Clonal deletion

[1][2] The process of clonal deletion helps prevent recognition and destruction of the self host cells, making it a type of negative selection.

[3] Clonal deletion can help protect individuals against autoimmunity, which is when an organism produces and immune response on its own cells.

[4][5] The combination of Traub's evidence and Owens' observations helped Burnet and his partner, Frank Fenner, to propose that 'self' markers for host cells were determined at an embryonic state.

[2][5] In part of this hypothesis, Burnet stated that an auto-reactive lymphocyte would be terminated before maturation in order to prevent further proliferation.

As a T or B lymphocyte develops, they can rearrange their genome in order to express a unique antigen that will recognize a specific epitope on a pathogen.

[2] It is important to note that not all lymphocytes expressing high affinity for self-antigen undergo clonal deletion.

[7] However, for both B and T cells in the primary lymphoid organs, clonal deletion is the most common form of negative selection.

[3] If the BCR demonstrates a high affinity attraction to self-antigen then clonal deletion can occur at this point.

Examples of mechanisms used in peripheral tolerance against auto-reactive B lymphocytes include anergy, and antigen receptor desensitization.

[2] Complete clonal deletion can lead to opportunities for molecular mimicry, which has adverse effects for the host.

[2] Clonal deletion provides an incentive for microorganisms to develop epitopes similar to proteins found within the host.

Because most autoresponsive cells undergo clonal deletion, this allows microorganisms with epitopes similar to host antigen to escape recognition and detection by T and B lymphocytes.

[2] Superantigens are composed of viral or bacterial proteins and can hijack the clonal deletion process when expressed in the thymus because they resemble the T-cell receptor (TCR) interaction with self MHC/peptides.