1. immunology

2. pathogen infection disease
an organism that causes disease:
bacteria &virus
pathogen
infection
in tissues
recognisable symptoms
specific to pathogen
disease

3. Appreciate the natural barriers to infection in humans
Spec.
Appreciate the natural barriers to infection in humans
Skin
Tears
Acid
Mucus (containing lysozyme)

5. general immune response specific immune response
phagocytes
specific immune response
lymphocytes

6. general immune response
blood
PLASMA
CHEMICAL
swelling
tissue
general immune response

8. pathogenic
vacuole
pathogen

9. antigen presentation

11. ANTIGEN
chemical capable of provoking the production of specific and complementary antibodies

12. clonal selection different lymphocytes non-self antigen
Specific complementary
lymphocyte selected
self antigen
clonal selection

14. Distinguish between antibody-mediated and cell-mediated immunity
Spec.
Distinguish between antibody-mediated and cell-mediated immunity
Antibody-mediated immunity involves the division of B-lymphocytes after exposure to foreign antigens to form:
Plasma cells capable of synthesising and secreting specific antibodies
Memory cells providing long-term immunity

15. Cell-mediated immunity involves the role of T-lymphocytes
spec
Cell-mediated immunity involves the role of T-lymphocytes
Division of T-lymphocytes sensitised by viral antigens, abnormal self-antigens (tumours) or transplanted foreign tissue antigens to form a pool of different types of T-lymphocytes:
Killer T-cells capable of direct enzymatic destruction of foreign invading antigens
Helper T-cells which cooperate with B-cells in the formation of some types of antibody
Memory T-cells providing long-term immunity to specific antigens

16. clones of B or T lymphocytes clonal expansion
Macrophage or antigen
T or B lymphocyte
differentiation
Division +
clones of
B or T lymphocytes
clonal expansion

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

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

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

21. damage bacterial cell walls
anti-toxins
neutralise toxins
produced by bacteria
agglutinins
clump bacteria and
phagocytes engulf them
attach to viruses
prevents them from entering cells
lysis
damage bacterial cell walls

22. Cell-mediated response
Clone cells differentiate (sub-divide) into:
Killer T-cells (cytotoxic T-cells)
destroy virus infected cells
destroy antigen directly by breaking cell wall
Memory T-cells
used in future infection by the same antigen to rapidly produce a bigger clone of T-lymphocytes
Helper T-cells
stimulate B and T cells to increase antibody production
attract and stimulate macrophages (phagocytosis)

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

24. Describe an antigen-antibody reaction
spec
Describe an antigen-antibody reaction
Agglutination involving formation of a specific antigen/antibody complex
Phagocytosis of this complex by polymorph (AS recall)
Destruction of the antigen by intracellular digestion involving lysosomal enzymes
Page 271 Froggy

25. Spec.
Concept of delay in such antibody-mediated reactions and consequences for the infected individual

26. delayed start
slower production
lower maximum
lasts shorter time
immediate start
faster production
higher maximum
lasts longer time

27. 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.

28. 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

29. Contrast active and passive immunity (in outline only)
spec
Contrast active and passive immunity (in outline only)
Active immunity involves an individuals own immune system producing specific antibodies, T-cells and memory cells to particular foreign antigens
Passive immunity involves donation of antibody from another source including:
Placental (uterine) transfer
Transfer from an individual convalescing from a clinical infection
Active immunity provides long-term immunity whereas passive immunity provides short-term immunity only

30. ACTIVE PASSIVE 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
Injection of dead/weakened antigen (vaccination)
Placental transfer:
Antibodies formed by mother cross placenta
Colostrol transfer:
Colostrum in breast milk contains antibodies
Antibodies made in individual or animal recovering from disease injected as a serum.
Quick way treating already ill people

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

32. Understand the concept of transplant rejection
spec
Understand the concept of transplant rejection
Transplanted/transfused tissue from a donor exposes a recipient’s immune system to foreign antigens
Production of specific T-cells/B-cells which attack and destroy introduced tissue

33. Understand the principle of immunosuppression and its consequences
spec
Understand the principle of immunosuppression and its consequences
Inactivation of specific B- and T- cell responses using irradiation by X-rays or using drugs which inhibit DNA replication
Introduced foreign antigens not recognised and therefore no immune response
Individual with a suppressed immune system is more susceptible to infection

34. Tissue transplants
The cells of tissues and organs carry protein markers on the cell membrane, which are identified as self. Different individuals have different markers, which initiate an immune response when transplanted into another individual.
Killer T-cells result in the recipient rejecting the new tissue or organ.

35. Flowchart
Immune response to
Transplanted tissue

36. foreign antigens/markers on transplanted tissue
complementary receptors
on specific T cells
attach to antigens/markers
on non-self 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

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

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

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

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

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

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

43. 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.
Immunosuppresion, using drugs to inhibit DNA replication, cell division and cloning of lymphocytes to delay rejection. Infections are more likely and it unpleasant side effects.

44. Understand human blood antigens and the basis of blood group polymorphism
Four blood groups recognised in the ABO system (A, B, AB and O)
Blood group specified by the antigen type present on the surface membrane of erythrocytes
Individuals possessing a particular type of antigen cannot possess complementary antibody in their plasma

45. Anti-rhesus antibodies do not naturally occur in any individual
Rhesus antigen (antigen D) may also occur on the surface membrane of erythrocytes
Anti-rhesus antibodies do not naturally occur in any individual
Production of anti-rhesus antibodies
Transfusion by error where a rhesus negative individual is given rhesus positive blood and the consequences thereof
A rhesus negative mother is exposed to the rhesus antigen of her rhesus positive baby, and the consequences for that child and future children

46. Appreciate the principles of blood transfusion compatibility
Comparison of donor antigens and recipient’s plasma antibodies to determine compatibility
Antibodies in donated blood have a negligible effect on the recipient’s erythrocytes

47. Appreciate the consequences of transfusion incompatibility
Formation of antigen/antibody complexes resulting in agglutination of erythrocytes
Potential blockage of the blood/O2 supply to a tissue and the consequences thereof

48. A B AB O A & B NONE RED BLOOD CELL BLOOD GROUP ANTIGEN
ANTIBODIES IN PLASMA a b b a

49. BLOOD TRANSFUSIONS

50. The person getting the blood transfusion 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.                 A B AB O RECIPIENT BLOOD DONOR BLOOD
ANTIBODY
anti b
anti a
NONE
anti a + anti b    
antigen A    
antigen B    
ANTIGEN
antigens A+B    
NONE

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

53. AGGLUTINATION
antigen a a a a
antibody a

54. AB A B O AB

55. + + + + + 1st pregnancy Mother rhesus negative Baby rhesus positive-
Baby’s Rh+ RBC enter
mother’s bloodstream
Mother makes antibodies
to destroy Rh+ antigen + + + +
2nd preganancy
Rh+ antibodies enter
baby’s bloodstream
Agglutination occurs -
Rhesus negative RBC +
Rhesus positive RBC
Rhesus antibody