HLA AND CANCER
The theoritical model, which explains the manner through which there is unrestrained growth of cells that are different from those of the tissue from which they originate, is based on the modification of surface molecules that determine the recognition of celf-cells by the immunes ystem. Tumour cells do not respond to the regulatory stimuli that normally limit tissue proliferation. Carcinogens and oncogenic viruses activate gens that destabilize cell proliferation and repair. As a result, some cell-surface antigens are lost and others are expressed. At the end of this process, the tumour may no longer be recognized by the immune system. Structural and functional changes in HLA, loss of expression of tumour antigens, lack of co-stimulatory molecules and production of immunosuppresive cytokines are some of the possible mechanisms that cause tumour cells to escape immune surveillance.
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