1. immunology

2. pathogen infection disease
an organism that causes disease:
Bacteria, virus, protoctist, fungi
pathogen
infection
in tissues
recognisable symptoms
specific to pathogen
disease

3. natural barriers to infection in humans
Skin: a tough physical barrier
Lysozyme: in tears, saliva & sweat, Antibacterial hydrolyses bacterial cell walls
HCl in stomach: kills most pathogens – denatures enzymes
Epithelial lining in respiratory tract covered in mucus, traps pathogens & prevents them reaching the cells beneath. Cilia sweep mucus & pathogen to trachea.

4. Non specific immune response specific immune response
phagocytes
specific immune response
lymphocytes

5. Non specific immune response
blood
PLASMA
CHEMICAL
swelling
tissue
Non specific immune response

6. Non specific immune response
Infection causes an inflammatory response
pathogen enters the tissues and releases chemicals
blood flow to the area increases
& capillaries become more leaky and plasma moves in to the surrounding tissue
phagocytes are attracted to the site & leave the blood by squeezing through the capillary walls: polymorphs arrive first in greatest numbers, followed by macrophages (made from monocytes) which are larger and longer lived.

7. phagocyte membrane invaginates and encloses around the pathogen
which is engulfed and forms a vesicle, called a phagosome.
lysosomes move to the phagosome and their membranes fuse
releasing hydrolytic enzymes which digest the pathogen
the soluble products are absorbed into the cytoplasm.
phagocytes, dead pathogens and cell debris form pus which results in swelling
temperature increases at the site of infection helping to denature pathogenic enzymes

8. Diagram page 20
A2 text book

10. pathogenic
vacuole
pathogen

11. specific immune response
This relies on the ability of lymphocytes to recognise self and non-self tissue.
All cells have polysaccharides, glycoproteins and glycolipids on their surface membrane that form antigens. These antigens can trigger an immune response.
Antigens present on the membrane our own cells are called self antigens.
Antigens present on the membrane of cells from other organisms, including other people, animals, bacteria, fungi, plants and virus’ are called non-self antigens.
These non-self antigens may trigger an immune response.

12. Different pathogens have different antigens; therefore, the immune response needs to be specific to each.
Lymphocytes have receptors on their cell surface membranes. These are complementary in shape to antigens allowing antigens and receptors to fit together.
The lymphocytes with receptors to self antigens are switched off in the developing foetus, leaving only those that are not complementary to self cells.
There are many millions of different lymphocytes, but only a few of each. Consequently this form of response is slow.

14. B & T lymphocytes B Lymphocyte T Lymphocyte
Where formed
Stem cells in the bone marrow
Mature
Bone marrow
Thymus gland
Type of response
Antibody mediated
Cell mediated
How they respond
Produces antibodies in response to non-self antigens, usually on bacteria and virus’ in body fluids such as blood and tissue fluid
Produces a range of cells in response to non-self antigens, usually from viral infections, attached to body cells

16. initial response of B & T lymphocytes to non-self antigens
The non-self antigen attaches to the complementary receptor on a specific B or T lymphocyte.
The lymphocyte is sensitised and becomes activated.
It divides by mitosis to produce clones.
B lymphocytes produce B clones that will form antibodies.
T lymphocytes produce T clones, with different cells carrying out different functions.
This is often called clonal expansion.

17. clones of B or T lymphocytes clonal expansion
non-self antigen
receptor
Macrophage or antigen
T or B lymphocyte
differentiation
Division +
clones of
B or T lymphocytes
clonal expansion

18. cell mediated immunity
This response is triggered by the body’s own cells that have been changed due to the presence of non-self material within them.
Non-self antigens are presented on the cell surface membrane, marking them as different to the other body cells. Examples include:
Macrophages – after engulfing and breaking down a pathogen they cut out and present the pathogen non-self antigens on their own surface membrane.
Body cells that have been invaded by a virus present non-self viral antigens on the body cell membrane.
Cancer (tumour) cells present abnormal antigens on their cell-surface membrane.

