2mks
iii)Identify cells 1,2,3. 2mks
iv) Explain the role of the complement system in non specific
immunity.3mks
v)If infection lasts a while the specific immune system is
stimulated. What is the ‘specific Immunity”.1mk
vi) Explain the role of cell 3 in stimulating the specific immune
system. 3mks
• 12 a Plasma/effector cells [1]
• b See Figure 11.9 in Biology Unit 2 for CAPE® Examinations
• c • Hinge region: gives molecule flexibility/allows molecule to
• bind to more than one epitope/antigen/pathogen [1]
• • Disulphide bonds: hold two heavy chains together/hold
• heavy and light chains together/maintain the quaternary
• structure of the molecule/maintain the shape of the
• molecule [1]
• d • To bind to different antigens
• • Specific to antigen/complementary shape/lock and key Well explained [1]
• e i • Any substance that when introduced into the blood or
• tissue induces the production of antibodies
• • Foreign substance which stimulates an immune
• response/production of antibodies
• ii Living:
• • Antibody response/primary response would be greater
• • More memory cells produced/lifelong protection [1]
• Attenuated:
• • Would not cause disease/no harm/lack of symptoms of
• disease
• f i • No memory cells to detect antigen
• • Time taken for degradation and presentation of antigen
• by APC to T- and B-cells
• • Time taken for specific clone to be selected
• • Time taken for clonal expansion
• • Time taken for the plasma cells to differentiate
• • And produce antibodies
• ii • Primary response is slower than secondary response
• • Primary response is smaller than secondary response
• • Secondary response remains higher after 40 days Any 2 points [2]
• iii • Secondary response is faster because of many memory
• cells present
• • Memory cells have to go through fewer differentiations
• to form plasma cells
• • More antibodies produced because many memory cells
• were present to stimulate many plasma cells production
• 13 a i • Natural: acquired through disease/illness [1]
• • Artificial: achieved through injections/given
• intentionally [1]
• ii With active immunity, the antigen enters body and
• antibody production is stimulated. In passive immunity,
• antibodies are supplied directly to the body. [2]
• b
• Example Type of immunity
• Baby feeding on breast milk Natural passive
• Child exposed to a friend with chicken pox Natural active
• Receiving the MMR vaccine as a child Artificial active
• Receiving the H1N1 vaccine as an adult Artificial active
• Getting an emergency tetanus injection after
• stepping on a rusty nail Artificial passive
• c • Vaccine contains antigen
• • Antigen activates the immune response
• • Memory cells (both T and B) would be made, which
• remain in circulation in body
• • When infected again, secondary response would
be faster
• d • Given an anti-venom/specific antibodies to
toxin
• • Through injection
• • Provides immediate protection
 Resources
National Health ServicesUK.2015. Retrieved from http://www.
nhs.uk/conditions/Bloodgroups/pages/intro duction.aspx

Ramesar, M. J. (2011). Biology Unit 2 for CAPE Examinations.

Cambridge University Press.

Taylor, D. G. (2012). Biological Science Third edition. Cambridge

University Press.

Tylor,N., Dodds,J., Dodds,J.,Bradfield,P.(2002).A2 Level Biology.

Pearson Limited Edition.