Specific Immune System 12.6 Flashcards
Antigens
These are molecules that exist on the cell surface of all cells, whether they are self antigens or non-self antigens which means they belong to something foreign. They trigger an immune response which means antibodies which are polypeptides are produced.
Specific Immune System
This is a lot slower than the non-specific system and can take up to 14 days to take affect. However if there is a second invasion of the same pathogen, the response will be a lot faster.
What are antibodies?
These are y shaped glycoproteins called immunoglobulins. They bind to antigens on a pathogen that has triggered the immune response and there’s a specific antibody for each type of antigen, they aren’t all the same.
Structure of antibodies
They are made up of 2 long polypeptide chains called heavy chains and 2 shorter chains called light chains. the heavy and light chains are bonded together with disulphide bridges and they are also in the chains structure to make it more solid. They also have antigen binding sites on each side of the antibody. They also have hinge regions on the antibody where each heavy chain angles off into the y shape and this makes it more flexible and allows it to bind to two antigens at the same time.
How can antibodies bind to antigens?
They have antibody binding sites which is an area on the variable region which is 110 amino acids on the heavy and light chain on both sides of the antibody. Each antibody will have it’s own specific variable region that can be different shapes and will bind to the antigens in a lock and key mechanism in the same way as enzymes and substrates. When they bind they form antigen-antibody complex. The rest of the antibody is called the constant region which is the same for all antibodies. This also has a receptor binding site for when it joins to cells.
How do antibodies defend the body?
- They act as opsonins so it’s easier for a phagocyte to engulf an antigen-antibody complex.
- Once in an antigen-antibody complex, the pathogen cannot enter the host cell and cause any more damage
- They act as agglutinins which causes pathogens carrying antigen-antibody complexes to clump together so they cannot move around the body and also to make it easy for the phagocyte to engulf many pathogens at the same time.
- They can act as anti-toxins and make the toxins produced by pathogens harmless.
Lymphocytes
The immune system is based on these white blood cells called lymphocytes. There are both B and T lymphocytes. B lymphocytes mature in the bone marrow, T lymphocytes mature in the thymus gland
T lymphocytes
These are covered with receptors to bind to the specific antigens. There are: T helper cells, T killer cells, T memory cells and T regulator
T helper cells
These have CD4 receptors on their cell-surface membranes that bind the the antigens on an APC. They produce interleukins which are a type of cytokine. This stimulates the activity of B cells so that more antibodies are produced, and they attract more phagocytes to engulf the pathogens with antigen-antibody complexes attached to them.
T killer cells
These destroy pathogens carrying the antigen by producing perforin which makes holes in its cell membrane so it’s freely permeable. This will kill it
T memory cells
These live for a long time and are part of the immunological memory. They are created after the first time a certain pathogen has been encountered. if the pathogen enters again, they will divide rapidly into many clones of T killer cells and destroy them quickly.
T regulator cells
These cells will control and suppress the immune system. This means that when a pathogen has been removed and everything is normal, the immune system needs to be stopped. They also make sure the body can recognise a self antigen so it doesn’t produce an autoimmune response.
B lymphocytes
They are covered in antibodies that will bind with antigens. There are: Plasma cells, B effector cells and B memory cells
Plasma cells
This produces many antibodies for a specific antigen and releases them into the blood stream so they can produce an immune response. These don’t live long but they produce around 2000 antibodies.
B effector cells
These will divide to form clones of plasma cells
B memory cells
They are part of the immunological memory and love for a long time. they are programmed to remember a specific type of antigen to produce a rapid immune response when necessary.
Cell Mediated Immunity
The T lymphocytes will respond to the cells of an organism that have been altered in some way. That could be virus infection or mutation (cancer cells) etc…
- If a pathogen is present, the macrophages will engulf them by phagocytosis and become an antigen presenting cell
- The receptors on T helper cells will fit the antigens and produce interleukins which will stimulate more clones of the T helper cells to be made by mitosis. They will carry the right receptors to bind to the pathogen
- The cloned T cells may develop into T memory cells, produce interleukins to make B cells divide or stimulate more phagocytosis. They could also become T killer cells to destroy infected cells.
Humoral Immunity
This is when antibodies are produced and released into the blood so they aren’t attached to any cell. This is when antigens are found outside the cells.
When a pathogen enters the body, it will either have antigens on it or will release toxins which act as antigens. The B cell that has complimentary antibodies to the antigen will bind to them and engulf them to become APCs.
Clonal Selection
Once the APC has been made by the B cell, the T helper cell that has been activated will bind to the APC. This is called clonal selection as the B cell that can fight off the pathogen with it’s antibody is selected to be cloned.
Clonal Expansion
The T helper cells that have bound to the B cell in clonal selection will then release interleukins to activate the B cells. These B cells will then divide by mitosis to give clones of the plasma cells and B memory cells which is clonal expansion
Primary Immune Response
This is when cloned plasma cells that have been produced as a result of clonal expansion and have the complimentary antibodies to bind to the antigen, will bind to it and disable them or act as opsonins or agglutinins. It can take weeks for this to become effective and for there to be enough plasma cells to fight the pathogen which is why we get ill because it’s the result of our body reacting when pathogens are dividing freely, before the immune response can act properly.
Why is the primary response slow?
It’s slow because there aren’t many of the complimentary plasma cells and B cells needed to fight off the pathogen, so more need to be produced.
Secondary Immune Response
Some of the B plasma cells will develop into B memory cells which stores information about the specific antigen it was fighting before. If the pathogen enters again, the B memory cells will rapidly divide into plasma cells and it will produce the right antibody to wipe out the pathogen very quickly before symptoms of the disease start to show.
Autoimmune Diseases
This is when the body no longer recognises ‘self antigens’ and will start destroying body tissues. This could be because of genetics, because of a mild pathogen that gives bad reactions or the T regulator cells aren’t working effectively. It can cause mass inflammation or even destruction of healthy organs and tissues. Some people can be given immunosuppressant drugs to combat this.
Type of autoimmune diseases
Type 1 diabetes, Lupus and Rheumatoid Arthritis
Type 1 Diabetes
This is when the insulin secreting pancreatic cells are attacked. It can be managed with insulin injections, pancreatic transplant or immunosuppressant drugs but there is no cure. They are looking at stem cell treatments.
Rheumatoid Arthritis
This is where your joints in your hands, feet, wrists and ankles. It is treated with pain relief, anti inflammatories, steroids etc.. There is no cure
Lupus
It affects the skin and joints and causes fatigue. It can attack any organ e.g. the kidney, liver etc… You can use anti-inflammatories, steroids, transplants etc… but no cure.