20. Cell-mediated response
Clone cells differentiate (sub-divide) into:
Killer T-cells (cytotoxic T-cells)
destroy virus infected cells
attach to the antigens on the cell-surface membrane & produce chemicals
e.g perforin (punches holes in cell-surface membrane) & nitric acid
Destroying the cell

21. Helper T-cells Memory T-cells
stimulate B to divide to increase antibody production
promote and speed up the process of phagocytosis
Attach opsonins to pathogens, marking them for attention of phagocytes
Secrete interferon that limits the ability of viruses to replicate
Memory T-cells
Circulate in body fluids & respond to future infection by the same pathogen.
As they are already sensitised they rapidly produce a large clone of T lymphocytes.

22. abnormal self-antigens/ transplanted foreign tissue
Virus /
abnormal self-antigens/ transplanted foreign tissue
T-helper
T-lymphocyte
Division +
differentiation
T-killer
T-memory

23. Antibody-mediated Response
antbodies
are globular proteins which are complementary to specific antigens and which can react with the antigens leading to their destruction

24. B lymphocytes that have complementary receptors to a pathogen’s antigens are sensitised.
The specific B lymphocyte divides by mitosis and clones
to produce large numbers of plasma cells and a small quantity of memory cells.
Plasma cells are short lived (a few days) but each produce millions of antibodies.
Antibodies neutralise pathogens by carrying out antigen-antibody reactions.

25. antibodies
Plasma cell
differentiates
into either
B-lymphocyte
memory cell

26. the action of antibodies
The antibodies produced by a specific antibody mediated response will be complementary in shape to the antigens on the invading bacterium.
The antibodies attach to the antigens and cause the antigens to clump together (agglutinate), forming an antigen-antibody complex.
This immobilises the pathogen and eventually the complex will be engulfed by polymorphs and other phagocytes.

27. B-memory pathogen B-lymphocyte mitosis & differentiation B-plasma
antibodies
pathogen
polymorph/
macrophage/
phagocyte
agglutination
pathogen
Ingestion &
digestion

28. invading cells directly
The antibodies can also use other methods to defend against infection:
attach to and destroy
invading cells directly
act as opsonins
attaching to pathogens &
marking them for phagocytosis

29. B memory cells can live for many years in the body fluids.
They remain inactive until stimulated by the same antigen again.
They are able to divide rapidly, as they are already sensitised and produce vast numbers of plasma cells.
This is possible because there are more memory cells than there were correct B cells initially.

30. The plasma cells produce the antibodies to destroy the pathogen, the memory cells guarantee a long term protection.
The initial response to the antigen when meeting it for the first time is called the primary immune response.
The production of plasma cells and antibodies from memory cells on subsequent encounters with the antigen is called the secondary immune response.

31. Primary response
Production of antibodies by B-plasma cells in response to pathogen entering the body.
Delay in their production allows the pathogen to reproduce and damage the body, producing the characteristic symptoms associated with the pathogen
As antibodies destroy the antigens, fewer B-cells are made and their level falls.

32. secondary response
When a person encounters the pathogen at a later date B-memory cells rapidly divide to produce plasma cells.
The response is rapid as the B memory cells are already activated.
Larger numbers of plasma cells are produced, so larger numbers of antibodies.
There is not enough time for symptoms of the disease to develop

33. SECONDARY
RESPONSE
PRIMARY RESPONSE
delayed start
slow production
low maximum
lasts shorter time
immediate start
faster production
higher maximum
lasts longer time
time interval
weeks/years

