a reasonable if fairly narrow essay (narrow in subject that is) can't remember
How does the body achieve the functional silencing of antigen reactive clones?
The central tenet of the immune system is the ability to recognise and remove non-self components without affecting self components. The T cells and B cells of the immune system express a vast repertoire of antigen receptors. It is thought that the germline TCR repertoire is composed of in the region of at least 109 different specificities. Considering the potential number of antigens that may be bound by these receptors it is inevitable that a proportion of them will be targeted against self components.
Tolerance in the T cell repertoire.
three T cell mechanisms for self tolerance: clonal deletion, clonal anergy and antigen specific suppressor T cells.
Burnet proposed theory of clonal deletion in 1955.
Marrack (1987) showed that T cells bearing receptors containing a member of the Vb17 family were absent from mice expressing the MHC class-II molecule I-E, with which the Vb17 chain is reactive.
Further support has been provided by the absence of self-reactive clones in mice expressing a superantigen such as minor lymphocyte stimulating antigen - an antigen which binds to the TCR in a manner that is independent of the Va chain and thus binds a much larger proportion of T cells than conventional antigens.
in the thymus self reactive TCR present at the CD4+8+stage, not at the CD4+8- or CD4-8+ stage ÃÂ deletion occurred during thymocyte development.
There is evidence that deletion occurs while thymocytes are in their double positive state -
CD8+ thymocytes bearing receptors specific for class II MHC molecules are deleted during thymocyte development - surprising since CD8+cells are usually MHC I restricted
If deletion was mediated via an interaction between TCR/CD8 and...