Non-specific immune response -Inflammation -Phagoc
- The damaged white blood cells and mast cells release histamine, they cause arterioles to dilate increasing the blood supply to certain areas.
- This causes the holes to open between the endothelial cell in the capillary walls.
- Causing swelling(odema)
- This will let the monocytes and neutrophils into the infected area, they engulf and destroy the foreign bodies and pathogens.
- The immune system destroys the pathogen.
- During this process the pathogen will be engulfed and destroyed.
- The Phagocyte (Macrophage) recognises the antigens on the pathogen.
- The cytoplasm of the phagocyte moves around the pathogen, engulfing it by endocytosis.
- The pathogen is in the phagocytic vacuole inside the cytoplasm of the phagocyte.
- Lysosomes fuse with the vacuole, hydrolytic enzymes breaking down pathogen and digesting it.
- The phagocyte will then present pathogen's antigens. Which will stick the antigens on its surface to activate the immune system cells.
- This is called APC (Antigen-Presenting Cell).
Non-specific immune response -Interferon
Its a protein made when the cells are infected with viruses.
Interferons help stop the virus spreading to other cells it does this in different ways:
- It will block RNA synthesis so replication is inhibited, which produces the viral proteins.
- Interferons activate the cells which are involoved in specific immune response, killing the infected cells.
- They will activate mechanisms of non-specific immune response by promoting inflammation causing immune system cells to the site of infection.
Pathogens have protien on the surface of the cell, the immune system can recognise it as foreign, these protiens are called ANTIGENS.
T cells, B cells and macrophage all can recognise an antigen and when it does recognise it will trigger the immune response.
When a pathogen is engulfed and destroyed the major histocompatabillity complex will attach to pathogenic antigen.
It will present foreign antigen and activate the T and B cell responses.