34. ACTIVE PASSIVE NATURAL ARTIFICIAL INVOLVES:
Individuals own immune system producing specific antibodies
Donation of antibodies from another source
CELLS INVOLVED:
B cells, T helper cells
None
RESPONSE LENGTH:
Long term (as memory cells produced)
Short term
(no memory cells, antibodies contain foreign antigens that evoke immune response so are destroyed)
NATURAL
ARTIFICIAL
HOW IT WORKS:
contract disease
e.g. chicken pox
Injection of dead/weakened antigen, modified toxins from pathogen, isolated antigens (vaccination) e.g. Measles
Placental transfer:
Antibodies formed by mother cross placenta
Colostrol transfer:
Colostrum in breast milk contains antibodies
Serum containing antibodies made in individual or animal recovering from disease injected. Monoclonal antibodies are made by removing sensitised & cloned B cells from mice that have been injected with specific antigens. B cells are hybridised with cancer cells & the resulting long lived lymphocytes are grown in fermenters. Large numbers of antibodies are made. Adv: single type of antibody produced, less allergies
Quick way treating already ill people e.g. tetanus

35. immunity ACTIVE PASSIVE T helper cells PRIMARY B plasma cells RESPONSE
Antibodies
Memory cells
PRIMARY
RESPONSE
body makes
long latent period
e.g.
chickenpox
measles
NATURAL
ACTIVE
1st antigen
encounter
get disease TB
meningitis
rubella
tetanus
subsequent
encounters
short latent period
ARTIFICIAL
ACTIVE
e.g.
ACTIVE
vaccination
Long term
immunity
SECONDARY
RESPONSE
immunity
rapid production
of plasma cells and
antibodies
placental
transfer
placenta
NATURAL
PASSIVE
from mother
body receives
antibodies
PASSIVE
breast milk
colostrum
serum
ARTIFICIAL
PASSIVE
e.g.
tetanus
Body does not make antibodies
against non-self antigens
Short term
immunity

36. Tissue transplants
The immune response usually occurs as a result of infection.
Transplanted tissues and organs contain non-self antigens, which also initiate an immune response (unless from within same person e.g. skin grafts or between identical twins).
Transplant rejection is the main reason for failing transplants.
T lymphocytes are sensitised by the non-self antigens in the transplanted tissue.
These clone producing Killer T-cells that destroy the transplanted cells.

37. Flowchart
Immune response to
Transplanted tissue

38. complementary receptors on specific T cells
Non-self antigens on
transplanted tissue
complementary receptors
on specific T cells
attach to non-self antigens
on transplanted cells
T cell sensitised
& divides by mitosis
producing clones
HELPER T CELLS
Play a smaller role
aiding B plasma cells to
produce antibodies
clones differentiate
KILLER T CELLS
destroy targeted non-self cells
by producing perforins
non-self cells lyse
MEMORY T CELLS
Respond if non-self cells
transplanted on a second occasion
from same donor

39. true
false or
Inject foreign antigens into patients so that their immune system is too busy to recognise the new organ
false

40. inject drugs to destroy antibodies produced in the immune response
true
false or
inject drugs to destroy antibodies produced in the immune response
false

41. inject drugs that prevent cell division
true
false or
True
called
immunosuppressants
inject drugs that prevent cell division

42. true false True X-rays or
use radiation to prevent stem cells in the bone marrow from differentiating

43. Inject antibodies to destroy recipients B & T lymphocytes
true
false or
Inject antibodies to destroy recipients B & T lymphocytes
false

44. Check donated tissue for non-self antigens
true
false or
True
Tissue typing
Check donated tissue for non-self antigens

45. Successful transplants require:
Tissue typing where markers on the donor and recipient tissue are checked, and that with the most matched markers will be used. Tissue matching is most likely to occur between close relatives.
X-rays to irradiate bone marrow and lymph tissue to inhibit lymphocyte production and slow down rejection. Unfortunately this increases the chances of infection during treatment and has unpleasant side effects.

46. Immunosuppresion, using drugs to inhibit DNA replication, & therefore cell division and cloning of lymphocytes to delay rejection. Need to be taken for the life of the transplant. It compromises the immune system & infections are more likely as the whole immune response is depressed. Other strategies such as monoclonal antibodies, anti-viral drugs & anti-bacterial mouthwashes help fight any infections.
There needs to be a delicate balance between reducing the risk of rejection and restricting side-effects from the immunosuppressant.

