- Created by: ebcrankomills
- Created on: 27-05-19 11:10
- Y- shaped glycoproteins called Immunoglobins
- They bind to specific regions on the pathogen triggering the immune response
- Heavy Chains - Two identical long polypeptide chains
- Light Chains - Two much shorter identical chains
- Disulfide bridges hold the chains in place.
- Bind with a lock and key mechanism
- Variable region - An area of 110 amino acids on both the heavy and light chains, it's a different shape on every antibody giving it specificity.
- Constant region - The rest of the antibody is always the same
- When an antibody binds to an antigen it forms an antigen-antibody complex.
- Hinge region - provides flexibility, this allows it to bind to two separate antigens, one at each bonding site.
- The Hinge region can be found where all points of the Y meet.
How antibodies work
- In the antigen- antibody complex, the antibody acts as an opsonin, this means that the complex can be easily engulfed and digested by pahogcytes.
- Many pathogens cannot invade host cells effectviely after they are part of an antigen-antibody complex.
- The antibodies are able to act as agglutinins. Agglutinins cause the pathogens- that are carrying the antigen-antibody complex- to clump together. As a result of this they are less able to spread through the body.
- It is also easier for phaggocytes to engulf pathogens
- The antibodies can act as anti-toxins, they bind to the toxins that are made by the pathogens and render them harmless.
Lymphocytes are white blood cells, they are partciularly important within the specific immune system.
T-Lymphocytes mature in the Thymus gland, they include:
- T-helper cells
- T-killer cells
- T-memory cells
- T-regulator cells
B-Lymphocytes mature in the Bone marrow, they include:
- Plasma cells
- B effector cells
- B memory cells
- They have CD4 receptors on their cell surface membranes these are able to bind to the surface antigens on APC's.
- They make a form of cytokines called interlukins, these are able to stimulate the activity of B cells.
- By stimulating B cells, there is an increase in the number of anitbodies made and stimulates the production of other types of T cells.
- It attracts and stimulates macrophages to ingest pathogens with antigen-antibody complexes.
- Capable of destroying the pathogen that is carrying the antigen.
- Produce perforin, a chemical which kills the pathogen.
- It is able to kill the pathogen by making many holes in the cell membrane.
- The effect of this is that the membrane becomes freely permeable.
- Live for a long time
- They are part of the immunological memory.
- If they come into contact with an antigen for a second time then they are able to divide rapidly to form a large number of clones of T-killer cells.
- These cells are able to suppress the immune system, they act in a way that means that they can control and regulate it.
- Once a pathogen has been eliminated they stop the immune response.
- As well as this they ensure that the body recognises self antigens and does not set up an autoimmune response.
- Interleukins are important in this control.
- Produce antibodies to a particular antigen.
- The antibodies are released into circulation
- Active plasma cells only live for a few days but are able to make around 2000 antibodies every second whilst they are alive and active.
- Divide to form the plasma cell clones
- They provide the immunological memory.
- They live for a very long time.
- Programmed to remember a specific antigen and enable the body to make a very rapid response when a pathogen carrying that antigen is encountered again.
T-lymphocytes respond to the cells of an organism which have been changed in some way and to the cells from transplanted tissue. The cell-mediated response is particularly important against viruses and early cancers.
- Macrophages engulf and digest pathogens by phagocytosis in the non-specific defence system. They process the antigens from the surface of the pathogen to form APC's.
- Receptors ofn some of the T-helper cells fit the antigens. These T-helper cells are then activated, they can now produce interleukins.
- The production of interleukins stimulates more T cells to divide rapidly (by mitosis). They form clones of identical activated T helper cells which all carry the correct antigen to bind to a specific pathogen.
- The cloned T-cells may:
- Develop into T-memory cells, these give a rapid response if the same pathogen invades again.
- Produce interleukins to stimulate phagocytosis or that stimulate the division of B cells
- Stimulate the development of a clone of T-killer cells which are specific for the presented antigen and are then able to destory infected cells.
The body responds to antigens that are found outside of the cells and to APC's. The humoral immune system is able to prodcue antibodies which are soluble in the blood and tissue fluid and are mobile (not attached to cells),
B lymphocytes have antibodies on their surface, when a pathogen invades the B cells with the compliemtnary antibody with bind to the antigens. The B cell engulfs and processes the antigens.
- Clonal Selection: Activated T helper cells bind to the APC of the B cell.
- Interleukins produced by the activated T helper cells activate the B cells.
- Clonal Expansion: The activated B cell divides via mitosis to create clones of plasma cells and B memory cells.
- Primary Immune Response: Cloned Plasma cells make antibodies which fit the antigens on the surface of the pathogen bind to them and disable them, or they acts as opsonins or aggluntinins. It can take a few days or weeks, this is why we become ill.
- Secondary Immune Response: some of the cloned B cells develop into B memory cells. These are able to divide rapidly to form plasma cell clones if the body is re-infected with the pathogen again. They produce the correct antibody and wipe out the pathogen very quickly before they can cause any symptoms.
- Sometimes the immune system can stop recognising its own cells, as a result it can start attacking healthy body tissue. This is an autoimmune disease.
- Scientists still don't completely know what causes this to happen.
- Immunosuppressant drugs can be used as treatments but they deprive the body of its natural defences, this leaves people much more susceptible to future pathogens.
- Examples include: type 1 diabetes, rheumatoid arthritis and lupus.