BIO - Immunology processes

Allergic response (6)

1. Allergen binds to B cells

2. B cells produce IgE antibodies

3. IgE binds to mast cells

4. When the allergen is encountered again, it binds to the activated mast cells via the IgE antibodies

5. When the allergen bridges the gap between 2 antibodies it triggers the release of histamine

6. Histamine causes blood vessels to dilate and become more permeable, increasing the inflammatory response. It also contracts the muscles of the airways which causes difficulty breathing and increases mucus production.

Inflammatory response (9)

1. A pathogen gets past the first line of defence through a cut

2. Injured cells release cytokines

3. Platelets release clotting factors

4. Cytokines attract neutrophils, macrophages and mast cells to the area

5. Mast cells release histamine that dilates the blood vessels and makes them more permeable to increase blood flow to the area

6. Neutrophils secrete defensins and hydrogen peroxide to kill pathogens

7. Macrophages are activated and secrete cytokines to attract more immune cells

8. Macrophages and neutrophils phagocytose pathogens

9. The inflammatory response continues until the pathogen is eliminated and the wound is healed

Phagocytosis (4)

1. Receptors on the phagocyte bind to a foreign pathogen

2. The phagocyte engulfs the pathogen in a phagosome

3. Lysosomes fuse with the phagosome and secrete lysozyme that breaks down the pathogen

4. Indigestible material is exocytosed from the cell

Humoral immunity (5)

1. Clonal selection - an antigen or APC reaches the lymph nodes and binds to a specific B cell that recognises the antigen

2. Helper T cells bind to the antigen and release cytokines that activate B cells and stimulate them to divide

3. Clonal expansion - B cells differentiate into plasma B cells and memory B cells

4. Plasma B cells secrete lots of antibodies that bind to antigens to form antibody-antigen complexes that are flagged for phagocytosis

5. Memory B cells remain in the body after infection has passed to recognise antigens faster when they are encountered again for a quicker, stronger immune response

Cell-mediated immunity (5)

1. APCs displaying foreign antigens on MHC-II markers bind to specific helper T cells

2. Helper T cells release cytokines that stimulate clonal selection and expansion to produce more helper T cells, cytotoxic T cells and memory T cells

3. Helper T cells secrete cytokines that activate cytotoxic T cells

4. Cytotoxic T cells bind directly to infected body cells displaying abnormal MHC-I markers and release perforin to induce apoptosis

5. Memory T cells remain in the body after infection to recognise antigens faster when they are encountered again to provide a quicker, stronger immune response

Monoclonal antibody production (6)

1. A mouse is injected with antigens from the cancer cell, causing it to produce specific plasma B cells

2. Plasma B cells are extracted from the spleen of the mouse

3. Plasma B cells are fused with tumor cells or myeloma cells to form hybridoma cells

4. Hybridoma are screened to determine which are producing useful antibodies

5. The selected hybridoma is allowed to divide and produce clones

6. Hybridomas are used to produce large amounts of antibodies that bind to cancer cells to kill them or flag them for destruction

Indirect ELISA test

1. Wells are pre-coated with antigens

2. Pipette the sample serum from the patient into the wells. If the serum contains primary antibodies to the antigen, they will bind.

3. Wash the wells to remove unbound substances

4. Pipette secondary antibodies (monoclonal) that are linked to an enzyme. They will bind to the primary antibodies. 

5. Wash the wells to remove unbound substances

6. Pipette substrate that reacts with the enzyme to cause a colour change if antibodies are present