The interaction between an antigen and its specific cell surface receptor may result either in the activation and differentiation of the cell (positive selection) or in its inactivation or even death (negative selection). Positive selection usually results in a cell leaving G0 and entering the cell cycle giving rise to a clone of increasingly differentiated effector cells, e.g. cytotoxic T cells and plasma cells. This process is known as clonal selection. By contrast, when an antigen-receptor interaction results in negative selection leading to cell death, it is known as clonal deletion (Figure 4.13). Although only a single cell is destroyed, the host has lost the potential to develop the clone of cells that would recognise the epitope in question. When the self-reactive cell is not killed but made functionally inactive the outcome is known as clonal anergy.
The theory of clonal deletion was proposed first by Burnett to explain the lack of self-reactivity in the immune system. This suggested that all cells bearing receptors which recognise self-antigen were destroyed, thus preventing the development of an autoimmune response. Death usually results from the induction of apoptosis (often referred to as cellular suicide or programmed cell death) in the self-reactive cells.
An autoimmune response is one directed against antigens expressed by the host's own tissues (auto) which leads to tissue damage. If the antigen is restricted to one particular organ or tissue (e.g. the thyroid), the resulting signs and symptoms are typical of a disease affecting that organ. However, if the antigen is expressed in several tissues or organs, the signs and symptoms will be more generalised.
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