47. Level of immunosuppression
LOW
LOW
Level of
immunosuppression
Risk of rejection
HIGH
Increased infection risk
Increased side effects of toxic drugs e.g. hair loss
HIGH

48. BLOOD TRANSFUSIONS

49. Erythrocytes (RBCs) have antigens on their cell-surface membrane.
The blood of any one person will not have the antibodies that correspond to the antigens on their RBCs, as this would trigger an immune response.
This is because the B lymphocytes that would produce the antibodies that correspond to these self-antigens are switched off during foetal development.

50. There is a variety of different antigens on the erythrocytes of different people.
In the ABO system there are 2 different antigens, but 4 different possible blood groups (known as polymorphism).
Donated blood must be compatible with the recipient to avoid an immune response.
This happens because the person getting the blood transfusion (recipient) has antibodies that will react with antigens on the red blood cells that they receive.
Recipients red blood cells are not damaged by the donors antibodies because there are not enough to cause a response.

51. If antigen and antibody are mixed they will form antigen-antibody complexes causing the RBCs to agglutinate or clump.
This agglutination could block capillary networks (particularly in the kidney) leading to organ failure and death.
antigen a a a a a
antibody

52. A B AB O A & B NONE RED BLOOD CELL BLOOD GROUP ANTIGEN
ANTIGENS & ANTIBODIES PRESENT IN THE ABO BLOOD GROUP SYSTEM
RED BLOOD CELL
BLOOD GROUP A B AB O
ANTIGEN
A & B
NONE
ANTIBODIES IN PLASMA a b b a
anti-b
anti-a
anti-a & anti-b

53. INTERACTIONS BETWEEN ABO BLOOD GROUPS
RECIPIENT BLOOD A B AB O
DONOR
BLOOD
ANTIBODY
anti-b
anti-a
NONE
anti-a + anti-b    
antigen A    
antigen B    
ANTIGEN
antigens A+B    
NONE

54. examples
A donor with blood group A can give blood to a recipient with blood group A because the recipient has no anti-a antibodies that correspond to the A antigens on the donor’s RBCs.
A donor with blood group A cannot give blood to a recipient with blood group B because the recipient has anti-A antibodies which will react with the A antigens on the donor’s RBCs, causing agglutination.

55. group O = universal donor group AB = universal recipient
Has no antigens to be agglutinated
Universal Recipient
Has no antibodies to agglutinate donated antigens

56. AB A B O AB

57. The Rhesus System
The rhesus antigen (or antigen D) is either present or absent on the cell-surface membrane of erythrocytes.
Approx. 85% of individuals possess the antigen and are described as rhesus positive (Rh+)
Rhesus negative individuals (Rh-) do not possess the rhesus antigen.

58. Antibodies for the rhesus antigen are not naturally produced by the body, therefore are absent form the plasma.
HOWEVER, they may be produced as a result of
Rhesus positive blood being donated to a rhesus negative recipient (rare due to blood matching techniques)
A rhesus negative mother carrying a rhesus positive baby.

59. 1st pregnancy
Mother rhesus negative
Baby rhesus positive
Baby’s Rh+ RBC enter mother’s bloodstream
Mother makes anti-D antibodies to destroy Rh+ antigen, a slow process, so baby born before significant numbers are produced
2nd pregnancy
If baby is Rh+ & foetal RBCs enter maternal circulation, relevant B lymphocytes are already sensitised and large numbers of anti-D antibodies are produced immediately.
Anti-D antibodies cross the placenta & enter baby’s bloodstream
causing agglutination of foetal RBCs

60. - + + + + -
Rhesus negative RBC +
Rhesus positive RBC
Rhesus antibody

61. 2nd pregnancy
This is known as haemolytic disease of the newborn
Few cases occur as mothers identified as rhesus negative are given an injection of anti-D antibodies during pregnancy.
These attach to any foetal RBCs that may have entered the maternal circulation before the mother’s B lymphocytes are stimulated to produce ant-D antibodies.
Following birth the mother is given another injection of anti-D antibodies, if the baby is rhesus positive.
If the mother is not identified as rhesus negative the baby can be treated with a blood transfusion.