Receptor editing is a process that occurs during the maturation of B cells, which are part of the adaptive immune system. This process forms part of central tolerance to attempt to change the specificity of the antigen receptor of self reactive immature B-cells, in order to rescue them from programmed cell death, called apoptosis.[1] It is thought that 20-50% of all peripheral naive B cells have undergone receptor editing making it the most common method of removing self reactive B cells.[2]

During maturation in the bone marrow, B cells are tested for interaction with self antigens, which is called negative selection. If the maturing B cells strongly interact with these self antigens, they undergo death by apoptosis. Negative selection is important to avoid the production of B cells that could cause autoimmune diseases. They can avoid apoptosis by modifying the sequence of light chain V and J genes (components of the antigen receptor) so that it has a different specificity and may not recognize self antigens anymore. This process of changing the specificity of the immature B cell receptor is called receptor editing.

References

  1. ↑ Meffre, E; Wardemann, H (2008). "B-cell tolerance checkpoints in health and autoimmunity". Current Opinion in Immunology. 20 (6): 632–638. doi:10.1016/j.coi.2008.09.001. PMID 18848883.
  2. ↑ Halverson R, Torres RM, Pelanda R (2004). "Receptor editing is the main mechanism of B cell tolerance toward membrane antigens". Nature Immunology. 5 (6): 645–650. doi:10.1038/ni1076. PMID 15156139. S2CID 20869465.
    3. Kleinfield R, Hardy RR, Tarlinton, D (1986). 'Recombination between an expressed immunoglobulin heavy-chain gene and a germline variable gene segment in a          
Ly1+ B-cell lymphoma'. Nature 322 (6082): 843-6.
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