The Immune System Master Notes
Key: Local Immune Response, Activation of Helper T-cells, Activation of B cells, Activation of Killer T-
cells, Immunological memory
1. The barrier is breached (perhaps a cut)
2. The cells around the site that are damaged/dying/just traumatised scream for help releasing
chemical alarm signals - HISTAMINE
3. Macrophages (soldiers) – phagocytosis – they secrete cytokines which attract neutrophils
4. Neutrophils (suicide warriors/marine cells) – vomit chemicals and phagocytosis (collateral
damage to both sides) some even explode
5. INFLAMMATION – fluid moves in – bringing in complement proteins (rips holes in bacteria etc)
6. Dendritic Cell (special intelligence) – collect samples and cover themselves in antigens etc (like a
soldier covering themselves in the guts of their enemy) *note dendritic cells can also be called
Macrophage APCs
7. Dendritic Cell leaves battle field and enters the lymph system – it is looking for a specific helper T-
cell in the lymph nodes
8. After a few hours it finds a complementary/specific helper T-cell for the antigen and activates the
helper T-cell T-helper call has a complementary receptor which fits the non-self-antigen the
macrophage is carrying - the binding activated the T-helper cell
9. Activated helper-T cell replicates (mitosis) to create thousands
10. Some T-cells move to the battle field (becoming the commanders) and reactivate (motivate) tired
macrophages (soldiers) and turns on serious macrophage killing mode
11. Antigens from the battlefield float through the lymph node, where a virgin B-Cell connects to it
(matching/complementary)
12. The B-cell engulfs the antigen and then displays the antigen fragments to its MHC II molecules
(windows) (it is now activated on a low level and makes lots of copies of itself)
13. This attracts the help of a matching mature helper T-cell. Cytokines secreted by the T-cell help
the B-cell to multiply faster and differentiate faster into plasma cells
14. Plasma cells release antibodies which lock onto matching antigens allowing them to be cleared
by the complement cascade and also neutralisation (block ability to bind to host cell) &
opsonisation (promote phagocytosis by neutrophils and macrophages)
15. The cytokines released by the helper T-cells also activate cytotoxic T cells (T-killers)
16. An activated cytotoxic T-cell binds to the MHC I molecule on an infected cell
17. The T-cell released perforin molecules – form pores in infected cell and enzymes enter the cell
triggering apoptosis, the Cytotoxic T-cell now moves onto its next prey
18. Some Cytotoxic T-cells become memory cells. Some B-cells become memory cells allowing a
faster response the next time this pathogen is encountered.
19. Cut is cleared out, clotting prevents further entry of pathogens, and tissue heals.
Key: Local Immune Response, Activation of Helper T-cells, Activation of B cells, Activation of Killer T-
cells, Immunological memory
1. The barrier is breached (perhaps a cut)
2. The cells around the site that are damaged/dying/just traumatised scream for help releasing
chemical alarm signals - HISTAMINE
3. Macrophages (soldiers) – phagocytosis – they secrete cytokines which attract neutrophils
4. Neutrophils (suicide warriors/marine cells) – vomit chemicals and phagocytosis (collateral
damage to both sides) some even explode
5. INFLAMMATION – fluid moves in – bringing in complement proteins (rips holes in bacteria etc)
6. Dendritic Cell (special intelligence) – collect samples and cover themselves in antigens etc (like a
soldier covering themselves in the guts of their enemy) *note dendritic cells can also be called
Macrophage APCs
7. Dendritic Cell leaves battle field and enters the lymph system – it is looking for a specific helper T-
cell in the lymph nodes
8. After a few hours it finds a complementary/specific helper T-cell for the antigen and activates the
helper T-cell T-helper call has a complementary receptor which fits the non-self-antigen the
macrophage is carrying - the binding activated the T-helper cell
9. Activated helper-T cell replicates (mitosis) to create thousands
10. Some T-cells move to the battle field (becoming the commanders) and reactivate (motivate) tired
macrophages (soldiers) and turns on serious macrophage killing mode
11. Antigens from the battlefield float through the lymph node, where a virgin B-Cell connects to it
(matching/complementary)
12. The B-cell engulfs the antigen and then displays the antigen fragments to its MHC II molecules
(windows) (it is now activated on a low level and makes lots of copies of itself)
13. This attracts the help of a matching mature helper T-cell. Cytokines secreted by the T-cell help
the B-cell to multiply faster and differentiate faster into plasma cells
14. Plasma cells release antibodies which lock onto matching antigens allowing them to be cleared
by the complement cascade and also neutralisation (block ability to bind to host cell) &
opsonisation (promote phagocytosis by neutrophils and macrophages)
15. The cytokines released by the helper T-cells also activate cytotoxic T cells (T-killers)
16. An activated cytotoxic T-cell binds to the MHC I molecule on an infected cell
17. The T-cell released perforin molecules – form pores in infected cell and enzymes enter the cell
triggering apoptosis, the Cytotoxic T-cell now moves onto its next prey
18. Some Cytotoxic T-cells become memory cells. Some B-cells become memory cells allowing a
faster response the next time this pathogen is encountered.
19. Cut is cleared out, clotting prevents further entry of pathogens, and tissue heals.
