immunology

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

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

general immune response specific immune response phagocytes specific immune response lymphocytes

general immune response blood PLASMA CHEMICAL swelling tissue general immune response

pathogenic vacuole pathogen

antigen presentation

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

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

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

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

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

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

antibodies Plasma cell differentiates into either B-lymphocyte memory cell

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

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

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)

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

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

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

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

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.

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

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

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

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

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

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

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.

Flowchart Immune response to Transplanted tissue

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

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

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

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

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

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

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

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.

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

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

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

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

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

BLOOD TRANSFUSIONS

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.

                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

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

AGGLUTINATION antigen a a a a antibody a

AB A B O AB

+ + + + + 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