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For some diseases, the TCR code is highly restricted. In the case of immunodeficiencies, the TCR does not recognize autologous MHC molecules, resulting in the presentation of self-antigens. Although this is not a disease of the immune system, it can be dealt with by matching the TCR with a different set of MHC molecules, or by introducing HLA-transgenic mice into the situation. In order to match the TCR with the appropriate MHC molecule, an enormous range of possibilities is now easily available. This can be a practical problem for a patient in whom a disease of the immune system is not known. Patients with these conditions are referred to as having immunodeficiency disorders. Certain TCRs are encoded by genes that have deletions, mutations or translocations. These result in defective T cells. This can be due to a defect of the chain of machinery that transports TCR into the cell. Alternatively, the cell can be unable to assemble a functional TCR. This is the case for T cells that undergo apoptosis (programmed cell death) following receptor activation. Some patients have a lack of the necessary signals required to activate these cells (see Chapter 5). As is common in such situations, the immune system is not working properly and the patient is susceptible to infection and cancer. Finally, some patients are unable to express TCRs that can recognize autologous MHC molecules. This is caused by a mutation in a gene involved in the assembly of TCR (see Chapter 6).
Once TCR genes have been identified, they are introduced into the cells of interest. Such cells include B cells, NK cells and the various types of T cells. The process of gene transfer, and the conditions that have to be met, are described in the chapters on these cells. In the case of B cells, gene transfer is relatively straightforward. This is because they are relatively small, they are always associated with each other and they do not have a long life. The result is that there are few restrictions on the number of times a gene can be introduced into them. In contrast, T and NK cells are much larger and they have a much longer life. When gene transfer is attempted, the target cells are very sensitive to the method used and the process is quite often unsuccessful.
Like microbial vaccines, autoantigens are generally not very immunogenic and do not induce strong immune responses. A number of strategies have been developed to improve their immunogenicity. Most importantly, they need to be presented in a way that will induce the immune system to mount an effective immune response. One approach is to use adjuvants.
A final approach to ameliorating autoimmune disease is through vaccination. Until now this has been the approach that has taken the greatest interest. Vaccines are designed to induce immunity to microbial pathogens. They are made by taking microbial cells or parts of them, and exposing them to the immune system so that it can recognize them and mount an effective immune response. This is the approach that has been used for decades to produce vaccines against polio, measles, and a number of other infections that cause significant morbidity and mortality. This strategy is also the foundation of vaccination against cancer. It is now time to apply this approach to other diseases. Autoimmune disease is one such disease. The immune system is able to recognize and mount an effective immune response to microbial antigens, so the idea is to take advantage of this mechanism to generate immunity to autoantigens. 827ec27edc