Rejection of an Organ
The rejection of an organ is determined by the similarity between patient and donor MHC class makers. The more indistinguishable difference between MHC class markers the higher the chance that T and B cells will recognise the cells as self, increasing the chance success.
When an organ is placed into a person T helper cells determine whether or no to classify the cells as self or non-self considering MHC class makers. If the T helper cells concludes that the cell is foreign, then it signals a cascade of events to occur. A B cell that is specific to the foreign antigen binds to the cell which then causes the B cells to multiply into plasma B cells and memory B cells, spreading antibodies and killing off all infected cells.
This is a problem as it could potentially kill of the organ that has been transplanted into the body, causing organ rejection. This makes the patient incredibly sick , showing signs of fever, inflammation and body aches as the third line of defence takes place. Plasma B cells create mass amount of antibodies specific to the antigen, so when a B cells binds to an antigen it replicates to try and kill of cells presenting the specific antigen (antigen-presenting cells)
To prevent the activation of T cells a series of drugs must be taken constantly for the rest of the patients life. These drugs are called immunosupressions, which suppress or reduce the immune system. There are four classes of iummunosupressions; azathioprine, cyclosporine, monoclonal antibodies and prednisone. Although these drugs prevent organ rejection, the increase chances of infection as immune system is lowered. There is a higher risk of cancer as T cells are down which activate B cells as the body is less resistant. The specific drug given to the patient (depends or how serious case is) must be taken regularly, if the patient were to stop taking the drug then the body immune levels will increase threatening to kill the organ. The medicines may also cause high blood pressure and high cholesterol and increase the risk for diabetes.
When an organ is placed into a person T helper cells determine whether or no to classify the cells as self or non-self considering MHC class makers. If the T helper cells concludes that the cell is foreign, then it signals a cascade of events to occur. A B cell that is specific to the foreign antigen binds to the cell which then causes the B cells to multiply into plasma B cells and memory B cells, spreading antibodies and killing off all infected cells.
This is a problem as it could potentially kill of the organ that has been transplanted into the body, causing organ rejection. This makes the patient incredibly sick , showing signs of fever, inflammation and body aches as the third line of defence takes place. Plasma B cells create mass amount of antibodies specific to the antigen, so when a B cells binds to an antigen it replicates to try and kill of cells presenting the specific antigen (antigen-presenting cells)
To prevent the activation of T cells a series of drugs must be taken constantly for the rest of the patients life. These drugs are called immunosupressions, which suppress or reduce the immune system. There are four classes of iummunosupressions; azathioprine, cyclosporine, monoclonal antibodies and prednisone. Although these drugs prevent organ rejection, the increase chances of infection as immune system is lowered. There is a higher risk of cancer as T cells are down which activate B cells as the body is less resistant. The specific drug given to the patient (depends or how serious case is) must be taken regularly, if the patient were to stop taking the drug then the body immune levels will increase threatening to kill the organ. The medicines may also cause high blood pressure and high cholesterol and increase the risk for diabetes.